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Healing Of Oral Wounds Important Notes

1. Types Of Healing
   • Healing by the first Intention
     • Hero edges of the wound are approximated
     • The healing process is fast
   • Healing by secondary intention
     • There is tissue loss, wound edges cannot be opposed
     • The wound contracts to reduce in size, granulation tissue fills the wound and epithelisation occurs
     • This is healing by secondary intention
2. Factors Affecting Healing
   • Physical factors
     • Location of wound – A wound in an area with a good vascular bed heals more rapidly
     • Immobilization – constant movement causes disruption of new connective tissue formation
     • Severe trauma – arrest rapid healing
     • Local temperature
       • Hyperthermia – accelerates healing
       • Hypothermia – delays healing
     • X-ray radiations
       • Low doses – stimulates healing
       • Large doses – suppresses healing
     • Anaemia – delays healing
     • Age of patient
       • Young patient – heals rapidly
       • Elder patient – healing is retarded
   • Nutritional factors – protein, vitamin deficiency delays healing
   • Hormonal factors – ACTH and cortisone inhibit the growth of granulation tissue formation
     • Diabetes mellitus – retards repair of wound
3. Types Of Biopsy
   • Incisional – removal of small piece for examination
   • Excisional – total excision of small lesion
4. Methods Of Biopsy
   • Surgical excision by scalpel
   • Surgical removal by cautery
   • Laser
   • Removal by biopsy forceps
   • Aspiration
   • Exfoliative cytology technique
5. Result Of The Cytology Smear
   • Class 1 – Normal – only normal cells are observed
   • Class 2 – Atypical – Presence of minor atypia
   • Class 3 – Indeterminate – Wider atypia, represents precancerous lesion
   • Class 4 – Suggestive of cancer – few malignant cells, many cells with borderline characteristics
   • Class 5 – positive for cancer – malignant cells present
6. Complications Of Fracture Wounds
   • Delayed union
   • Fibrous union
   • Nonunion
   • Lack of calcification
7. Storage Media For The Preservation Of Teeth
   • Milk
   • Saliva
   • Saline
   • HBSS
   • Propolis
   • Viaspan
   • Coconut water
8. Types Of Oral Implants
   • Endodontic
   • Endosseous
   • Subperiosteal

Healing Of Oral Wounds Short Question And Answers

Question 1. Write about the healing of extraction wound and mention its complications
Answer:

Healing Of Extraction Wound

1. Immediate reaction
   • Coagulation of blood
   • Entrapment of RBC into fibrin mesh
   • Vasodilation and engorgement of blood vessels
   • Mobilization of leukocytes
   • Presence of areas of contraction of clot
2. First week
   • Growth of fibroblast into wound
   • Formation of granulation tissue
   • The proliferation of epithelium at the periphery
   • The osteoblastic activity of alveolar bone
   • Organization of blood clot
3. Second week
   • Penetration of new capillaries into centre of clot
   • Degeneration of remnants of PDL
   • Fraying of bony socket
   • Epithelium proliferation at periphery
   • Fragments of necrotic bone
4. Third week
   • Complete formation of granulation tissue
   • Presence of young trabeculae
   • Early bone formation
   • Remodeling of cortical bone
5. Fourth week
   • Bonefilling
   • Healing of crest of the bone

Read And Learn More: Oral Pathology Question And Answers

Healing of Extraction Wound Complications:

1. Dry socket
   • It is focal osteomyelitis of the tooth socket in which the blood clot has disintegrated or been lost
   • Dry socket Clinical Features:
     • Loss of blood clot
     • Radiating pain
     • Foul odour
     • Metallic taste
2. Fibrous healing of extraction wound
   • Occurs when extraction is accompanied by loss of lingual and labial or buccal cortical plates and periosteum
   • It is asymptomatic
   • Fibrous Healing Of Extraction Wound Treatment
     • Excision of lesion
     • Bony repair

Question 2. Dry socket
Answer:

Dry Socket

Dry Socket is focal osteomyelitis of the tooth socket in which the blood clot has disintegrated or been lost

Dry Socket Etiology:

1. Bim’s hypothesis

2. Nitzan’s theory

• Suggests a relationship between the fibrinolytic activity of anaerobic bacteria and dry socket

Dry Socket Predisposing Factors:

• Infection
• Decreased blood supply
• Debilitating conditions

Dry Socket Clinical Features:

• Loss of blood clot
• Radiating pain
• Foul odour
• Metallic taste

Dry Socket Management:

• Irrigation of socket
• Smoothening of bony margins
• Packing with pompom
• Analgesics
• Hot saline mouth bath
• Chemical cauterization
• Regular follow up

Dry Socket Prevention:

• Doing extraction gently
• Instruct the patient not to rinse for 24 hours
• Prescribe vitamin B complex and vitamin C

Question 3. Exfoliative cytology
Answer:

Exfoliative Cytology

Exfoliative cytology is introduced by Papanicolaou and Traunt

Exfoliative Cytology Indications:

• Herpes simplex
• Herpes zoster
• Pemphigus Vulgaris
• Pemphigoid
• Squamous cell carcinoma
• Aphthous ulcer
• Candidiasis

Exfoliative Cytology Technique:

Exfoliative Cytology Results:

Question 4. Factors affecting the healing of oral wound
Answer:

Factors Affecting The Healing Of Oral Wound

1. Age
   • Faster healing occurs in younger individuals compared to older individuals
2. Type of tissue
   • Fast healing occurs in epithelial tissues
   • Delayed healing in neural tissues
3. Location of wound
   • Good vascular area- fast healing
4. Mobility of wound
   • Movement of the site of wound delays healing
5. Trauma
   • Mild trauma- fast healing
   • Severe trauma- retards healing
6. Local temperature
   • High temperature- Fast healing
   • Low temperature- delay healing
7. Radiation
   • Low dose- stimulates healing
   • High dose- Retards healing
8. Nutritional factors
   • Nutritional deficiency- delays healing
   • Vitamins and proteins- speed up healing
9. Infections
   • Low-grade infection- stimulates healing
   • Severe infections- interfere with healing
10. Hormonal factors
    • Trephones- accelerate healing
    • ACTH, cortisone- delays healing

Question 5. Healing of fractured wound
Answer:

Healing Of Fractured Wound

• Bleeding occurs immediately at the site of the fracture, hematoma is formed which is converted into blood clot
• Stages of healing
• Stage 1 – formation of fibrous callus
  • The proliferation of fibroblasts and endothelial cells in the bone marrow as periosteum
  • These cells enter the fracture site and organise the clot
  • Development of edema
  • Inflammatory cell infiltration
  • Removal of necrotic cells, connective tissue, and bone fragments from fracture site by phagocytosis, proteolysis and osteolysis
  • Replacement of clot by granulation tissue
  • Formation of fibrous callus at fracture site
• Stage 2 – Formation of primary bone callus
  • Replacement of fibrous callus by immature bone
  • Formation of primary bone callus
  • Fibrous and primary bone callus binds the fracture fragments of bone together
• Stage 3 – Formation of secondary bone callus
  • Replacement of primary bone callus by mature bone
  • Remodelling of secondary callus by resorption
  • Restoration of normal jaw outline

Question 6. Biopsy
(or)
Types of biopsy
Answer:

Biopsy

Biopsy is the removal of part of tissue for the purpose of histological examination and analysis

Types Of Biopsy

Question 7. Complications of wound healing
Answer:

Complications Of Wound Healing

1. Infection
   • Wounds provide a portal of entry to microorganisms and result in infection
2. Keloid and hypertrophic scar formation
   • Keloids are overgrown scar tissues
   • Hypertrophic scars are more cellular and vascular
3. Hypopigmented or hyperpigmented areas
4. Cicatrization
   • It refers to late reduction in the size of scar
5. Implantation cyst
   • Epithelial cells may get entrapped in the wound and proliferate to form cyst

Question 8. Reimplantation
Answer:

Reimplantation

Reimplantation refers to the insertion of a vital or nonvital tooth into the same alveolar socket from which it was removed

Reimplantation Indications:

• Broken instruments in canals
• Presence of foreign body In periapical tissue
• Tooth apex present in close proximity to nerve and vessels
• Inaccessible areas
• Persistent chronic pain
• Accidental avulsion of tooth

Reimplantation Contraindications:

• Medically compromised
• Periodontal involvement
• Missing buccal/lingual plate
• Nonrestorable tooth

Reimplantation Technique:

Question 9. Complications of healing of extraction socket
Answer:

Complications Of Healing Of Extraction Socket

1. Dry socket
   • It is focal osteomyelitis of the tooth socket In which the blood clot has disintegrated or been lost
   • Clinical features
     • Posh of blood dot
     • Radiating pain
     • Foul odour
     • Metallic taste
2. Fibrous healing of extraction socket
   • Occurs when extraction Is accompanied by loss of lingual or buccal cortical plates and periosteum
   • It is asymptomatic

Healing Of Oral Wounds Viva Voce

1. Healing refers to the replacement of damaged tissue by living tissue to restore function
2. Replacement of lost tissue by granulation tissue is called repair
3. Cicatrization refers to late reduction in the size of scar
4. Biopsy refers to removal of tissue from a living organism for the purpose of microscopic examination and diagnosis
5. Granulation tissue formation occurs in healing by secondary intention
6. Exfoliative cytology is the study of cells that exfoliate or abraded from body surfaces
7. Replantation refers to the insertion of a vital or nonvital tooth into same alveolar socket from which it was removed or lost
8. Dry socket is most common and painful complication in the healing of extraction wound
9. Implants are any foreign material fixed or inserted into body tissue
10. Osseointegration is a direct structural and functional connection between ordered living bone and the surface of a load-carrying implant

Regressive Alteration Of The Teeth Important Notes

1. Types Of Secondary Dentin
   • Physiological
     • Secondary Dentin is a regular, uniform layer of dentin around the pulp chamber that is laid down throughout the life of the tooth as a result of age and tooth eruption
   • Reparative secondary dentin
     • Reparative secondary dentin is the dentin that forms around the pulp chamber in response to irritation or attrition
2. Forms Of Pulp Calcifications
   • Discrete pulp stones (denticles)
     • True denticles
       • They are made up of localized masses of calcified tissue that resemble dentin because of their tubular structure
       • They are further divided into
         • Free denticles and
         • Attached denticles
     • False denticles
       • Composed of localized masses of calcified material
       • They do not exhibit dentinal tubules
   • Diffuse calcification
     • Mostly seen in the root canals

Regressive Alteration Of The Teeth Short Question And Answers

Question 1. Describe in detail regressive alterations of teeth
Answer:

Regressive Alterations Of Teeth:

• Regressive Alterations Of Teeth are a group of retrogressive changes in the teeth occurring due to nonbacterial causes and resulting in
• wear and tear of tooth structure along with Impairment of function
• Regressive Alterations Of Teeth are
  • Attrition
  • Abrasion
  • Erosion

Question 2. Classify resorption of teeth. Describe external resorption.
Answer:

Resorption Of Teeth: Resorption of teeth can be defined as chronic progressive damage or loss of tooth structure due to the action of odontoclasts

Resorption Of Teeth Classification:

1. Physiological
   • Resorption of roots of deciduous teeth
2. Pathological
   • External resorption
   • Internal resorption

Resorption Of Teeth External Resorption:

• Pathological resorption that begins peripherally on the surface of the tooth root and moves toward the pulp is called external resorption

Resorption Of TeethCauses:

• Periapical inflammation
• Reimplantation of teeth
• Tumors and cysts
• Excessive mechanical or occlusal forces
• Impaction of teeth

Resorption Of Teeth Radiographic Features:

• Loss of continuity in peripheral and external outlines of teeth
• Root canals are intact
• Presence of blunting of root apex
• Larger lesions produce a moth-eaten appearance due to irregular or uneven destruction of tooth
• External resorption in apical regions appears as if the root canal-filling materials are projecting beyond the apex
• Obliteration of PDL space

Read And Learn More: Oral Pathology Questions and Answers

Resorption Of Teeth Complications:

• Loss of vitality of the tooth
• Risk of fracture of the tooth
• Ankylosis of teeth

Question 3. Hypercementosis
Answer:

Hypercementosis Definition: It is a prominent thickening of cementum on the root surfaces of the tooth due to excessive cementogenesis

Hypercementosis Etiology:

• Accelerated elongation of a tooth
• Periapical inflammation
• Tooth repair
• Paget’s disease of bone
• Mechanical stimulation- orthodontic forces
• Functionless or unerupted teeth

Hypercementosis Types:

• Localized
• Generalized
• Clinical Features:
• Asymptomatic
• Identified on routine radiograph

Hypercementosis Radiographic Appearance:

• Thickening and apparent blunting of the roots
• Rounding of the root apex
• Well-defined periodontal space
• Histological Features:
• Excessive deposition of cellular and acellular cementum
• This occurs over the entire root or only at the root apex
• This cementum is arranged in concentric layers

Hypercementosis Complications:

• Obliteration of periodontal space
• Ankylosis of tooth
• Difficulty in extraction
• Concrescence of teeth

Question 4. Age changes in pulp
Answer:

Age Changes In Pulp

• Age Changes In Pulp
• Decreased cellularity
• Increased vascularity
• Increased fibrosis
• Impaired pulpal response to tissue injury
• Decrease in pulpal volume
• Pulp calcification- pulp stones
• Pulp Stones/ Denticles:
• Deposition of calcified mass within the dental pulp for no apparent reason is called pulp calcification

Age Changes In Pulp Types:

• Depending on the microscopic structure

• Depending upon location

Question 5. Internal resorption or Pink tooth of mummery
Answer:

Internal Resorption Or Pink Tooth Of Mummery

Internal resorption refers to the resorption process that starts internally within the tooth itself and the dentin is gradually resorbed from the pulpal side toward the periphery

Internal Resorption Or Pink Tooth Of Mummery Etiopathogenesis:

• Hyperplastic pulpal tissues occupy the spaces created due to dentinal re4sorption

Internal Resorption Or Pink Tooth Of Mummery Clinical Feature:

• Can involve the crown portion or root portion of teeth
• Any tooth can ho Involved
• Initially asymptomatic
• Later there Is the appearance of the pink-hued area on the crown of the tooth
• Also known as the pink tooth of mummery
• The affected tooth is vital

Internal Resorption Or Pink Tooth Of Mummery Radiographic Features:

• The involved tooth shows a round or ovoid radiolucent area In the central portion of the tooth
• Well well-defined, spherical-shaped, radiolucent area occurs in dentin
• The external outline of the tooth is intact

Internal Resorption Or Pink Tooth Of Mummery Types:

• Internal inflammatory resorption
• Internal replacement resorption

Internal Resorption Or Pink Tooth Of Mummery Treatment:

• Extirpation of pulp
• Endodontic treatment
• Extraction

Question 6. Age changes in dentin
Answer:

Age Changes In Dentin

1. Formation of secondary dentin
   • It causes
     • Reduction in size of pulp chamber
     • Obliteration of pulp chamber
2. Dentinal sclerosis
   • This occurs due to the continued production of peritubular dentin
   • It causes
     • More brittle roots
     • Increased translucency of roots

Question 7. Attrition
Answer:

Attrition Definition Loss by wear of surface of tooth or restoration caused by tooth tooth-to-tooth contact during mastication or parafunction

Attrition Clinical Features:

• Wear on occluding surfaces
• Shiny facets on amalgam contacts
• Fracture of cusps or restorations

Attrition Types:

• Physiological-Causes
• Old age- increasing age causes attrition
• Pathological-causes
• Abnormal occlusion
• Premature extraction of teeth
• Abnormal chewing habits
• Structural defects in teeth

Question 8. Abrasion
Answer:

Abrasion Definition: Loss by wear of dental tissue caused by abrasion by foreign substances

Abrasion Clinical Features:

• Located at cervical areas of teeth
• Lesions are more wide than deep
• Premolars and cuspids are commonly affected
• Saucer shaped indentations
• Smooth, shiny surface

Question 9. Erosion
Answer:

Erosion Definition Progressive loss of hard dental tissue by a chemical process not involving bacterial action

Erosion Causes:

• Intrinsic causes
• Eating disorders
• Gastrointestinal disorders
• Chronic alcoholism
• Pregnancy morning sickness
• Extrinsic causes

Erosion Clinical Features:

• Broad concavities within smooth surface enamel
• Cupping of the occlusal surface
• Increased incisal translucency
• Wear on non-occluding surfaces
• Raised amalgam restorations
• The clean, non-tarnished appearance of amalgams
• Preservation of enamel cuff in gingival service
• Hypersensitivity
• Pulp exposure in deciduous teeth

Question 10. Pink Tooth
Answer:

Pink Tooth

Pink Tooth occurs due to internal resorption

Pink Tooth Clinical Features:

• Can involve the crown portion or root portion of teeth
• Any tooth can be involved
• Initially asymptomatic
• Later there is the appearance of the pink-hued area on the crown of the tooth
• So it is known as the pink tooth of mummery
• The affected tooth is vital

Question 11. Cementicles
Answer:

Cementicles

• The calcified bodies found in the periodontal ligament are called cementless
• These bodies are seen in older individuals

Cementicles Appearance:

• May remain free in the connective tissue
• May join with the cementum
• May fuse into large calcified masses

Cementicles Origin: Degenerated epithelial cells from the nidus for the calcification of cementless

Question 12. Hypercementosis
Answer:

Hypercementosis Definition: It is a prominent thickening of cementum on the root surfaces of the tooth due to excessive cementogenesis

Hypercementosis Etiology:

• Accelerated elongation of a tooth
• Periapical inflammation
• Tooth repair
• Paget’s disease of bone
• Mechanical stimulation- orthodontic forces
• Functionless or unerupted teeth

Hypercementosis Types:

• Localized
• Generalized

Hypercementosis Clinical Features:

• Asymptomatic
• Identified on routine radiograph

Hypercementosis Radiographic Appearance:

• Thickening and apparent blunting of the roots
• Rounding of the root apex
• Well-defined periodontal space

Question 13. Secondary dentin
Answer:

Secondary Dentin

• Secondary Dentin is a narrow band of dentin bordering the pulp
• Secondary Dentin represents continued, slower deposition of dentin by odontoblasts
• There is greater deposition on the roof and floor of the chamber than on other parts
• Secondary Dentin contains fewer tubules which sclerose more readily
• This reduces the overall permeability of the dentin
• Due to the regular arrangement of dentinal tubules, it is also called regular secondary dentin

Question 14. Factors causing external resorption of teeth
Answer:

Factors Causing External Resorption Of Teeth

• Periapical inflammation
• Reimplantation of teeth
• Tumors and cysts
• Excessive mechanical or occlusal forces
• Impaction of teeth
• Idiopathic

Question 15. Dead tracts
Answer:

Dead Tracts

• Dentinal tubules are emptied by complete retraction of the odontoblast process from the tubule or through death of the odontoblast
• The dentinal tubules then become sealed off so that in-ground section air-filled tubules appear by transmitted light as black dead tracts
• They are most often in coronal dentin
• Frequently bound by bands of sclerotic dentin
• These areas demonstrate decreased sensitivity
• They are the initial step in the formation of sclerotic dentin

Regressive Alteration Of The Teeth Viva Voce

1. Attrition is defined as the physiological wearing away of tooth surface as a result of tooth to tooth contact
2. Abrasion is the pathological wearing away of tooth substance through some abnormal mechanical process.
3. Erosion is defined as the irreversible loss of dental hard tissue by a chemical process that does not involve bacteria
4. Abfraction is loss of tooth surface at cervical areas of teeth caused by tensile and compressive forces during tooth flexure
5. Dentinal sclerosis is a regressive alteration in tooth substance that is characterized by calcification of the dentinal tubules
6. Sclerotic dentin under carious lesion is harder than adjacent normal dentin
7. Secondary dentin is the dentin that is formed and deposited in response to normal/ slightly abnormal stimulus after root completion
8. Hypercementosis is the excessive deposition of cementum on the root surface
9. Cementicles are small foci of calcified tissue not necessarily true cementum which lie free in the periodontal ligament of the lateral and apical root areas.

Spread Of Oral Infections Important Notes

1. Ludwig’s Angina
   • Ludwig’s angina is an overwhelming diffuse, suppurative cellulitis, which simultaneously involves the submandibular, sublingual, and submental space.
   • Ludwig’s Angina produces a rapidly spreading, large, diffuse, and broad-like aggressive swelling; which involves the upper part of the neck and floor of the mouth bilaterally with brawny induration, swelling causes elevation of the tongue.
   • The enlarged tongue may protrude outside the mouth and the condition is called woody tongue.
   • Bull neck
   • Ludwig’s Angina Complications
     • Cavernous sinus thrombosis,
     • Meningitis,
     • Brain abscess and
     • Suppurative encephalitis, etc.
     • Death due to asphyxia
2. Focal Infection
   • Metastases of microorganisms or their toxins from a localized site of infection to any distant part of the body with subsequent injury are called “focal infections.”
3. Focus Of Infection
   • A circumscribed area of tissue, which is infected by exogenous pathogenic organisms and is usually located near the skin or mucosal surface is called a focus of infection.
4. Cellulitis
   • Cellulitis is a diffuse inflammation of soft tissues that tends to spread through tissue spaces and along fascial planes
   • Causative organisms – streptococci and anaerobes
   • Cellulitis Clinical features
     • The patient is moderately ill with increased temperature and leukocytosis
     • Swelling is painful, diffuse, firm, and brawny
     • The overlying skin is inflamed
     • Regional lymphadenitis is present
     • Treatment
       • Administration of antibiotics
5. Spread Of infection
   
   
6. Maxillary Sinusitis
   • Maxillary Sinusitis is an acute or chronic inflammation of sinusitis
   • Maxillary Sinusitis Features
     • Moderate to severe pain in the sinus region
     • Discharge of pus into the nose with fetid breath
   • Water’s view is a radiographical technique used for it
   • Clouding of the maxillary sinus is seen over radiograph
7. Cavernous Sinus Thrombosis
   • Cavernous Sinus Thrombosis is characterized by the formation of septic thrombi within the cavernous sinus and its numerous communicating branches
   • Sources of infection
     • External source
       • Infection from face
     • Internal source
       • Periapical abscess
       • Otitis media
       • Fracture of skull
       • Meningitis
       • Septicaemia
   • Cavernous Sinus Thrombosis Clinical features
     • Tachycardia, tachypnoea
     • Stiffness of neck
     • Photophobia
     • Increased lacrimation
     • Proptosis
     • Chemosis
     • Dilatation of pupil
     • Paralysis of extraocular muscles
     • Fixation of eyeball
     • Complete paralysis of 3rd, 4rd and 6th cranial nerves

Spread Of Oral Infections Short Question And Answers

Question 1. Describe in detail chronic osteomyelitis affecting the jaw.
Answer:

Chronic Osteomyelitis

Chronic Osteomyelitis is defined as the inflammation of bone and bone marrow along with the surrounding periosteum

Chronic Osteomyelitis: Osteomyelitis persisting for more than one month is known as chronic osteomyelitis

Chronic Osteomyelitis Causative Organism:

• Staphylococci
• Streptococci
• Bacteroids
• Actinomyces

Chronic Osteomyelitis Pathogenesis:

Chronic Osteomyelitis Clinical Features:

• Age- before 20 years of age
• Site- Mandibular first molar is commonly affected
• Fever, tachycardia
• Mild and vague pain
• Insidious in nature
• jaw swelling
• Mobility of teeth
• Sinus tract formation
• Purulent discharge
• Anesthesia and paraesthesia of lip
• The affected tooth is carious

Chronic Osteomyelitis Radiographic Features:

• The moth-eaten appearance of lesion
• Ill-defined radiolucency with ragged borders
• Radiolucency with multiple radiopaque foci within it represents sequestra
• A dense zone of radiopacity with faint radiolucency at the margin

Chronic Osteomyelitis Histopathology:

• Accumulation of exudates and pus within medical spaces
• Presence of inflammatory cells like lymphocytes, plasma cells, and macrophages
• Formation of irregular bony trabeculae
• Presence of sequestrum

Chronic OsteomyelitisTreatment:

• Antibiotics- penicillin, metronidazole, clindamycin for 2-4 months
• Sequestromy
• cauterization of bone
• decortication
• Hyperbaric oxygen therapy

Read And Learn More: Oral Pathology Questions and Answers

Question 2. Ludwig’s angina
Answer:

Ludwig’s Angina

• Ludwig’s angina was described by Wilhelm Fredrich Von Ludwig in 1836
• Ludwig’s Angina is rapidly spreading cellulitis invoking simultaneously submandibular, sublingual, and sub-mental spaces

Ludwig’s Angina Etiology:

• Odontogenic infections
• Traumatic injuries
• Infective conditions
• Pathologic conditions

Ludwig’s Angina Predisposing Factors:

• Diabetes mellitus
• HIV infection
• Oral transplant
• Aplastic anemia

Ludwig’s Angina Pathogenesis

Ludwig’s Angina Clinical Features:

• Rapidly spreading, large, diffuse, and broad-like aggressive swelling
• Elevation of tongue leading to open mouth appearance
• Swollen area of the neck is firm, painful, and non fluctuant
• Swelling is bilateral
• Massive swelling in the neck above the hyoid bone results in bull neck
• High fever with chills
• Rapid pulse
• Dysphagia
• Sore throat
• Hoarseness of voice
• Stridor
• Drooling of saliva

Ludwig’s Angina Treatment:

• High dose of antibiotics
• Incision and drainage
• Tracheostomy in case of airway obstruction

Question 3. Capillary and cavernous haemangiomas
Answer:

Capillary And Cavernous Haemangiomas

Hemangiomas are relatively common benign proliferative lesions of vascular tissue origin

Capillary Haemangioma:

• They begin as endothelial cell neoplasms that are absent at birth
• Common in females
• They exhibit two phases of growth
• Proliferative phase
• Occurs from 8-18 months
• Characterized by the increased number of endothelial and mast cells
• Involution phase
• Characterized by slow regression of haemangioma
• Decrease in endothelial and mast cell activity
• Vascular spaces are lined with endothelial cells

Capillary Haemangioma Types:

• Salmon’s patch
• Port-wine stain
• Strawberry angioma

Cavernous Haemangioma:

• Occurs in areas of abundant venous space like lip, cheek, tongue, posterior triangle of neck
• Age-3rd-5th decade of life
• Swelling is compressible, bluish, warm and nontender
• Associated with arteriovenous communication
• Characterized by large, irregularly shaped, dilated, endothelial lining sinuses
• Contains large aggregates of erythrocytes

Capillary Haemangioma Treatment

• Injection of boiling water or hypertonic saline
• Excision

Capillary Haemangioma Complications:

• Ulceration
• Bleeding
• Infection
• High-output cardiac failure

Question 4. Focal infection
Answer:

Focal infection

Focal infection is a localized or general infection caused by the dissemination of micro-organisms or toxic products from a focus of infection

Focal infection Mechanism:

• Spread of pathogenic micro-organisms from their primary site of infection to the distant part of the body via blood vessels or lymphatics
• Spread of toxins liberated by the pathogenic microbes to distant organs either via blood vessels or lymphatics

Focal infection Significance:

• It causes a great number of systemic diseases like
  • Arthritis
  • Valvular heart diseases
  • Gastrointestinal diseases
  • Ocular diseases
  • Skin diseases
  • Renal diseases

Question 5. Cellulitis
Answer:

Cellulitis Definition: It is an acute, edematous, purulent inflammatory process that spreads diffusely through different tissue spaces

Cellulitis Sources of Infections:

• Periapical abscess
• Pericoronitis
• Periodontal abscess
• Osteomyelitis
• Infected post-extraction wound
• Gunshot injuries
• Oral soft tissue infections
• Blood borne infections

Cellulitis Clinical Features:

• Large, diffuse, painful swelling over the face or neck
• The overlying skin appears purplish
• Fever, chills
• Leukocytosis
• Regional lymphadenopathy
• Pus discharging sinuses

Cellulitis Complications:

• Trismus
• Dyspnoea
• Dysphagia

Question 2 Spaces involved in Ludwig’s Angina
Answer:

Spaces Involved In Ludwig’s Angina

• Spaces involved in Ludwig’s angina are
• Submandibular spaces
• Sub-lingual spaces
• Sub-mental spaces

Question 3. Definitions: Focus of infection, focal infection
Answer:

The Focus Of Infection:

• Circumscribed area of tissue, which is infected by exogenous pathogenic organisms and is usually located near the skin or mucosal surface is called the focus of infection

Focal Infection:

• Focal Infection is a localized or general infection caused by the dissemination of micro-organisms or toxic products from a focus of infection

Spread Of Oral Infections Viva Voce

1. 2nd and 3rd molars are the most common teeth for the source of infection.
2. Submasseteric space is situated between the masseter muscle and the lateral surface of mandibular vaunts
3. Canine space is between the anterior surface of the maxillary anti overly log levator muscle of the upper Up
4. A tracheostomy is done to ease airway obstruction in Ludwig’s angina
5. Cellulitis is a diffuse inflammation of soft tissues
6. Pterygomandibular space lies between the inter not pterygoid muscle and ramus of the mandible
7. Rheumatic fever occurs due to hypersensitization of tissues to hemolytic streptococci
8. Subacute bacterial endocarditis is more often related to dental infection

Diseases Of The Pulp And Periapical Tissues Important Notes

1. Classification Of Pulp Disease
   • Inflammatory disease
     • Focal reversible pulpitis
     • Acute pulpitis
     • Chronic pulpitis
     • Chronic hyperplastic pulpitis
   • Miscellaneous
     • Aerodositalgsa
     • Necrosis
     • Reticular atrophy
     • Cakifscatkm
     • Palpal metaplasia
2. Focal Reversible Pulpitis Or Pulp Hyperemia
   • It is a mild, transient localized inflammatory reaction in the pulp that can be treated by conservative means without involving any form of direct pulp therapy
   • The tooth is sensitive to cold
   • The involved tooth has a large carious lesion, large restoration, or restoration with defective margins
   • Histopathology
     • Dilatation of pulpal vessel
     • Collection of edema fluid
     • Displacement of odontoblast cell nuclei into dentinal tubules
     • Infiltration of leukocytes
3. Acute Pulpitis
   • Mode of development
     • Extension of focal reversible pulpitis
     • As de novo
     • As acute exacerbation of chronic pulpitis
   • Clinical features
     • The tooth is extremely sensitive to hot or cold
     • Has short and severe lancinating pain
     • Associated with microabscess formation
     • Draining pus has a noxious odor
4. Chronic Pulpitis
   • The tooth may be asymptomatic
   • There may be an intermittent dull and throbbing pain
   • Less sensitive to hot or cold stimuli
   • Treatment
     • Root canal treatment
     • Extraction
5. Pulp Polyp Or Chronic Hyperplastic Pulpitis
   • Characterized by the overgrowth of tissue outside the boundary of the pulp chamber as a protruding mass
   • Teeth commonly involved are
     • Deciduous molars
     • First permanent molar
   • Affected tooth always has a large open carious cavity
6. Periapical Granuloma
   • Sequence of pulpitis
   • It is a localized mass of chronic granulation tissue formed from infection
   • Involved tooth is usually nonvital
   • May produce dull sounds on percussion
   • The patient may complain of pain on biting or chewing on solid food
   • Radiographically appears as a thickening of the ligament at the root apex
   • Loss of lamina dura
   • Epithelium of it may arise from
     • Respiratory epithelium
     • Oral epithelium growing in through fistula
     • Oral epithelium proliferating apically from a periodontal pocket
   • Consists of
     • Granulation tissue mass
     • Chronic inflammatory cells
     • Epithelial islands, cholesterol clefts, foam cells
     • Giant cells
     • Plasma cells
   • Sequel
     • Resorption of the root apex
     • Acute exacerbation
     • Suppuration
     • Radicular cyst
     • Osteosclerosis in apical region
     • Hypercementosis
7. Osteomyelitis
   • Osteomyelitis Definition
     • Osteomyelitis is defined as inflammation of bone and bone marrow along with surrounding periosteum
   • Osteomyelitis Classification
     • Acute osteomyelitis
       • Acute suppurative osteomyelitis
       • Acute subperiosteal osteomyelitis
       • Acute periostitis
     • Chronic osteomyelitis
       • Nonspecific type
         • Chronic intramedullary osteomyelitis
         • Chronic focal sclerosing osteomyelitis
         • Chronic diffuse sclerosing osteomyelitis
         • Chronic osteomyelitis with proliferative periostitis
         • Specific type
         • Tuberculous osteomyelitis
         • Syphilitic osteomyelitis
         • Actinomycotic osteomyelitis
   • Radiation-induced osteomyelitis
   • Idiopathic osteomyelitis

Diseases Of The Pulp And Periapical Tissues Long Essays

Question 1. Define and classif pulpitis. Write in detail about the pathogenesis, features, and histopathological features of acute pulpitis.
Answer:

Classify Pulpitis Definition: Pulpitis is the inflammation of dental pulp resulting from intreated caries, trauma, or multiple restorations

Classif Pulpitis Classification

1. Inflammatory diseases
   • Acute pulpitis
   • Chronic pulpitis
2. Depending on the extent of involvement of pulp
   • Partial pulpitis
   • Generalized pulpitis
3. Based on the presence or absence of direct communication between dental pulp and oral environment
   • Open pulpitis
   • Closed pulpitis

Acute Pulpitis:

• Acute pulpitis is an irreversible condition characterized by acute, intense inflammatory reaction in the pulpal tissue

Acute Pulpitis Pathogenesis:

• Acute Pulpitis occurs through
• Extension of focal reversible pulpitis
• As a de novo condition, where inflammation is acute from the beginning
• Acute exacerbation of chronic pulpitis

Read And Learn More: Oral Pathology Questions and Answers

Acute Pulpitis Clinical Features:

• Occurs in the tooth with large carious lesion or restoration
• Severe pain occurs in the involved tooth
• It is sensitive to hot or cold stimuli
• Pain is not relieved even after the removal of the stimuli
• Pain increases during sleep
• Associated with micro-abscess formation along with liquefaction degeneration
• Formation of drainage
• The pus has a noxious odor
• Patients are apprehensive and ill
• When intrapulpal pressure increases, it may collapse of apical blood vessels
• This is known as the pulp-strangulation

Acute Pulpitis Histopathology

• Characterized by continued vascular dilatation
• Accumulation of edema fluid in connective tissue surronding
• Micro-abscess formation untreated
• Liquefaction and necrosis of pulp due to destruction of the odontoblastic cell layer of pulp
• Death of pulp along with tissue dehydration occurs
• This is known as dry gangrene of pulp

Question 2. Define and classify osteomyelitis. Write about the etiology, pathology, and clinical features of acute suppurative osteomyelitis
Answer:

Osteomyelitis Definition: Osteomyelitis is defined as inflammation of the bone narrowsrrow along with surrounding periosteum

Osteomyelitis Classification:

1. Acute osteomyelitis
   • Acute suppurative osteomyelitis
   • Acute subperiosteal osteomyelitis
   • Acute periostitis
2. Chronic osteomyelitis
   • Nonspecific type
     • Chronic intramedullary osteomyelitis
     • Chronic focal sclerosing osteomyelitis
     • Chronic diffuse sclerosing osteomyelitis
     • Chronic osteomyelitis with proliferative periostitis
     • Chronic subperiosteal osteomyelitis
   • Specific type
     • Tuberculous osteomyelitis
     • Syphilitic osteomyelitis
     • Actinomycotic osteomyelitis
3. Radiation-induced osteomyelitis
4. Idiopathic osteomyelitis

Acute Suppurative Osteomyelitis

• Acute suppurative osteomyelitis is diffuse spreading inflammation characterized by extensive tissue necrosis

Acute Suppurative Osteomyelitis Etiology:

• Dental infection due to
• Fracture
• Gunshot wound
• Hematogenous spread
• Causative organisms
• Staphylococcus aureus
• Staphylococcus albus
• Variant streptococci
• Anaerobes- bacteroids, prevotella

Acute Suppurative Pathology:

Acute Suppurative Clinical Features

• Age-after 30years of age
• Sex-common in males
• Site- maxilla or mandible
• In the maxilla, the disease is well-localized
• In mandible disease is more diffuse and widespread
• Severe throbbing, deep-seated pain in the in
• Diffuse large swelling on the jaw
• Trismus
• Paraesthesia of lip
• Rise in body temperature
• Regional lymphadenopathy
• Regional teeth are loose and sore
• Difficulty in eating
• Exudation of pus from gingival margin
• Excessive salivation
• Bad breath
• In advanced cases, reddening of overlying skin or mucosa
• Anorexia, vomiting
• Metastatic spread of disease-causing cellulitis, bacteremia, septicemia
• Distension of periosteum due to pus accumulation
• Exfoliation of necrotic bone fragments or sequestrum spontaneously
• Pathological fracture may occur

Question 3. Enumerate periapical lesions. Describe the etiology, histopathological, clinical, and radiographic features of periapical granuloma and mention its consequences
Answer:

Periapical Lesions:

• Acute apical periodontitis
• Periapical abscess
• Periapical granuloma
• Periapical cyst
• Dentigerous cyst
• Periapical scar
• Giant cell granuloma
• Osteomyelitis
• Periapical cemental dysplasia
• Langerhans cell disease

Periapical Granuloma:

• Periapical granuloma is a localized mass of granulation tissue around the root apex of a non-vital tooth

Periapical Lesions Etiology:

• Extension of pulpal inflammation or infection beyond the root apex
• Occlusal trauma
• Orthodontic tooth movement
• Acute trauma
• Perforation of root apex during endodontic therapy
• Spread of periodontal infection
• Chemical irritation

Periapical Lesions Clinical Features:

• The involved tooth is nonvital and slightly tender on percussion
• Mild pain occurs on biting or chewing on solid food
• The tooth may be slightly elongated in its socket
• Sensitivity occurs due to hyperemia, edema, and inflammation of the apical periodontal ligament
• The tooth is usually asymptomatic
• Pain occurs during acute exacerbations

Periapical Lesions Histopathology:

• Inflammation and locally increased vascularity of tissue are associated
• There is the proliferation of fibroblasts and endothelial cells formation of more tiny vascular channels occurs
• New capillaries are lined by swollen endothelial cells
• Cells present are
  • Macrophages
    • Indicates chronic inflammation
  • Lymphocytes
    • Indicates delayed hypersensitivity reaction
  • Plasma cells
    • Produces immunoglobulin
  • Epithelial islands and foam cells
    • Deposit of cholesterol and hemosiderin are present
    • Cholesterol crystals appear clear needle-like spaces or clefts
    • Presence of collagen bundles in connective tissue

Periapical Lesions Radiographic Features:

• Thickening of the periodontal ligament at the root apex
• Periapical granuloma appears as a radiolucent area of variable size attached to the root apex
• It is well-circumscribed, well-demarcated from surrounding bone
• The thin radiopaque line representing the zone of sclerotic bone outlines the lesion
• In some cases, radiolucency may blend with the surrounding bone
• Advance lesions show root resorption and loss of apical dura

Periapical Lesions Complications:

Diseases Of The Pulp And Periapical Tissues Short Essay

Question 1. Chronic hyperplastic pulpitis
(or)
Pulp polyp
Answer:

Chronic Hyperplastic Pulpitis

• Pulp polyp is an unusual type of hyperplastic granulation-responsive pulp
• It is characterized by the overgrowth of tissue outside the boundary of the pulp chamber as a protruding mass

Pulp Polyp Clinical Features:

• Occurs in children and young adults
• Pulp Polyp involves teeth with large, open carious lesions
• Pulp Polyp appears as a small, pinkish-red, lobulated mass protruding out from the pulp chamber
• The teeth mostly involved are deciduous molars and the first permanent molar
• Lesion bleeds profusely on slight provocation
• If traumatized, the pulp polyp becomes ulcerated
• Then it appears as a dark red, fleshy mass with fibrinous exudate

Pulp Polyp Histopathology:

• Hyperplastic tissue is made up of delicate connective tissue fibers interspersed with a variable number of small capillaries
• Inflammatory cell infiltration includes lymphocytes, plasma cells, and polymorphonuclear leukocytes
• Presence of fibroblast and endothelial cell proliferation
• Granulation tissue gets epithelialized
• The epithelium is stratified squamous with well-formed rete pegs
• Pulp Polyp contains desquamated cells from the buccal mucosa, gingiva, and salivary gland carried by the saliva
• There is hyperemia and edema of pulpal tissue
• Focal areas of pulpal necrosis surrounded by fibrosis are seen
• Reparative secondary dentin may be formed

Question 2. Garre’s osteomyelitis
Answer:

Garre’s Osteomyelitis

• Garre’s Osteomyelitis represents a reactive periosteal osteogenesis in response to low-grade infection or trauma

Garre’s Osteomyelitis Clinical Features:

• Occurs at a young age
• Site involved
• The posterior part of the mandible
  • Maxilla
  • Toothache
• Pain in jaw
• Bony hard swelling on the outer surface of the jaws size of swelling varies from a  few centimeters to the entire length of the mandible
• Slight pyrexia
• Moderate leucocytosis

Garre’s Osteomyelitis Radiographic Features:

• Presents as a mottled radiolucent lesion with few radiopaque foci
• The cortex of bone exhibits many concentric or parallel opaque layers giving onion skin appearance
• Garre’s Osteomyelitis shows focal overgrowth of bone on the  outer surface of the cortex
• Described as a duplication of the cortical layer of bone
• Few newly formed bony trabeculae are oriented perpendicular to onion skin layers

Garre’s Osteomyelitis Histopathology:

• The lesion consists of new bone and osteoid
• Osteoblasts border the trabeculae
• Trabeculae are oriented perpendicular to the cortex
• They are arranged parallel to each other
• Connective tissue contains lymphocytes and plasma cells
• Garre’s Osteomyelitis is fibrous
• There may be the  presence of sequestrum

Question 3. Chronic focal sclerosing osteomyelitis
Answer:

Chronic Focal Sclerosing Osteomyelitis

• Chronic focal sclerosing osteomyelitis is a rare nonsuppurative inflammatory condition of bone

Chronic Focal Sclerosing Osteomyelitis Etiology:

• Chronic pulpitis
• Traumatic malocclusion

Chronic Focal Sclerosing Osteomyelitis Clinical Features:

• Occurs in children and young adults
• Common in mandibular first molars
• Presents as a large carious lesion
• The associated tooth is non-vital
• Asymptomatic condition

Chronic Focal Sclerosing Osteomyelitis Radiographic Features:

• Presents as a well-circumscribed radiopaque mass of sclerotic bone surrounding the apex of the root of the involved tooth
• Lamina dura is intact
• Widening of periodontal ligament
• The border of the lesion is smooth and distinct

Chronic Focal Sclerosing Osteomyelitis Histopathology:

• Consist of a dense mass of bony trabeculae with little interstitial marrow tissue
• Osteocytic lacunae are empty
• Bony trabeculae exhibit many resting and reversal lines
• Bone marrow if present, is fibrotic and infiltrated by chronic inflammatory cells

Question 4. Focal Reversible Pulpitis
Answer:

Focal Reversible Pulpitis

Focal Reversible Pulpitis is an acute inflammatory response to noxious stimuli

Focal Reversible Pulpitis Etiology

• Trauma
• Thermal injury
• Chemical stimulus
• Deep restoration

Focal Reversible Pulpitis Symptoms:

• Sharp sudden pain on stimulus
• Pain relieves on removal of stimuli

Focal reversible Pulpitis Diagnosis:

• Clinically – caries
• Traumatic occlusion
• Percussion test – Negative
• Radiograph – Normal PDL and lamina dura
• Vitality – Early response

Focal Reversible Pulpitis Treatment:

• No endodontic treatment is  required Sedative dressing placed
• Desensitize the tooth
• Use of cavity varnish

Question 5. Apical Periodontal cyst
Answer:

Apical Periodontal Cyst

Apical Periodontal Cyst is also called a radicular cyst

Apical Periodontal Cyst Clinical Features:

• Age- young age
• Sex- common in males
• Site- common in maxillary anterior
• Involved teeth are nonvital
• Smaller cysts are asymptomatic
• Larger lesions produce slow enlarging, bony hard swelling
• Expansion and distortion of cortical plates
• Severe bone destruction
• The springiness of jaw bones
• Pain occurs if a secondary infection is present
• Intraoral and extraoral pus discharge
• Pathological fractures
• Formation of abscess called “cyst abscess”

Question 6. Alveolar abscess
Answer:

Alveolar Abscess

• Also called a periapical abscess
• Alveolar Abscess is the acute or chronic suppurative process of the periapical region

Alveolar Abscess Clinical Features:

• Involved teeth are extremely painful
• It is slightly extruded from its socket
• Regional lymphadenitis
• There may be swelling of the tissues
• Fever
• There may be swelling of the tissues
• May develop into osteomyelitis
• Chronic condition leads to mild symptoms

Question 7. Classification of osteomyelitis
Answer:

Classification Of Osteomyelitis

1. Acute osteomyelitis
   • Acute suppurative osteomyelitis
   • Acute subperiosteal osteomyelitis
   • Acute perseids
2. Chronic osteomyelitis
   • Nonspecific type
     • Chronic intramedullary osteomyelitis
     • Chrome focal sclerosing osteomyelitis
     • Chronic diffuse sclerosing osteomyelitis
     • Chronic osteomyelitis with proliferative periostitis
     • Chronic subperiosteal osteomyelitis
   • Specific type
     • Tuberculous osteomyelitis
     • Syphilitic osteomyelitis
     • Actinomycotic osteomyelitis
3. Radiation-induced osteomyelitis
4. Idiopathic osteomyelitis

Question 8. Sequestrum
Answer:

Sequestrum

• Sequestrum is a fragment of dead tissue, usually bone, that has separated from healthy tissue as a result of injury disease
• Sequestrum is a vascular

Sequestrum Types:

• Primary sequestrum
• A piece of dead bone that completely separates from sound bone during the process of necrosis
• Secondary sequestrum

Sequestrum Treatment:

• Removed by sequestrum

Question 9. Garre’s osteomyelitis
Answer:

Garre’s Osteomyelitis

Garre’s Osteomyelitis represents a reactive periosteal osteogenesis in response to low-grade infection or trauma

Garre’s Osteomyelitis Clinical Features:

• Occurs at a young age
• Site involved
• The posterior part of the mandible
• Maxilla
• Toothache
• Pain in jaw
• Bony hard swelling on the outer surface of the jaw
• The size of swelling varies from a few centimeters to the entire length of the mandible
• Slight pyrexia
• Moderate leucocytosis

Question 10. Acute suppurative osteomyelitis
Answer:

Acute Suppurative Osteomyelitis

Acute suppurative osteomyelitis is diffuse spreading acute inflammation of the bone characterized by extensive tissue necrosis

Acute Suppurative Osteomyelitis Clinical Features:

• Age- after 30 years of age
• Sex- common in males
• Site- maxilla or mandible
• In the maxilla, the disease is well-localized
• In the mandible, the disease is more diffuse and widespread
• Severe throbbing, deep-seated pain in the involved jaw
• Diffuse large swelling of the jaw
• Trismus
• Paraesthesia of lip
• Rise in body temperature
• Regional lymphadenopathy
• Regional teeth are loose and sore
• Difficulty in eating
• Exudation of pus from gingival margin
• Excessive salivation
• Bad breath
• In advanced cases, reddening of overlying skin or mucosa
• Anorexia, vomiting
• Metastatic spread of disease pausing cellulitis, bacteremia, septicemia
• Distension of periosteum duo to pus accumulation
• Kxfollatlou of necrotic bono fragment or sequestrum spontaneously
• Pathological fracture may occur

Diseases Of The Pulp And Periapical Tissues Viva Voce

1. Osteocalcin is a glycoprotein present In presenting
2. Young people more often develop focal reversible pulpit Ih
3. During acute inflammation, Intropulmonary pressure becomes very high causing the collapse of the apical blood vessels. This is called pulp strangulation
4. Death of pulp along with I Issue dehydration is called dry gangrene of pulp
5. Untreated pulpitis leads to necrosis of the pulp
6. Aerodontalgia is dental pain during high altitude or deep sen diving
7. Acute exacerbation of n chronic periapical lesion is known as a Phoenix abscess
8. The presence of sequestrum is a feature of osteomyelitis

Physical And Chemical Injuries Of The Oral Cavity Important Notes

1. Smear Layer
   • Smear Layer is an amorphous microlayer deposited on the prepared tooth surface
   • Consists of inorganic enamel and dentin debris, organic pulp materially dentinal fluid, bacteria, and saliva
   • Thickness -1-5 mm
   • Smear Layer Functions
     • Forms physical barrier
     • Reduces permeability of dentin
     • Prevents exit of dentinal fluid
     • Acts barrier against micro-organisms
2. Effect Of Restorative Materials
   
   
3. Cracked Tooth Syndrome
   • Cracked Tooth is characterized by sharp pain on chewing without any obvious reason
   • Cracked Tooth Causes
     • Attrition
     • Bruxism
     • Trauma
     • Accidental biting on a hard object
     • Presence of large restoration
     • Improper endodontic treatment
   • Cracked Tooth Treatment
     • Stabilization by stainless steel band/crown
4. Symptoms Of Sodium Hypochlorite Accidents
   • Hemolysis
   • Ulceration
   • Facial nerve weakness
   • Necrosis
   • Inhibits neutrophil migration
   • Damages endothelial cells and fibroblasts
5. Drugs Causing Gingival Hyperplasia
   • Dilantin sodium
   • Cyclosporine
   • Nifedipine

Physical And Chemical Injuries Of The Oral Cavity Short Question And Answers

Question 1. Describe the predisposing factors and clinical features of osteoradionecrosis.
Answer:

Osteoradionecrosis:

• Osteoradionecrosis is a radiation-induced pathologic process characterized by chronic and painful infection and necrosis is accompanied by late sequestration and sometimes permanent deformity
• This is one of the most serious complications of radiation to the head and neck

Osteoradionecrosis Predisposing Factors:

• Irradiation of an area of previous surgery before adequate healing had taken place
• Irradiation of lesion near the bone
• Poor oral hygiene
• Continued use of irritants
• Poor patient cooperation in managing irradiated tissue
• Surgery in the irradiated area
• Failure to prevent trauma to the irradiated area

Osteoradionecrosis Clinical Features:

• Nonhealing dead bone
• The bone becomes hypovascular, hypocellular, and hypomineralised
• Mandible is more effected than maxilla
• Necrosis of bone
• Infection of tissues
• Sequestration of bone
• Bone deformity

Osteoradionecrosis Treatment:

• Debridement of necrotic tissue should be done along with removal of the sequestrum
• Administration of intravenous antibiotics and hyperbaric oxygen therapy
• Maintenance of oral hygiene
• Chemotherapy- Bleomycin, Cisplatin, 5- Fluorouracil

Read And Learn More: Oral Pathology Questions and Answers

Question 2. Traumatic bone cyst
Answer:

Traumatic Bone Cyst

• Traumatic bone cyst is a pseudo cyst
• Traumatic Bone Cyst is not lined by epithelium

Traumatic Bone Cyst Etiopathogenesis:

Traumatic Bone Cyst Clinical Features:

• Age- between 10-20 years
• Sex- Females are commonly affected
• Site- in mandible, above the mandibular canal
• Painful, bony hard swelling of the jaw
• Paraesthesia of lip
• Expansion of the cortical plates
• Displacement of regional teeth

Traumatic Bone Cyst Radiographic Features:

• Smooth radiolucent area
• Size- centimeter in diameter
• Cysts involving roots of teeth have a scalloped appearance
• Intact lamina dura
• The cystic margin is well-demarcated

Traumatic Bone Cyst Histological Features:

• Absence of epithelial lining
• The cystic cavity is surrounded by loose vascular connective tissue wall
• Connective tissue stroma is made up of fibrous tissue, areas of hemorrhage, hemosiderin pigmentation, and bone resorption
• Presence of red blood cells, or giant cells adhering to the bone surface

Traumatic Bone Cyst Treatment:

• Surgical exploration

Question 3. Effects of radiation on oral tissues
Answer:

Effects Of Radiation On Oral Tissues

1. Oral mucous membrane
   • Mucositis
   • Desquamation of epithelial layer
   • Infection of the oral cavity
   • Candidiasis
   • Atrophic mucosa
   • Ulceration
   • Radiation necrosis
2. Taste buds
   • Degeneration
   • Loss of taste sensation
3. Salivary glands
   • Xerostomia
   • Loss of salivary secretion
   • Difficult and painful swallowing
   • Decreased buffering capacity
   • Susceptibility to radiation caries
4. Teeth
   • Retards growth of teeth
   • Inhibits cellular differentiation
   • Premature eruption
   • Retard root formation
   • Pibroatrophy of pulp
   • Radiation caries
5. Bone
   • Osteonecrosis
   • Hypocellularity
   • Hypoxia
   • Hypovascuiarity

Question 4. Internal resorption
Answer:

Internal Resorption

• Internal resorption refers to the resorption process that starts internally within the tooth itself and the dentin is gradually resorbed from the pulpal side toward the periphery

Internal Resorption Etiopathogenesis

Internal Resorption Clinical Features:

• Can involve the crown portion or root portion of teeth
• Any tooth can be Involved
• Initially asymptomatic
• Later there appearance of pink pink-lined area on the crown of the tooth
• Also known as the pink tooth of mummery
• Affected tooth Is vital

Internal Resorption Radiographic Features:

• involved tooth shows the round or ovoid radiolucent area in the central portion of the tooth
• Well well-defined, spherical-shaped, radiolucent area occurs in dentin
• The external outline of the tooth is intact

Internal Resorption Types:

• internal inflammatory resorption
• internal replacement resorption

Internal Resorption Treatment:

• Extirpation of pulp
• Endodontic treatment
• Extraction

Question 5. Clinical and histologic features of nicotine stomatitis
Answer:

Nicotine Stomatitis

Nicotine stomatitis or smoker’s keratosis is tobacco-related keratosis of the oral mucosa

Nicotine Stomatitis Clinical Features:

• Affects both the hard and soft palate
• Hyperkeratosis of the epithelium
• Inflammatory swelling of palatal mucous glands
• Palatal mucosa becomes red initially and later becomes white
• On the surface, there is the presence of red dot-like areas surrounded by elevated white keratotic rings
• The surface is rough, fissured, or wrinkled

Nicotine Stomatitis Histopathological Features:

• Hyperorthokeratosis and acanthosis of surface epithelium
• Inflamed and swollen palatal mucous glands
• Squamous metaplasia of ductal epithelium
• Atrophic changes of minor salivary glands
• Moderate inflammatory cell infiltration

Question 6. Tooth ankylosis
Answer:

Tooth Ankylosis

Tooth ankylosis is a fusion between the tooth and bone

Tooth Ankylosis Etiology:

• Partial root resorption
• Traumatic injury to teeth
• Periapical inflammation

Tooth Ankylosis Clinical Features:

• Lack of mobility of tooth
• If a deciduous tooth is affected, they do not exfoliate and become submerged
• Pulpal infection
• Dull, muffled sound on percussion of tooth

Tooth Ankylosis Radiographic Features:

• Loss of periodontal ligament
• Mild sclerosis of the bone
• Blending of bone with tooth root

Question 7. Plumbism
Answer:

Plumbism

Plumbism or lead poisoning is an occupational hazard

Plumbism Etiology:

• Inhalation of lead vapor or dust in adults
• Ingestion while chewing on wood painted with lead-containing paint- in infants

Plumbism Clinical Features:

• Nausea, vomiting, constipation
• Peripheral neuritis
• Wrist drop or foot drop
• Encephalitis
• Hypochromic anemia
• Basophilic stippling of RBC
• Grey bluish-black line on marginal gingiva
• Ulcerative stomatitis
• Excessive salivation
• Metallic taste
• Swelling of salivary glands

Plumbism Treatment: Treatment of oral lesions

Question 8. Amalgam tattoo
Answer:

Amalgam Tattoo

Amalgam tattoo of oral mucous membrane is a relatively common finding in dental practice

Amalgam Tattoo Etiology:

• Therapeutic use of silver nitrate
• Condensation of amalgam in gingiva during restoration work
• From broken pieces introduced into the socket during extraction of the restored tooth
• Retrograde amalgam filling

Amalgam Tattoo Clinical Features:

• Permanent bluish-grey pigmentation of skin and mucosa
• Black or olive brown granules present in gingival areas
• Differential Diagnosis:
• Malignant melanoma

Question 9. Pink disease or Acrodynia
Answer:

Pink Disease Or Acrodynia

Pink Disease Or Acrodynia is also known as Swift’s disease

Pink Disease Or Acrodynia Etiology:

• Mercury toxicity

Pink Disease Or Acrodynia Clinical Features:

• Age- infants below the age of 2 years
• The raw beef appearance ofthe  skin
• The patient has a cold, clammy feeling
• Presence of pruritic maculopapular rash
• Extreme irritability
• Photophobia with lacrimation
• Muscular weakness
• Tachycardia, hypertension
• Insomnia
• Gastrointestinal upset
• Stomatitis
• Profuse salivation
• Painful gingiva
• Bruxism
• Loosening and premature shedding of teeth

Question 10. Bruxism
Answer:

Bruxism Definition: Habitual grinding of teeth either during sleep in the night or during daytime

Bruxism Etiology:

• Local factors-hereditary
• Psychologic factor- emotional upset
• Occupational causes- carpenters

Bruxism Clinical Features:

• Attrition of teeth
• Loosening and drifting of teeth
• Gingival recession
• Hypertrophy of masticatory muscles
• Trismus
• Facial pain
• Sensitivity of teeth

Bruxism Treatment:

• Removal of irritating factors
• Use of occlusal splints

Physical And Chemical Injuries Of The Oral Cavity Viva Voce

1. Demineralization of dentin widens tubules
2. Peritubular dentin demineralizes quicker than Intertubular matrix
3. A concussion is produced by an injury that is not strong enough to cause serious, visible damage to the tooth and the periodontal structures
4. Abrasion is the wearing away of tooth substance due to mechanical means
5. Subluxation is the abnormal loosening of the tooth without displacement due to sudden trauma
6. An avulsion is the discoloration of a tooth from its socket due to traumatic injury
7. Fusion between tooth and bone is termed ankylosis
8. The most common physical injury of the bone is fractured
9. The linea alba is a white line seen on the buccal mucosa extending from the commissures posteriorly at the level of the occlusal plane
10. Sialolithiasis is common in the submandibular salivary gland
11. Rhinoliths are calcareous concentrations occurring in the nasal cavity
12. Radiation causes osteoradionecrosis in bone
13. Local application of aspirin causes blanching and sloughing of the epithelium of oral mucosa
14. Pink’s disease or acrodynia occurs due to mercury toxicity
15. Green stains frequently seen on children’s teeth are caused by chromogenic bacteria.

Dental Caries Important Notes

1. Dental Caries – It is an irreversible microbial disease of the calcified tissues of the teeth, characterized by demineralization of the inorganic part and destruction of the organic substance of the tooth which often leads to cavitation
2. Caries Theory Regarding Etiology
   
   
3. Classification Of Caries:
   • Based on the anatomical site
     • Pit and fissure caries develops on
       • Occlusal surfaces of molars and premolar
       • Buccal and lingual surfaces of molar
       • Palatal surfaces of maxillary incisor
     • Smooth surface caries
       • Proximal surfaces of teeth or
       • On the gingival third of buccal and lingual surfaces
     • Cervical caries
       • Extends from the area opposite to the gingival crest occlusal to the convexity of the tooth surface
     • Root caries
       • Found anywhere on root surfaces
   • Based on severity and rate of progression
     • Acute caries
       • Runs rapidly and results in early pulp involvement
     • Chronic caries
       • Progresses slowly and involves pulp much later
   • Other
     • Rampant caries
       • Characterised by sudden, severe destruction of teeth affecting surfaces that are relatively caries-free
     • Nursing caries
       • Affects deciduous dentition due to prolonged use of nursing bottles containing milk or milk formula
4. Caries Activity Tests
   • Lactobacillus colony test
   • Snyder test
   • Swab test
   • Buffer capacity test
   • Salivary reductase test
   • Salivary s.mutans level test
   • Dip slide test
5. Caries Vaccine
   • Caries Vaccine is a suspension of an attenuated or killed micro-organism administered for the prevention, amelioration, or treatment of infectious diseases

Route Of Administration

• Oral route
  • Increases stimulation of IgA antibodies
• Systemic route
  • Subcutaneous administration of s.mutans leads to an increase in IgG, IgM, and IgA antibodies
  • Active gingivosalivary route
  • Localizes the immune response by using gingival crevicular fluid as a route
• Active immunization
  • Synthetic peptides
  • Derived from glucosyl transferase enzyme Coupling with cholera toxin subunits
  • Coupling of the protein with a nontoxic unit of cholera toxin suppresses colonization of S. mutans
  • Fusing with avirulent strains of salmonella
  • Liposomes- increases IgA antibodies
• Passive immunization
  • External supplements are included
  • Bovine milk and whey
  • Egg yolk
  • Transgenic plants

Dental Caries Long Essays

Question 1. Define and classify dental caries. Describe clinical and histopathologic features of dentinal caries.
Answer:

Dental Caries Definition:

• Dental caries is an infectious, microbiologic disease of the teeth that results in localized dissolution and destruction of the calcified tissues of the teeth
• Dental Caries leads to weakening of tooth structure, cavity formation, and eventual loss of tooth

Dental Caries Classification:

1. Based on occurrence
   • Primary caries- affects the intact surface
   • Secondary caries- Occurs around margins of restoration
2. Based on the anatomical site
   • Pit and fissure caries
   • Smooth surface caries
   • Linear enamel caries
   • Cervical caries
   • Root caries
3. Based on the rate of progression
   • Acute caries
   • Chronic caries
   • Rampant caries
   • Nursing bottle caries
   • Recurrent caries
   • Arrested caries
   • Incipient caries
   • Radiation caries

Dental Caries Clinical Features:

• Dental Caries occur on pit and fissures/smooth surfaces and roots of teeth
• Initially brown or black in color
• Soft and examined through a catch by tip of the explorer
• The enamel bordering it appears opaque bluish-white
• Due to undermining enamel, caries spreads laterally at DEJ

Histopathologic Features Zones in Dentinal Carles:

1. Zone 1- Normal dentin
   • Zone of fatty degeneration of odontoblast process
   • Represents the innermost layer of carious dentin
   • No crystals are present in the lumen of tubules
   • No bacteria present in tubules
   • Intertubular dentin has normal collagen
2. Zone 2- Sub-transparent dentin
   • Zone of dentinal sclerosis characterized by deposition of calcium sails in dentinal tubules
   • The superficial layer shows areas of demineralization and damage to odontoblastic processes
   • It is capable of remineralization
   • No bacteria is present in tubules
3. Zone 3- Transparent dentin
   • Zone of decalcification of dentin, a narrow zone preceding bacterial invasion
   • It is softer than normal dentin
   • Large crystals are present within the lumen of dentinal tubules
   • No bacteria is present in tubules
   • It is capable of self-repair and remineralization
4. Zone 4- Turbid dentin
   • Zone of bacterial invasion of decalcified but intact dentin
   • Widening and distortion of dentinal tubules
   • Cannot undergo self-repair or remineralization
   • Must be removed before restorative treatment
5. Zone 5- Infected dentin
   • Zone of decomposed dentin
   • Infected is the outermost zone of carious dentin
   • Characterised by the complete destruction of dentinal tubules
   • Areas of decomposition of dentin occur along the direction of dentinal tubules called liquefaction foci of Miller
   • Transverse clefts are seen due to the decomposition of dentin
   • Bacteria invade and destroy peri and intertubular dentin.

Question 2. Write about the theories of dental caries.
Answer:

Theories Of Dental Caries:

1. Acidogenic theory
   • Postulated by WD Miller in 1889
   • Dental Caries states that
     • Acids formed due to the fermentation of dietary carbohydrates by oral bacteria lead to progressive decalcification of the tooth structures with subsequent disintegration of organic matrix
   • Dental Caries states that process of dental caries involves two stages
     • Initial stage
       • Acid production due to fermentation of carbohydrates by plaque bacteria
     • Late stage
       • Decalcification of enamel followed by dentin by acids
       • This causes total destruction of enamel and dentin
       • According to Miller, the process of caries involves four factors
         • Dietary carbohydrates
         • Micro-organisms
         • Acids
         • Dental plaque
2. Proteolytic Chelation Theory
   • Proteolytic Chelation Theory states that there is simultaneous microbial degradation of the organic components and the dissolution of the minerals of the tooth by the process known as chelation
   • The chelating agent is negatively charged
   • Proteolytic Chelation Theory releases the positively charged calcium ions from the enamel or dentin
3. Sucrose chelation theory
   • Sucrose chelation theory proposes the sucrose itself and not the acid derived from it can cause the dissolution of enamel by forming ionized calcium saccharate
4. Autoimmune theory
   • Autoimmune theory suggests that few odontoblast cells at some specific sites within pulp are damaged by an autoimmune mechanism

Read And Learn More: Oral Pathology Question And Answers

Question 3. Discuss the role of carbohydrates in caries. Describe and histopathologic features of enamel caries
Answer:

Role Of Carbohydrates In Caries:

• Fermentable dietary carbohydrates play an important role in the causation of caries
• Glucose, sucrose, and fructose are rapidly diffused and fermented by cariogenic bacteria in the oral cavity to produce acid
• This causes the dissolution of hydroxyapatite crystals of enamel
• Risk of caries occurrence increases if dietary sugar is sticky and adheres to the tooth surface for a longer time
• Following its ingestion, the pH of plaque falls to 4.5-5 within 1-3 minutes and neutralization occurs after 10-30 minutes

Enamel Caries Histopathology:

• Early enamel caries
  • Loss of interprismatic or inter-rod substances with an increase in prominence of enamel rods
  • Appearance of transverse striations of enamel rods
  • Dark lines often appear at right angles to the enamel rods
  • Accentuation of incremental striate of Retzius

• Advanced enamel caries
  • Advanced enamel caries presents several zones in tissues
    • Zone 1- Translucent Zone
      • Advanced enamel caries are the deepest zone
      • Advanced enamel caries is slightly more porous
      • Contains 1% by volume
      • Pores are larger than usual pores seen in normal enamel
      • Dissolution of mineral occurs at the junction of prismatic and interprismatic enamel
    • Zone 2-Dark zone
      • Located superficial to the translucent zone
      • Excessive demineralization of enamel occurs
      • Dark zone is narrow in rapidly advancing caries and wide in slowly advancing caries
      • Contains 2-4% pore volume
      • Pores are smaller than those of the translucent zone
      • There is some degree of remineralization present
    • Zone 3- Body of lesion
      • Present between the dark zone and the surface layer of enamel
      • Represents the area of greatest demineralization
      • Pore volume is between 5-25%
      • Contains larger apatite crystals
      • Reprecipitation of minerals occurs
      • Dissolution of minerals occurs
      • Lost minerals are replaced by unbound water and organic matters
      • There is increased prominence of the striate of Retzius
    • Zone 4- Surface zone
      • The surface zone remains unaffected
      • The surface zone is 40 micrometers thick
      • Surface remineralization occurs due to active precipitation of mineral ions

Question 4. Describe the immunology of dental caries. Give a brief account of caries activity tests.
Answer:

Immunology of Dental Caries:

• Salivary immunoglobulin IgA protects the tooth from oral pathogenic bacteria by acting as specific agglutinin
  • Dental Caries binds and agglutinates specific oral bacteria
  • Prevents their adherence to the tooth
  • Removes it from the mouth
  • Inactivates surface glycosyltransferase
  • Reduces synthesis of extracellular glucans
  • Reduces plaque formation
  • Increases opsonization

Caries Activity Tests:

1. Synder’s Test

• Used for lactobacillus count

Synder’s Test Procedure:

• Paraffin-stimulated saliva is collected in test tubes
• Synder test is inoculated into glucose and agar media
• pH-4.7-5 is maintained along with color indicator bromocresol green
• Color change indicates pH change and is compared to the standardized color chart and scored
• Recordings are carried out at the end of 24 hours, 48 hours, and 72 hours

Synder’s Test Result

2. Lactobacillus Test

• Described by Hadley in 1933

Lactobacillus Test Procedure:

• Collect paraffin-stimulated saliva
• Dilute to 1:10 dilution by pipetting 1 ml of saliva into a 9 ml tube of sterile saline solution
• Similar again to 1:100 dilution using a 1:10 diluted sample
• Mix thoroughly
• Spread 0.4 ml of each dilution over agar plates
• Incubate for 3-4 days at 37 degrees C
• Count the number of colonies

Lactobacillus Test Result:

3. Swab Test

Swab Test Procedure:

• The oral flora is sampled by swabbing the buccal surfaces of the teeth with a cotton applicator
• Incubate it in media
• The change in pH following 48 hours incubation period is read by pH meter

Swab test Interpretation:

4. Salivary Reductase Test

Salivary Reductase Test Procedure:

• Paraffin-stimulated saliva is collected in a collection tube
• Salivary Reductase Test is then mixed with dye diazo-resorcinol
• Caries conduciveness reading or color change is done after 15 minutes

Salivary Reductase Test Result

Dental Caries Short Essays

Question 1. What is plaque? Describe its role in the pathogenesis of dental caries
Answer:

Plaque: Plaque is a soft non mineralized deposit of bacteria present on the tooth surface and other hard surfaces of the oral cavity

Role Of Plaque:

• Plaque harbors the cariogenic bacteria on the tooth surface
• Rapid production of high amounts of acids within the plaque occurs through fermentation of carbohydrates by cariogenic bacteria
• Plaque helps to hold these acids onto the tooth surface for a long duration
• Increased thickness of plaque does not allow the salivary buffers to enter into it to neutralize the acids produced by the cariogenic bacteria
• Plaque protects the acids produced by the cariogenic bacteria from getting neutralized in two ways
  • Plaque has diffusion limiting property that does not allow acids to escape
  • Does not allow the buffering agents from saliva to enter into it and cause neutralization of acids
    • Continued sugar production from bacterial intracellular polysaccharides helps to maintain a low pH and facilitates more tooth decay

Question 2. Describe the etiology of dental caries
Answer:

Etiology of Dental Caries: There are four etiological factors in dental caries

1. Tooth
   • Composition
     • Highly mineralized-less caries formation
     • High solubility leads to more caries formation
     • Increased permeability of enamel surfaces causes increased caries
     • An increase in mineral content leads to increased resistance to caries
   • Morphology
     • The presence of deep, narrow, and retentive pits and fissures leads to high caries incidence
   • Position
     • MolaHgned, rotated teeth Are more prone to caries due to more plaque accumuiulkm
2. Saliva
   • pH
     • A rise in pU neutrally adds attacks on the tooth surface during carle progression
   • Composition
     • Bicarbonateionscauses neutrailiftalton
     • Ammonia- causes a rise in pH
   • Quantity
     • Reduction of saliva leads to
     • Rampant caries
     • Exacerbation of caries
   • Viscosity
     • Extremely viscous saliva leads to carle-free mouth
     • Abundant, thin, watery saliva exhibits rampant caries
   • Antibacterial properties
     • Lysozyme-lyses endogenic and non-cariogenic bacteria
     • Salivary peroxidase- inactivates bacterial enzymes
     • Immunoglobulin- IgA protects against caries
3. Diet
   • Fibrous food
     • Keep teeth clean
     • Stimulates salivary flow
     • Reduces caries incidence
   • Soft and sticky food increases caries incidence
   • Dietary constituents that reduce the incidence of caries are
     • Phosphates
     • Traces of molybdenum and vanadium
     • Vega tables
     • Vitamins
     • Minerals
     • Fats
4. Systemic conditions
   • Hereditary
   • Pregnancy
   • Lactation

Question 3. Acidogenic theory of dental caries
Answer:

Acidogenic Theory Of Dental Caries

1. Populated by WD Miller In 1889
2. Dental caries stales that
   • Acids formed due to Ilia fermentation of dietary carbohydrates by oral Itadurla load to progressive decalcification of the tooth structures with subsequent disintegration of organic matrix
3. Dental caries states that process of denial Carles Involves two stages
   • Initial stage
     • Add production due to fermentation of carbohydrates by plaque harder
   • Late stage
     • Deealdflcalkm of enamel followed by dentin by adds
     • This causes total destruction of enamel and dentin
     • According to Miller, process of caries Involves four factors
       • Dietary carbohydrates
       • Micro-organisms
       • Adds
       • Dental plaque

Question 4. Microbiological aspects of dental Caries
Answer:

Microbiological Aspects Of Dental Caries

• Cariogenic bacteria are present in the oral cavity
• They accumulate In plaque and ferment carbohydrates present In the diet
• Produces add and results in dissolution of enamel to cause cavity formation
• Microorganisms Involved in the caries process are
  • Streptococcus mutans
    • Streptococcus mutans are catalase-negative, gram-positive cocci forming short or medium chains
    • Streptococcus mutans synthesizes Insoluble polysaccharides from sucrose
    • Streptococcus mutans results in production of lactic acid
    • This causes a drop in pH favoring caries
    • Streptococcus mutans also has the ability to store intracellular glycogen amylopectin
    • Provides a reservoir of substrate and enables prolonged periods of increased metabolic activity
  • Lactobacillus
    • Lactobacillus is long and thin, non-motile
    • Lactobacillus may occur singly in the palm or in chain
    • Lactobacillus could multiply in low-pH of plaque and carious lesions
    • Hence it is an important etiologic agent of dental caries
    • Lactobacillus is present in deep fissures and in deep dentinal caries
    • Lactobacillus causes progress of caries
    • Actinomycosis
    • Lactobacillus cause root caries

Question 5. Preventive measures for carIe’s control
Answer:

Preventive Measures For Caries Control: Preventive measures for caries control include

1. Chemical measures
   • Chemical includes sub lances that
     • Alter tooth surface or tooth structure
     • Interfere with carbohydrate degradation
     • interfere with bacterial growth and metabolism
   • Fluorine
     • It decreases microbial acid production
     • Enhances remineralization of underlying ename
   • Bis-biguandies- Chlorhexidine
     • Anti-plaque agent
   • Silver nitrate
     • Prevent or arrest dental caries
   • Zinc chloride and potassium ferrocyanide
     • It seals off Carie’s Invasion pathway
   • Vitamin K
     • Prevents acid formation
2. Nutritive measures
   • A diet rich in fag low in carbohydrates and free of sugar have low caries activity
   • A phosphate-rich diet causes a reduction in caries
3. Mechanical measures-includes
   • Oral prophylaxis by dentist
   • Tooth brushing
   • Mouth rinsing
   • Use of dental loss
   • Pit and fissure sealants

Question 6. Clinical types of caries
Answer:

Clinical Types Of Caries

1. Pit and fissure caries
   • Carles develops on occlusal surfaces of molars and promoters, buccal and lingual surfaces of motel’s, and palatal surfaces of maxillary Inch sors
   • Clinical Types Of Caries Appearance:
     • Initially brown or black in color
     • Soft and examined through catch by lip of explorer
     • Enamel bordering 2 appears opaque bluish-white
     • Due to undermining enamel, Caries spreads laterally at DEJ
2. Smooth surface caries
   • Develops on proximal surfaces of teeth or a gingival third of buccal and lingual surfaces
   • Begins just below the contact points
3. Incipient caries
   • Intact enamel surface
   • Destruction of enamel below surface layer
   • Appeal’s as chalky while tooth surface
   • It Is reversible process
   • Cured by remineraiization by salivary Ions
   • Prevented by topical fluorides
4. Rampant carles
   1. Present in oil age groups
   2. Both dentitions are effected
   3. It involves all teeth Including mandibular incisors
   4. Rapidly new lesions develop in addition to the present old lesions
   5. Carious tooth are with pulpal involvement
5. Nursing bottle caries
   • All teeth except mandibular anteriors are affected
   • They are protected by the position of tongue
   • Initially, caries appears as dull, white area along gingival margin
   • This progresses to the cervical margin to form a ring-like lesion
   • Finally, whole crown of Loolh is destroyed
   • Chronic caries
   • Progresses slowly
6. Common in adults
   • Dentin is stained dark brown
   • Surface destruction occurs with minimal softening of dentin
7. Arrested caries
   • Caries becomes static
   • Affects both dentition
   • Occurs on occlusal surfaces
8. Recurrent caries
   • Occurs in immediate contact of restoration
   • Due to inadequate extension of restoration, this favors food lodgement
9. Root caries
   • Periodontal attachment loss
   • Soft, irregular lesion
   • Round or oval in shape
   • Irregular outline
   • Common in males
   • Common in mandibular molars
10. Radiation caries
    • It is rampant caries in patients undergoing radiotherapy
    • Rate of progression is faster
    • Encircles entire crown cervical portion

Question 7. Write about nursing bottle syndrome
Answer:

Nursing Bottle Caries: Caries caused by prolonged use of a bottle filled with any liquid other than water

Nursing Bottle Etiology:

• Bovine milk and milk products
• Sweeteners like honey-dipped pacifiers
• Micro-organisms like streptococcus mutans
• Fermentable carbohydrates
• Hypoplasia of teeth
• Decreased salivary flow
• Malnutrition

Nursing Bottle Clinical Features:

• All teeth except mandibular interiors are affected
• They are protected by the position of tongue
• Initially caries appears as the dull, white area along the gingival margin
• This progresses to cervical margin to form ring-like lesion
• Finally, whole crown of tooth is destroyed

Nursing Bottle Treatment:

• Excavate and restore all caries lesions
• Pulpal therapy
• Drainage of abscess
• Topical fluoride application
• Diet counselling
• Extraction of unrestorable teeth

Question 8. Cemental caries
Answer:

Cemental Caries

Cemental caries is soft, progressive lesion that is found anywhere on the root surface that has lost its connective tissue attachment and is exposed to the environment

Cemental Caries Etiology:

• Streptococcus mulans
• Lactobacillus
• Actinobacillus

Cemental Caries Clinical Features:

• Periodontal attachment loss
• Soft/irregular lesion
• Round or oval in shape
• Irregular outline
• Common in males
• Common in mandibular molars

Cemental Caries Prevention:

• Plaque removal
• Diet modification
• Use of topical fluoride
• Soft tissue management
• Use of xylitol-containing chewing gums

Question 9. Smooth surface caries
Answer:

Smooth Surface Caries

• Develops on proximal surfaces of teeth or a gingival third of buccal and lingual surfaces
• Begins just below the contact points

Smooth Surface Caries Appearance:

• Initially, faint white opacity of enamel is seen
• In some cases, it appears yellow or brown pigment
• Later it becomes roughened due to superficial decalcification of enamel
• The enamel surrounding the caries is bluish-white
• Smooth Surface Caries extends both buccally and lingually
• There is formation of cavity

Question 10. Theories of dental caries
Answer:

Acidogenic Theory

• Postulated by WD Miller
• Acidogenic Theory states that acids formed due to fermentation of dietary carbohydrates by oral bacteria lead to progressive decalcification of the tooth structures with subsequent disintegration of organic matrix

Proteolytic Chelation Theory

• Proteolytic Chelation Theory states that there is simultaneous microbial degradation of the organic components and the dissolution of the organic components and the dissolution of the minerals of the tooth by the process known as chelation

Sucrose Chelation Theory

• Sucrose Chelation Theory proposes that the sucrose itself and not the acid derived from it can cause dissolution of enamel by forming ionized calcium saccharate

Autoimmune Theory

• Autoimmune Theory suggests that few odontoblast cells at some specific sites within pulp are damaged by an autoimmune mechanism

Dental Caries Short Question And Answers

Question 1. Lactobacillus
Answer:

Lactobacillus

• Lactobacilli are gram-positive, non-spore-forming rods that grow best under microaerophilic conditions
• Lactobacillus is long and thin, non-motile
• Lactobacillus may occur singly or in pairs or in chains
• Lactobacillus could multiple in low-pH of plaque and carious lesion
• Hence it is important etiologic agent of dental caries
• Lactobacillus is present in deep fissures and in deep dentinal caries
• Lactobacillus can be cultured on agar, in broth, in litmus milk, etc

Question 2. Streptococcus mutans
Answer:

Streptococcus Mutans

• Streptococcus mutans are catalase-negative, gram-positive cocci forming short or medium chains
• On agar media they grow as convex colonies
• Streptococcus Mutans synthesizes insoluble polysaccharides from sucrose
• Streptococcus Mutans results in the production of lactic acid
• This causes drop in pH favoring caries
• Streptococcus Mutans also has an ability to store intracellular glycogen amylopectin
• Provides a reservoir of substrate and enables prlonged periods of increased metabolic activity

Question 3. Pioneer bacteria
Answer:

Pioneer Bacteria

• Pioneer bacteria are the first group of bacteria that adheres to the dental plaque
• They are streptococci, Neisseria, Actinomyces and Captocytophaga
• Other bacteria co-adhere to the pioneer bacteria to increase the complexity of the association
• Dental caries results from the metabolism of this association which attacks the tooth enamel

Question 4. Cariogenic micro-organism
Answer:

Cariogenic Micro-organism

Question 5. Name organisms causing cervical caries
Answer:

• Organisms involved in cervical caries are
  • Actinomyces
  • Nocardia
  • Streptococcus mutans

Question 6. Define Caries
Answer:

Caries

• Dental caries is an infectious, microbiologic disease of the teeth that results in localized dissolution and destruction of the calcified tissues of the teeth
• Caries leads to the weakening of tooth structure, cavity formation, and eventual loss of tooth

Question 7. Enamel caries
Answer:

Enamel Caries

• Occurs in pit and fissures, smooth surface, and root
• Initially brown or black in color
• Soft and examined through catch by tip of the explorer
• The enamel bordering it appears opaque bluish-white
• Due to undermining enamel, caries spreads laterally at DEJ

Question 8. Zones in enamel caries
Answer:

Zones In Enamel Caries:

1. Zone 1- Translucent zone
2. Zone 2- dark zone
3. Zone 3- Body of the lesion
4. Zone 4- Surface zone

Question 9. Dentinal caries
Answer:

Dentinal Caries

• Dentinal Caries occurs on pit and fissures, smooth surfaces, and root caries
• Initially brown or black in color
• Soft and examined through catch by tip of explorer
• Enamel bordering it appears opaque bluish-white
• Due to undermining enamel, caries spreads laterally at DEJ

Question 10. Zones in dentinal caries
Answer:

Zones In Dentinal Caries:

1. Zone 1
   • Zone of fatty degeneration of odontoblast process
2. Zone 2
   • Zone of dentinal sclerosis characterized by deposition of calcium salts in dentinal tubules
3. Zone 3
   • Zone of decalcification of dentin, a narrow zone preceding bacterial invasion
4. Zone 4
   • Zone of bacterial invasion of decalcified but in that dentin
5. Zone 5
   • Zone of decomposed dentin

Question 11. Dental plaque
Answer:

Dental Plaque

Plaque is a soft non mineralized deposit of bacteria present on the tooth surface and other hard surfaces of the oral cavity

Dental plaque Classification:

Dental Plaque Composition:

• Dental plaque consists of
  • Bacteria
  • Epithelial cells
  • Macrophages
  • Leucocytes

Dental Plaque Effects:

• Calculus formation
• Dental caries
• Periodontal diseases

Question 12. Arrested caries
Answer:

Arrested Caries

• Caries becomes static
• Affects primary and permanent dentition
• Occurs on occlusal surfaces

Arrested CAries Appearance:

• Large open cavity
• Superficially softened and decalcified dentin
• Brown stained
• Sclerosis of dentinal tubules and secondary dentin formation
• It can also occurs on proximal surfaces revealing brown stained at or just below contact point
• Caries is arrested by fluoride application

Question 13. Nursing bottle caries
Answer:

Nursing Bottle Caries: Caries caused by prolonged use of a bottle filled with any liquid other than water

Nursing Bottle Caries Etiology:

• Bovine milk and milk products
• Sweeteners like honey-dipped pacifiers
• Micro-organisms like streptococcus mutans
• Fermentable carbohydrates
• Hypoplasia of teeth
• Decreased salivary flow

Nursing Bottle Caries 

• All teeth except mandibular interiors are affected
• They are protected by the position of tongue
• Initially, caries appears as the dull, white area along the gingival margin
• This progresses to the cervical margin to form a ring-like lesion
• Finally, the whole crown of the tooth is destroyed

Question 14. Caries susceptibility
Answer:

Caries Susceptibility

• Caries susceptibility refers to inherent tendency of the host and target tissue to caries process
• Microbiological test helps to measure the number of streptococcus mutants and lactobacillus acidophilus
• Two samples of paraffin-stimulated saliva is collected and diluted 10 times and each is cultivated in two different special media
• After incubation, the number of colonies that develop in two separate media are counted and then are multiplied by 10 to estimate the number of bacteria in 1 ml of saliva
• If the count is more than 10,00,000 S. mutans and more- than 1,00,000 L.acidophilus, then caries susceptibility of the individual is very high

Question 15. Role of Saliva in dental caries
Answer:

Role of Saliva in Dental Caries

Salivary factors that influence dental caries are as follows

1. pH
   • A rise in pH neutralizes acid attacks on tooth surface during caries progression
2. Composition
   • Bicarbonate ions- causes neutralization
   • Ammonia- causes rise in pH
3. Quantity
   • Reduction of saliva leads to
   • Rampant caries
   • Exacerbation of aeries
4. Viscosity
   • Extremely viscous saliva leads to caries-free mouth
   • Abundant, thin, watery saliva exhibit rampant carles
5. Antibacterial properties
   • Lysozyme- lyses cariogenic and non-cariogenic bacteria
   • Salivary peroxidase- inactivates bacterial enzymes
   • Immunoglobulin-IgA protects against caries

Question 16. Liquefaction foci of Miller
Answer:

Liquefaction Foci Of Miller

• Liquefaction foci of Miller are present in advanced caries of dentin
• These are formed by focal coalescence and breakdown of few dentinal tubules
• They occur along the direction of dentinal tubules

Question 17. Rampant caries
Answer:

Rampant Caries

Rampant Caries is an acute widespread caries with early pulpal involvement of teeth which are usually immune to decay

Rampant Caries Etiology:

• Multifactorial in nature
• Excessive sticky carbohydrates
• Decreased salivary flow
• Heredia try

Rampant Caries Clinical Features:

• Present in all age groups
• Both dentitions are affected
• Rampant Caries involves all teeth including mandibular incisors
• Rapidly new lesions develop in addition to the present old lesions
• Carious teeth with pulpal involvement

Rampant Caries Treatment: Pulpotomy is done

Question 18. Pit and fissure caries
Answer:

Pit And Fissure Caries

The shape of pit and fissure make it more susceptible to caries

Pit And Fissure Caries Features:

• Initial – Brown/Black in color
• Catch with an explorer
• Decalcification of enamel
• Enamel involvement – in the direction of the rod
• Shape – Triangular, base towards DE
• Progress to the involvement of dentinal tubules
• Result in cavitation
• Undermining of enamel

Question 19. Proteolytic chelation theory
Answer:

Proteolytic Chelation Theory

• Proteolytic Chelation Theory explains the process of dental caries
• According to it
  • Initially, all proteolytic breakdown of the organic portion of the enamel matrix takes place
  • Formation of a chelating agent by combining proteolytic breakdown products acquired pellicle and food debris
  • The negatively charged chelating agent releases positively charged calcium ions from enamel and dentin
  • This results in tooth decay

Question 20. Radiation caries
Answer:

Radiation Caries Pathogenesis:

Radiation Caries Types:

• Superficial
• Involving cervical region
• Dark pigmentation

Dental Caries Viva Voce

1. The most cariogenic carbohydrate is sucrose
2. Clinical significance of sclerotic dentin is that it is resistant to caries
3. The most significant organism for pit and fissure caries is Strep. Mutans and lactobacillus
4. The most significant organism for root surface caries is A. Viscosus
5. The lingual surface of the maxillary lateral incisor is more susceptible to caries
6. pH below 5.5 causes demineralization of the tooth surface
7. The inorganic phase of enamel consists of crystalline hydroxyapatite
8. The critical pH for tooth minerals to act as buffers is 5.5
9. Recurrent caries occurs near a restoration
10. Brown stains in newly erupted teeth are indicative of underlying decay
11. Brown stains in older individuals may be due to arrested lesions

Diseases Of The Periodontium Important Notes

1. Periodontium
   • Includes – gingiva, periodontal ligament, cementum, and bone
   • Periodontium Functions
     • Attaches tooth to the jaw bone
     • Maintains integrity of masticatory system
2. Gingiva
   • Gingiva Parts
     • Free gingiva
     • Attached gingiva
     • Interdental papilla
   • Color – coral pink
   • Surface – stippled- orange peel
   • Fibers
     • Circular
     • Dentogingival
     • Dentoperiosteal
     • Alveologingival
     • Transseptal
3. Functions Of Gingival Fluid
   • Cleanse material from the sulcus
   • Improves adhesion of epithelium to the tooth
   • Maintains structure of junctional epithelium
   • Has antimicrobial property
4. Periodontal Ligament
   • It is dense connective tissue attached to the cementum on one end and alveolar bone on the other
   • Principal fibers
     • Alveolar crest group
     • Horizontal Group
     • Oblique group
     • Apical group
     • Interradicular group
   • Cells
     • Cementoblasts
     • Osteoblasts
     • Osteoclasts
     • Epithelial remnants of Malassez
   • Width – 0.2-0.4 mm
   • Shape – hourglass shape
5.  AUG
   • Also known as Vincent’s infection, Vincent’s stomatitis, trench mouth, fetid stomatitis, putrid stomatitis
   • Smears from the lesions of ANUG show spirochaetes and fusiform bacilli
   • Clinical Features
     • Punched out crater-like depressions at the crest of interdental papilla covered by pseudomembrane and extending into marginal gingiva
     • The pseudomembranous slough is demarcated from the remaining gingival mucosa by linear erythema
     • c.Attached gingiva and alveolar mucosa are rarely involved
6. Drugs Causing Gingival Enlargements
   • Dilantin sodium
   • Cyclosporine
   • Calcium channel blockers
7. Papillon Lefevre Syndrome
   • Characterized by
     • Cutaneous lesions
       • Keratotic lesions of palmar and plantar surfaces
     • Oral lesions
       • Aggressive periodontitis
       • Severe destruction of alveolar bone
       • Rapid bone loss and pathological migration lead to loss of entire dentition at an early age
8. Peri-Implants
   • Peri-Implants is inflammation of the soft tissue surrounding the osseointegrated implant in function and progressive bone loss
   • Peri-Implants begins at the coronal portion of the implant.
   • Peri-Implants Clinical features:
     • Erythema over the area
     • Bleeding on probing
     • Pocket formation
     • Bone destruction
     • Suppuration
     • Presence of calculus
     • Tooth mobility present

Diseases Of The Periodontium Long Essays

Question 1. Classify periodontal diseases. Describe in detail about acute necrotizing ulcerative gingivitis (ANUG).
Answer:

Periodontal Diseases Classification:

1. Gingival diseases
   • Plaque-induced gingival diseases
   • Non-plaque-induced gingival diseases
2. Periodontitis
   • Chronic periodontitis
     • Localized
     • Generalized
   • Aggressive periodontitis
     • Localized
     • Generalized
   • Periodontitis associated with systemic diseases
   • Necrotizing periodontal diseases
     • Necrotizing ulcerative gingivitis
     • Necrotizing ulcerative periodontitis
   • Abscesses of the periodontium
     • Gingival abscess
     • Periodontal abscess
     • Periocoronal abscess
   • Periodontitis associated with endodontic lesion
   • Developmental or acquired deformities
     • Localized
     • Mucogingival lesion around teeth
     • Mucogingival lesion around edentulous ridges
   • Occlusal trauma

Read And Learn More: Oral Pathology Questions and Answers

Acute Necrotizing Ulcerative Gingivitis:

• Acute Necrotizing Ulcerative Gingivitis is an inflammatory destructive disease of the gingiva

Acute Necrotizing Ulcerative Gingivitis Etiology:

• Causative organisms are
• Prevotellaintermedia
• Fusobacterium
• Treponema
• Selenomonas species

Acute Necrotizing Ulcerative Gingivitis Precipitating Factors:

• Poor oral hygiene
• Trauma
• Smoking
• Stress
• Nutritional deficiency
• Chronic diseases
• Blood disorders

Acute Necrotizing Ulcerative Gingivitis Clinical Features:

1. Prodromal symptoms
   • Debilitating diseases
   • Psychologic stress
2. Intraoral signs
   • Punch out crater-like depression
   • Pseudomembranous slough
   • Gingival hemorrhage
   • Fetid odor
   • Increased salivation
   • Sensitive to pain
   • Radiating gnawing pain
   • Increased pain on having spicy food
   • Metallic foul taste
3. Extra-oral signs
   • Lymphadenopathy
   • Fever
   • Loss of appetite
   • Lassitude
   • Leucocytosis

Acute Necrotizing Ulcerative Gingivitis Histopathology:

1. Epithelial changes
   • The surface epithelium is destroyed
   • It is replaced by pseudomembrane
   • This membrane consists of fibrin, necrotic epithelial cells, neutrophils, and various micro-organisms
2. Connective tissue
   • It is hyperaemic
   • Contains numerous engorged capillaries
   • Consists of dense infiltration of neutrophils and plasma cells

Acute Necrotizing Ulcerative Gingivitis Treatment:

1. Antibiotics
   • Penicillin-500 mg TDS or
   • Metronidazole-200-400 mgBID
2. Removal of pseudomembrane with the help of pellet soaked in hydrogen peroxide
   • Scaling and root planning
   • In severe cases, gingivoplasty

Question 2. Enumerate causes of gingival enlargement. Discuss the pathogenesis, clinical features, and histopathology of leukemic enlargement.
Answer:

Causes Of Gingival Enlargement:

1. Inflammation
   • Acute
   • Chronic
2. Drug-induced
   • Phenytoin
   • Cyclosporins
3. Systemic diseases
   • Conditioned enlargements
     • Puberty
     • Pregnancy
     • Non-specific
   • Systemic diseases
     • Leukemia
4. Neoplastic
   • Benign tumors
   • Malignant tumors
5. False enlargements
6. Idiopathic

Leukaemic Gingival Enlargement Pathogenesis

Leukaemic Gingival Enlargement Clinical Features:

• Distribution
  • Diffuse or marginal
  • Localized or generalised
• It increases in size and gradually covers the tooth crown
• It appears as tumor enlargement
• Color-bluish red
• Surface-shiny surface
• Consistency-spongy-like and friable
• Gingiva bleeds spontaneously
• Increased susceptibility to infections

Leukaemic Gingival Enlargement Histopathology:

1. Epithelium
   • Hyperplastic
   • Diminished keratinization
   • Presence of inter and intracellular edema
   • Consists of pseudomembrane containing fibrin, necrotic cells, neutrophils, and bacteria
2. Reticular layer
   • Contains immature and proliferating leukemic cells
3. Papillary layer
   • Contains few leukocytes
4. Blood vessels
   • Contains leukemic cells and RBCs

Leukaemic Gingival Enlargement Treatment:

• Scaling and curretage
• Antibiotic prophylaxis
• Incision and drainage
• Cleanse the area with a cotton pellet soaked in hydrogen peroxide
• Application of pressure with gauze.

Diseases Of The Periodontium Short Essays

Question 1. Difference between supragingival and subgingival calculus
Answer:

Difference Between Supragingival And Subgingival Calculus

Question 2. Juvenile periodontitis or Aggressive periodontitis
Answer:

Juvenile Periodontitis

• Rapid loss of attachment and bone loss occurring in an otherwise clinically healthy patient with the amount of microbial deposits inconsistent with disease severity and familial aggregation of diseased individuals

Juvenile Periodontitis Or Aggressive Periodontitis Etiology:

• Hereditary
• A.actinomycetumcomitans
• Capnocytophaga

Juvenile Periodontitis Or Aggressive Periodontitis Types:

1. Localized Aggressive Periodontitis:
   • Localized Aggressive Periodontitis Clinical Features:
     • Age-20 years
     • Sex- common in females
     • Lack of inflammation
     • Deep pockets
     • A small amount of plaque
     • Mobility of first molars and incisors
     • Midline diastema
     • Root sensitivity
     • Deep dull radiating pain
     • Periodontal abscess
     • Lymphadenitis
   • Localized Aggressive Periodontitis Radiographic Features:
     • Vertical/ angular bone loss
     • Arc-shaped loss of alveolar bone extending from distal surface of 2nd premolar to mesial surface of 2nd molar
     • Bilateral involvement results in a “mirror image” pattern
2. Generalized Aggressive Periodontitis:
   • Characterized by generalized interproximal attachment loss affecting at least three permanent teeth other than the first molar and incisors
   • Generalized Aggressive Periodontitis Clinical Features:
     • Age- puberty to 30 years of age
     • Site- All teeth are affected
     • Severely inflamed tissue
     • Spontaneous bleeding
     • Suppuration
     • Deep pockets
     • Attachment and bone loss
     • Weight loss
     • Mental depression
     • General malaise
   • Generalized Aggressive Periodontitis Radiographic Features:
     • Severe bone loss
     • Osseous destruction

Question 3. Vincent infection or ANUG
Answer:

Vincent Infection Or ANUG

• Vincent infection is also known as acute necrotizing ulcerative gingivitis

Vincent Infection Or ANUG Clinical Features

• Gingival hemorrhage
• Fetid odor
• Increased salivation
• Sensitive to pain
• Radiating gnawing pain
• Increased pain on having spicy food
• Metallic foul taste
• Lymphadenopathy
• Fever
• Loss of appetite

Question 4. Micro-organisms causing ANUG
Answer:

Micro-Organisms Causing ANUG

• Causative organisms of ANUG are
  • Prevotella intermedia
  • Fusobacterium
  • Treponema
  • Selenomonas species

Question 5. Periodontal abscess
Answer:

Periodontal Abscess

• Papillon Lefevre syndrome is an autosomal recessive inherited disease

Periodontal Abscess Etiology:

• Mutation of chromosome
• Autosomal recessive disorder

Periodontal Abscess Clinical Features:

• Age- before 4 years
• Hyperkeratotic skin lesions
• Calcification of dura
• Early bone loss
• Severe periodontal destruction
• Premature loss of primary and permanent teeth

Question 6. Epulis
Answer:

Epulis

• Epulis refers to solid swelling situated on the gum

Epulis Types:

1. Granulomatous epulis
   • It manifests as a mass of granulation tissue around the teeth on the gums
   • It is a soft to firm fleshy mass and bleeds on touch
2. Fibrous epulis
   • Arises from the periodontal membrane
   • It may undergo a sarcomatous change
   • It is firm, polypoidal mass, slow growing, and non-tender
3. Giant cell epulis
   1. It is an osteoclastoma arising in the jaw
   2. It is present as hyperaemic vascular oedematous, soft to firm gums with indurated mass due to expansion of bone
   3. It may ulcerate and result in hemorrhage
4. Carcinomatous epulis
   • This is epithelioma arising from the mucous membrane of the alveolar margin
   • It presents as a non-healing painful ulcer
   • It slowly infiltrates the bone

Question 7. Staining Of Teeth
Answer:

Staining Of Teeth Causes:

1. Intrinsic stains
   • Pre-eruptive causes
     • Disease- hematological disorders
     • Medication-Tetracycline
   • Post-eruptive causes
     • Pulpal changes
     • Trauma
     • Aging
     • Dental caries
2. Extrinsic stains
   • Acquiredstains
     • Plaque
     • Tobacco use
     • Poor oral hygiene
     • Gingival hemorrhage
   • Chemicals
     • Chlorhexidine
     • Metallic stains

Question 8. Periodontal abscess
Answer:

Periodontal Abscess

• Periodontal abscess is a localized accumulation of pus within the gingival wall of a periodontal pocket

Periodontal Abscess Etiology:

• Presence of plaque and calculus

Periodontal Abscess Clinical Features:

• Involves deep periodontal structures
• Localized pain
• Deep pockets
• Vital tooth
• Tenderon lateral percussion
• Tooth mobility
• Associated fistula

Periodontal Abscess Treatment:

• Drainage
• Flap surgery

Question 9. Desquamative gingivitis
Answer:

Desquamative Gingivitis

• Desquamative gingivitis is characterized by intense erythema, desquamation, and ulceration of free and attached gingiva

Desquamative gGingivitis Clinical Features:

Question 10. Scorbutic gum
Answer:

Scorbutic Gum

• Scorbutic gum is seen in scurvy, vitamin C deficiency

Scorbutic Gum Clinical Features:

• The site involved- free and attached gingiva
• Color- brilliant red
• Swollen gums
• Spongy in consistency
• The disappearance of lamina dura
• Reduced bone density
• Loss of bony trabeculae
• Mobile teeth
• Impaired healing
• Increased bacterial pathogenicity

Question 11. Granulomatous diseases of periodontium
Answer:

Granulomatous Diseases Of Periodontium

• Granulomatous diseases of periodontium are:
  • Eosinophilic granuloma
  • Giant cell granuloma
  • Wegener’s granulomatosis
  • Pyogenic granuloma

Question 12. Dilantin gingival hyperplasia
Answer:

Dilantin Gingival Hyperplasia

• It occurs 3 months after initiation of phenytoin therapy
• Common in younger individuals
• Generalized distribution but severe in the maxilla
• The site involved- marginal gingiva and interdental papilla
• Appears as a painless, bead-like enlargement
• Interferes with occlusion n Has lobulated surface
• Firm to resilient in consistency
• No tendency to bleed

Question 13. Gum boil or parulis
Answer:

Gum Boil Or Parulis

• A gum boil is defined as a drainage point for an abscessed tooth

Desquamative Gingivitis Etiology:

• Dental caries
• Gum infection
• Failure of root canal treatment
• Weak immune response

Desquamative Gingivitis Features:

• Occurs around the root of the tooth
• Appears as small, red, bulging over gingiva
• When pressed it drains out pus
• Painful swelling
• Earache
• Fever
• A foul taste in my mouth
• Bad breath

Diseases Of The Periodontium Viva Voce

1. Epulis fissuratum is caused by ill-fitting dentures
2. Stippling is a form of adaptive specialization or reinforcement for the function
3. Halitosis is an unpleasant odor exhaled while breathing or talking
4. The mandibular third molar is commonly involved tooth in Pericoronitis
5. A.a. contains predominate organisms causing chronic periodontitis
6. A localized form of aggressive periodontitis is localized to the first molar and incisors
7. The generalized form of aggressive periodontitis involves at least 3 teeth other than 1st molar and incisor.

Mycotic Infections Of Oral Cavity Important Notes

1. Actinomycosis
   • Causative organisms – A. israelii, A.naeslundh, A.bovis, A.odontolyticus, and A.viscosus
   • Actinomycosis Types
     • Cervicofacial
     • Abdominal
     • Pulmonary
   • Actinomycosis Clinical features
     • Overlying skin
       • Dusky, red, or bluish-red
     • Appears as a wooden indurated area of fibrosis
     • Sinus contains pus which has sulphur granules
     • Colonies produce the ray-fungus appearance
2. Candidiasis
   • Candidiasis Classification
     • Acute
       • Acute pseudomembranous candidiasis
       • Acute atrophic candidiasis
     • Chronic
       • Chronic atrophic candidiasis
         • Denture stomatitis
         • Median rhomboid glossitis
         • Angular cheilitis
     • ID reaction
     • Chronic hyperplastic candidiasis
   • Chronic mucocutaneous candidiasis
     • Familial CMC
     • Localized CMC
     • Diffused CMC
     • Candidiasis endocrinopathy syndrome
   • Candidiasis Clinical features

Mycotic Infections Of Oral Cavity Long Essays

Question 1. Enumerate fungal Infections of the oral cavity. Write In detail about clinical features and Investigations of oral candidiasis
(or)
Describe the etiology, clinical features, and histopathology of oral candidiasis
Answer:

Fungal Infections Of The Oral Cavity:

• Candidiasis
• Coccidioidomycosis
• Histoplasmosis
• Cryptococcosis
• North American blastomycosis
• Mucormycosis
• Geotrichosis
• Phycomycosis
• Rhinosporidiosis
• Sporotrichosis

Oral Candidiasis:

• Candidiasis is the most common fungal infection of the oral cavity

Oral Candidiasis Etiology/Causative Organisms:

• Candidiasis is caused by
  • Mainly Candida albicans
  • Other species- C tropica C is, C.glabrala, C, Krusie, C.pseudotropicaiia

Read And Learn More: Oral Pathology Questions And Answers

Oral Candidiasis Clinical Features:

• Candidiasis may range from mild superficial mucosal involvement to severe, fatal, disseminated form

Oral Candidiasis Investigations:

1. Direct microscopy
   • Gram-stained smears and KOH mounts from lesions are used
   • They show budding Gram-positive yeast cells
2. Culture- sabouraud’s dextrose agar media
   • Media is inoculated and incubated at 25-37 degrees C for 24 hours
   • Cream-colored smooth pasty colonies appear
3. Identification
   • Candida albicans can be identified by
   • Germ tube test
   • Chlamydospores
4. Biochemical reactions
   • albicans can be identified by the assimilation and fermentation of ssugarSerology
   • OrOrganismsre identified by the precipitation test with a carbohydrate extract of group A antigens

Question 2. Write in detail about candidiasis concerning classification, histopathology, and management.
Answer:

Candidiasis Classification

1. Acute
   • Pseudomembranous candidiasis or oral thrush
   • Atrophic
2. Chronic
   • Atrophic
   • Hypertrophic
   • Angular cheilitis
3. Systemic
   • Candidal endocarditis
   • Candidal meningitis
   • Candidalsepticaemia
4. Mucocutaneous
   • Localized
   • Familial
   • Syndrome associated

Candidiasis Histopathology

Candidiasis Management

• Removal of etiological factor
• Improvement of oral hygiene
• In conventional – topical and systemic administration of Nystatin
• In immunosuppressed patients – systemic administration of amphotericin B and fluconazole

Mycotic Infections Of Oral Cavity Short Essays

Question 1. Histoplasmosis
Answer:

Histoplasmosis

• Histoplasmosis is a generalized fungal infection caused by Histoplasma capsulatum

Histoplasmosis Clinical Features:

• Fever, malaise
• Headache
• Productive cough
• Hepatomegaly
• Splenomegaly
• Lymphadenopathy
• Anaemia, leukopenia
• Subcutaneous nodules
• Chest pain
• Weight loss
• Granulomatous, verrucous, or necrotic ulcers

Histoplasmosis Oral Manifestations:

• Nodular, ulcerative lesions on the buccal mucosa, gingiva, tongue, palate o, or lips
• Ulcers are covered by a non-specific grey membrane
• Regional lymphadenopathy
• Jaw swellings
• Oral lesions heal with scarring

Histoplasmosis Histopathology:

• Granulomas contain large number of macrophages, lymphocytes, plasma cells, multiple multi-nucleated giant cells
• Liquefaction necrosis and exudation at the margins
• Epithelial hyperplasia
• Microabscess formation

Histoplasmosis Treatment:

• In mild infections- ketoconazole
• In severe cases- amphotericin B

Question 3. Candida Albicans
Answer:

Candida Albicans

• Candida albicans is an ovoid or spherical budding yeast cells
• Size- 3-5 micrometers in diameter
• Candida Albicans is a normal inhabitant of skin, GIT, oral and vaginal cavities
• Candida Albicans causes candidiasis
• Lesions caused by it in include mucocutaneous lesions
  • Skin and nail infections
  • Systemic candidiasis
  • Oral symptoms

Question 4. prPredisposingactors for candidiasis
Answer:

predisposing Factors For Candidiasis

• Diabetes
• Immunodeficiency
• Malignancy
• Prolonged administration of antibiotics
• Patients on immunosuppressive drugs and intravenous catheters

Question 5. Classification of oral candidiasis
Answer:

Primary Oral Candidiasis

1. Acute forms
   • Pseudomembranous
   • Erythematous
2. Chronic forms
   • Hyperplastic
   • Nodular
   • Plaque like
   • Erythematous
   • Pseudomembranous
3. Candida-associated lesions
   • Denture stomatitis
   • Angular cheilitis
   • Median rhomboid glossitis
4. Keratinized primary lesions superinfected with Candida
   • Leukoplakia
   • Lichen planus
   • Lupus erythematosus

Secondary Oral Candidiasis

1. Candidiasis endocrinopathy syndrome

Question 6. Identification of Candida albicans
Answer:

Identification Of Candida Albicans

1. Germ tube test
   • When incubated in human serum at 37 degrees, C.albicans form germ tubes within 2 hours
   • This is called Rethe Ynolds braude phenomenon
2. Chlamydospores
   • Chlamydospores develop in cornmeal agar at 20 degrees

Question 7. Actinomycosis
Answer:

Actinomycosis

• Actinomycosis is a chronic granulomatous disease

Actinomycosis Causative Organisms:

• Chiefly- Actinomyces Israeli
• Rarely
  • Actinomyces naeslundii
  • Actinomyces meyeri
  • Actinomyces odontolyticum
  • Actinomyces viscosus

Actinomycosis Forms:

• Cervicofacial
• Thoracic
• Abdominal
• Pelvic

Actinomycosis Clinical Features:

• Multiple abscess formation
• Tissue destruction
• Fibrosis
• Multiple sinus formation
• Painless indurated swelling
• Gingivitis
• Periodontitis

Question 8. Cervicofacial Actinomycosis
Answer:

Cervicofacial Actinomycosis

• Cervicofacial Actinomycosis is the ommonest form of actinomycosis

Cervicofacial actinomycosis Sites Involved:

• Cheek
• Submaxillary regions
• Route of Infections:
• Tonsils
• Carious tooth
• Periodontal disease
• Trauma following tooth extraction

Cervicofacial Actinomycosis Clinical Features:

• Initially, a firm swelling appears in the lower jaw
• Gradually the mass breaks down
• This leads to abscesses and sinus formation

Cervicofacial actinomycosis Complications:

• Spreading of infection into adjacent soft tissues
• Destruction of bone

Question 9. Rhinosporidiosis
Answer:

Rhinosporidiosis

• Rhinosporidiosis is charoniconic granulomatous disease

Rhinosporidiasis Causative Organism:

• Rhinosporidium seeberi

Rhinosporidiosis Mode of Infection:

•  Frequent contact with stagnant water

Rhinosporidiosis Clinical Features:

• Friable polyps
• The site involved nose, mouth, eyes
• Oropharyngeal lesions
• Appear as soft red polypoid growth and spreads to the pharynx and larynx
• Lesions contain mucoid discharge and are vascular

Question 10. Acute atrophic candidiasis
Answer:

Acute atrophic Candidiasis

• Acute atrophic Candidiasis occurs when the pseudomembranous covering of the oral thrush is lost

Acute Atrophic Candidiasis Features

• Site – dorsum of tongue and palate in patients receiving long-term antibiotics or steroid therapy
• Present as generalized red, painful peeling patches over the mucosa
• Causes tenderness, dysphagia, and a burning sensation

Acute Atrophic Candidiasis Histopathology

• The epithelium is thin, atrophic and non-keratinized
• There is occasional presence of candidal hyphae
• Resembles oral thrush without pseudomembrane
• Chronic inflammatory cell infiltration is seen in the epithelium as well as lamina propria

Question 11. Sulfur granules
Answer:

Sulfur Granules

• Sulfur Granules are features of actinomycosis
• In tissues affected by actinomycosis, there is a formation of numerous abscesses
• This abscess drains through discharging sinuses over the in
• The pus contains sulphur granules which contain colonies of actinomycosis

Mycotic Infections Of Oral Cavity Viva Sulfurphur granules in actinomycosis cocontainolonies of organisms of actinomycosis

1. Lumpy jaw is a cervicofacial form of actinomycosis
2. Chronic diagnosis of candidiasis is confirmed by the proliferation of inflamed pulp tissue
3. Oral candidiasis is also known as Moniliasis or oral thrush
4. Histoplasmosis is caused by Histoplasma capsulatum
5. Candida albicans spherical budding yeast cell
6. Cervicofacial is the common form norm of actinomycosis
7. GeA germ tube test is used for the didentificationtion of Candida albican

Viral Infections Of The Oral Cavity Important Notes

1. Mumps
   • It is an acute viral infection characterized by unilateral or bilateral swelling of the salivary glands
   • It is caused by RNA virus
   • Incubation period 14-18 days
   • Transmitted through the respiratory route
   • Complications
     • Meningoencephalitis
     • Orchitis
     • Mastoiditis
     • Encephalitis
     • Nerve deafness
2. Measles
   • It is an acute, contagious, hepatotropic viral infection
   • Characterized by fever, malaise, Koplik’s spots, cough, maculopapular rash
   • Koplik spots are prodromal and disappear after the onset of the rash
   • They usually occur on the buccal mucosa as small, irregular bluish-white flecks surrounded by a red margin
   • Histologically it shows multinucleated giant cells
3. Chickenpox
   • It is caused by the Varicella zoster virus
   • It rarely occurs second time
   • It is an extremely contagious disease usually occurring in children
   • Characterized by exanthematous vesicular rashes
   • It Is common in the winter and spring months
   • the incubation period is 14-21 days
   • Maculopapular or vascular eruptions begin on the trunk and spread to involve the face and extremities
   • Occasionally secondary infection of the vesicles results in the formation of pustules which may leave small pitting scars upon healing
4. AIDS
   • Caused by Human Immunodeficiency Virus
   • Mode of transmission
   • Sexual
     • Blood and blood products
     • Injected drug users
     • Occupational transmission
     • Maternal-fetal transmission
     • Other – via saliva, milk, and tears
   • Oral manifestations
     • Candidiasis
     • Erythematous
     • Hyperplastic
     • Pseudomembranous
     • Oesophageal
   • Herpes Simplex infection
   • Herpes Zoster infection
     Hairy leukoplakia
   • Kaposi’s sarcoma
   • Angular cheilitis HIV-gingivitis HIV – HIV-periodontitis Necrotizing ulcerative gingivitis Necrotizing stomatitis
   • Major aphthae
   • Vesiculobullous lesion
   • Parotitis
   • Toxoplasmosis
   • Purpura
   • Osteomyelitis
     • Diagnosis
       • Western blot
       • ELISA
       • PCR
       • Reverse ratio of T helper to T suppressor
       • Detection of antibodies in serum
       • Detection of virus
       • Lymphopenia
       • Hypergammaglobulinaemia
   • Treatment
     • Nucleoside reverse transcriptase inhibitor
     • Nonnucleoside reverse transcriptase inhibitor
     • Protease inhibitor

Viral Infections Of The Oral Cavity Long Essays

Question 1. Enumerate various viral infections affecting the oral cavity, write in detail about clinical features and oral manifestations of herpes simplex virus
Answer:

Viral Infections Affecting Oral Cavity:

1. RNA Viruses
   • Orthomyxovirus
     • Influenza
   • Paramyxovirus
     • Measles
     • Mumps
   • Rhabdovirus
     • Rabies
   • Arenavirus
     • Lassa fever
     • Lymphocytic choriomeningitis
   • Calicivirus
   • Coronavirus
     • Upper respiratory tract infection
   • Bunyavirus
   • Picornavirus
   • Reovirus
   • Retrovirus
2. DNA Viruses
   • Herpes virus
     • Herpes simplex virus 1 and 2
     • Varicella zoster virus
     • Cytomegalovirus
     • Epstein-Barr virus
   • Poxvirus
     • Smallpox
     • Molluscum contagiosum
   • Adenovirus
     • Pharyngoconjunctival fever
   • Papovavirus
     • Human warts or papillomas

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Herpes Simplex Virus:

• Herpes simplex is a DNA virus causing disease in man

Herpes Simplex Virus Types:

• Herpes simplex virus type-1
  • Acute herpetic gingivostomatitis
  • Herpetic eczema
  • Keratoconjunctivitis
  • Meningoencephalitis
  • Herpes labialis
• Herpes simplex virus type-2
  • Genital herpes
  • Neonatal herpes
  • Uterocervical cancer
  • Oral herpes

Herpes Simplex Virus Clinical Features:

Herpes Simplex Virus Oral Manifestations:

• Site involved
  • Gingiva
  • Hard palate
  • Dorsum of tongue
  • Lips
  • Vermillion border
  • Perioral skin
• Nasopharynx
• Reddening of oral mucosa
• Formation of numerous small, dome-shaped, or pinhead-type vesicle
• Size-2-3 mm in diameter
• Vesicles contain clear fluid and rupture to form ulcers
• Ulcers are multiple, small, circular, punctuate, shallow, and painful
• Have red margins and yellowish or greyish floor
• Small ulcers fuse to form diffuse, large, whitish ulcers
• They are surrounded by a red halo
• Gingival margins are red, swollen, and painful and have punched-out erosions
• Difficulty in taking food
• Difficulty in mastication
• Difficulty in swallowing
• Numerous vesicle formations over the tonsillar area and posterior pharynx

Question 2. Describe in detail histological features, and lab investigations of primary herpetic gingivostomatitis
Answer:

Primary Herpetic Gingivostomatitis:

• Primary Herpetic Gingivostomatitis is an acute infection of the oral cavity caused by the herpes simplex type-I virus

Primary Herpetic Gingivostomatitis Histological Features:

• Formation of sharply defined vesicles in the superficial part of keratinized epithelium
• Ballooning degeneration of prickle cells with intranuclear inclusion body and marginated chromatin
• Presence of multiple multinucleated giant cells

Primary Herpetic Gingivostomatitis Lab Investigations:

• Cytologic smear
• The presence of inclusion bodies and ballooning degeneration of infected cells
• Culture
• Produces change In culture cells
• Serology
• Detects HSV-specific antibodies

Viral Infections Of The Oral Cavity Short Essays

Question 1. Herpangina
Answer:

Herpangina Clinical Features:

• Age- young age
• Incubation period-2-10 days
• Site- Posterior pharynx, tonsil, faucial pillars, and- soft palate

Herpangina Prodromal Symptoms:

• Fever, chills
• Headache
• Anorexia, vomiting
• Abdominal pain
• Sore throat
• Dysphagia
• Laceration
  • The lesion initially appears as a punctuate macule
  • This turns into papules and vesicles
  • Within 24-48 hours, vesicles rupture to form a 1-2 mm ulcer
  • They show a grey base
  • They generally heal without treatment

Herpangina Differential Diagnosis:

• Primary herpes simplex infection
• Herpes zoster

Herpangina Treatment:

• Palliative treatment is done

Question 2. Herpes zoster
Answer:

Herpes Zoster

• Herpes Zoster is a recurrent regional infection caused by the Herpes Zoster virus

Herpes Zoster Clinical Features:

• Age- 5th, 6th and 7th decade of life
• Prodromal symptoms
  • Fever, malaise
  • Headache
  • Painful lymphadenopathy
  • Severe pain, irritation or burning sensation develops in the dermatome of the involved nerve
  • Affects the first branch of the trigeminal nerve
• Later symptoms
  • Intense pain
  • Formation of clusters of vesicles over skin and oral mucosa unilaterally
  • Vesicles develop over buccal mucosa, soft palate, and tongue
  • Causes stinging pain, paraesthesia, and severe stomatitis
  • Vesicles rupture to form crateriform ulcers
  • Ulcers heal without scar formation
  • Stimulates toothache

Herpes Zoster Histopathology:

• Presents as swelling of infected epithelial cell cytoplasm called ballooning degeneration
• Margination of nuclear chromatin
• Formation of intranuclear inclusion bodies
• Reticular degeneration of epithelial cells
• The presence of multinucleated giant cells and polymorphonuclear neutrophilic infiltration in connective tissue

Question 3. Lipschutz bodies
Answer:

Lipschutz Bodies

• Lipschutz bodies are characteristic histologic features seen in primary herpetic stomatitis
• It is intranuclear inclusion present in herpetic vesicle
• These are eosinophilic, ovoid homogenous structures within the nucleus that tend to displace the nucleolus and nuclear chromatin peripherally
• This displacement of chromatin produces a perinuclear halo

Question 4. Oral manifestations of AIDS
Answer:

Oral Manifestations Of AIDS

1. Bacterial infections
   1. Tuberculosis
   2. M. avium complex
   3. Salmonellosis
2. Viral infection
   • Herpes simplex
   • Varicella zoster
   • Epstein Barr virus
3. Mycotic infections
   • Pneumocystis pneumonia
   • Candidiasis
   • Aspergillosis
   • Cryptococcosis
4. Parasitic infection
   • Toxoplasmosis
   • Cryptosporidiosis
5. Malignancies
   • Kaposi’s sarcoma
   • B cell lymphoma

Question 5. Measles
Answer:

Measles Clinical Features:

• Insidious in onset
• Moderate fever
• Tachycardia
• Sore throat
• Formation of greyish-greenish pseudomembrane on tonsils
• Associated nausea and vomiting
• Bull neck- swollen neck
• Tender lymphadenopathy
• Nasal infection
• Hoarseness of voice
• Cough
• Respiratory obstruction
• Toxaemia
• Acute peripheral circulatory failure
• Nerve paralysis
• Dysphagia
• Dysphonia
• Paraesthesia

Question 6. Reiter’s syndrome
Answer:

Reiter’s Syndrome

• Reiter’s Syndrome consists of a triad of non-gonococcal urethritis, arthritis, and conjunctivitis

Reiter’s Syndrome Clinical Features:

• Genital lesions
  • Balanitis circinata over glans penis
  • Genital ulcers
• Oral lesions
  • Seen over buccal mucosa, palate, and gingiva
  • Present as painless, aphthous-like ulcers
  • Geographic tongue
  • The presence of few elevated areas of erythema on oral mucosa
  • Pruritic spots on the palate
• Skin lesions
  • Well-circumscribed erythematous erosions with irregular white border

Question 7. Infectious mononucleosis
Answer:

Infectious Mononucleosis

• Infectious Mononucleosis is a benign acute infectious disease caused by to Epstein-Barr virus affecting B-lymphocytes

Infectious Mononucleosis Clinical Features:

• Incubation period-10-40 days
• Age-young age individuals
• Sore throat
• Fever-101-103 degrees – F
• Headache
• Photophobia
• Nausea, vomiting, diarrhea
• Erythematous macular rash
• Splenomegaly, hepatomegaly
• Lymphadenopathy
• Myalgia, arthralgia
• Depression and cognitive defect

Infectious Mononucleosis Oral Manifestations:

• Petechiae over soft palate
• Ulcerative gingivitis, periodontitis
• Stomatitis
• Inflamed and enlarged tonsils
• Tonsils are covered by pseudomembrane
• Sore throat
• Dysphagia
• Bleeding from the oro-nasopharyngeal region and gingiva

Infectious Mononucleosis Complications:

• Airway obstruction
• Splenic rupture
• Neurological involvement
• Hemolytic anemia

Question 8. Herpes labialis
Answer:

Herpes Labialis

• Herpes Labialis occurs in patients with no prior infection with Herpes Simplex Virus-1

Herpes Labialis Clinical Features:

1. Age- children and young adults
2. Incubation period-5-7 days

• Prodromal generalized symptoms
  • Fever
  • Malaise
  • Headache
  • Nausea, vomiting
  • Painful mouth
  • Sore throat
  • Irritability
  • Excessive drooling of saliva
  • Lack of tactile sensation
  • Cervical lymphadenopathy
• Later symptoms
  • Numerous vesicle formations over keratinized mucosa
  • Vesicles are thin-walled
  • They contain clear fluid
  • They rupture leaving multiple, small, punctuate shallow painful ulcers of 2-6 mm
  • Ulcers are surrounded by a red ring of inflammation
  • Ulcers may become secondarily infected
  • Healing starts in about 3 days and is completed within 7-14 days

Herpes Labialis Treatment:

• To prevent secondary infection- antibiotics are used
• To control fever- Antipyretics are given

Question 9. Ramsay Hunt syndrome
Answer:

Ramsay Hunt Syndrome

• Ramsay Hunt is a zoster infection of the geniculate ganglion with involvement of external ear and oral mucosa

Ramsay Hunt Syndrome Features:

• Facial paralysis
• The pain of the external auditory meatus and pinna of the ear
• Vesicular eruption in oral cavity and oropharynx
• Hoarseness of voice
• Tinnitus
• Vertigo

Question 10. Chickenpox
Answer:

Chickenpox

• Chickenpox is caused by Varicella zoster virus
• Chickenpox seldom occurs a second time
• The virus enters the mucosa of the upper respiratory tract and spreads by droplets from the throat

Chickenpox Clinical Features:

• It involves young children and adults
• The incubation period is 14-21 days
• Malaise
• Low-grade fever followed by a rash
• Rash is maculopapular
• Heals by scabs formation
• Sites Involved:
  • Skin lesions- over trunk and face then spread to peripheral parts of the body
  • Mucosal lesions- affects the mucosa of the pharynx and vagina

Chickenpox Complications:

• Superinfection of skin due to frequent scratching
• Encephalitis
• Cerebellar ataxia
• Myocarditis
• Osteomyelitis
• Septic arthritis
• Septicaemia
• Hepatitis
• Pneumonia

Question 11. Rubella
Answer:

Rubella

• Rubella is a mild childhood disease
• Rubella may be acquired, congenital, or postnatally

Rubella Features:

• Infection is acquired by inhalation
• Incubation period-2-3 weeks
• Fever, malaise
• Headache
• Mild conjunctivitis
• Lymphadenopathy
• Rash develops on the forehead and face
• It spreads downward to the trunk and extremities
• It lasts for 1-5 days

Rubella Prevention: It is prevented by MMR vaccine

Question 12. Koplik’s spots
Answer:

Koplik’s Spots

• Koplik’s spot is an important clinical feature of measles
• Appears over buccal mucosa
• The mucosa becomes inflamed
• They appear as small, irregularly shaped flecks surrounded by a bright red margin
• Over it, there is the presence of white or white-yellow pinpoint papules
• Koplik’s Spots is followed by red maculopapular rashes on the skin

Question 13. Behcet’s syndrome
Answer:

Koplik’s Spots

• Koplik’s Spots is a triad of recurring oral ulcers, recurring genital ulcers, and eye lesions

Behcet’s Syndrome Clinical Features:

• Genital lesions
  • Consist of recurrent aphthae
  • Larger than mucosal lesions
  • Site
    • In males- penis, inner thigh, scrotum
    • In females- vulva
    • It is painful in females
    • Healing of these lesions leads to severe scarring
• Oral lesions
  • Recurrent aphthae ulcers develop
  • Size- varies from several mm to cm
  • They are painful lesions
  • They have erythematous borders and are covered by exudate
  • Can occur anywhere in the oral mucosa
• Eye lesions
  • Initially, ocular lesions develop
  • Consist of conjunctivitis, keratitis, uveitis, optic trophy and, and retinal this may
  • May lead to visual damage and eventually blindness
  • Photophobia
• Other features
  • Skin lesions- Small pustules or papules develop on the trunk or limbs
  • Neurological degeneration
  • Intestinal ulceration
  • Arthralgia
  • Visceral involvement

Question 14. Herpetic whitlow
Answer:

Herpetic whitlow

• Herpetic whitlow is caused by Herpes Simplex Virus
• Herpetic whitlow is the infection of the finger by a virus through the break in the skin
• Dentists may experience it through contact with lesions of the mouth or saliva of patients who are asymptomatic carriers of HSV
• The lesions are usually preceded by prodromal symptoms of burning or tingling sensation

Viral Infections Of The Oral Cavity Viva Voce

1. Infectious mononucleosis is caused  in the oral cavity  by Ebstein-Burr most common malignancy in AIDS is Kaposi’s sarcoma
2. Lipschutz bodies is seen in primary herpetic stomatitis
3. Herpes simplex virus causes oral ulcerations in immunocompromised patients
4. Herpes virus shows prodromal symptoms preceding local lesions
5. Reiter’s syndrome is a triad of non-gonococcal urethritis, arthritis, and conjunctivitis
6. Ramsay Hunt syndrome is a zoster infection of the geniculate ganglion with involvement of external ear and oral mucosa
7. Behcet’s syndrome is a triad of recurring oral ulcers, recurring genital ulcers, and eye lesions
8. Koplik’s spot is an important clinical feature of measles
9. Ballooning degeneration is seen in herpes zoster infection.

Bacterial Infections Of Oral Cavity Important Notes

1. Tuberculosis
   • Tuberculosis is caused by Mycobacterium tuberculosis
   • The hard tubercle consists of epithelioid cells, Langhans giant cells, plasma cells, and fibroblasts Central part of the lesion contains caseous, soft, and cheesy necrotic material Causative organism is seen in ZN or acid-fast stain
   • Diagnosis can be confirmed by
     • Presence of acid-fast bacilli
     • Tuberculin/ Mantoux test
   • Tuberculosis Treatment
     • Isoniazid + rifampicin for 9 months or
     • Isoniazid + rifampicin + pyrazinamide for 2 months followed by isoniazid + rifampicin for 4 months
2. Ghon’s Complex
   • Ghon’s complex is primary complex tuberculosis – infection of an individual who has not been previously infected/ immunized
   • Ghon’s complex Components
     • Pulmonary component
     • Lymphatic vessel component
     • Lymph node component
3. Leprosy
   • Caused by mycobacterium leprae
   • Forms: tuberculoid type and lepromatous type
   • Sheets of lymphocytes with vacuolated macrophages called lepra cells are a distinct histological feature
   • Leprosy Clinical features
     • Leonine facies
     • Collapse of nasal bridge
     • Dry, wrinkled skin
     • Loss of smell sensation
     • Loss of hair
     • Facial and trigeminal neuralgia paralysis
     • The difficulty is dosing eyes
4. Features Of Tetanus
   • Lockjaw
   • Risus sardonicus
   • Trismus
   • Opisthotonus
   • Laryngospasm
   • Dysphagia
   • Caused by Clostridium tetani
   • Toxins produced by it are
     • Tetanospasmin
     • Tetanolysin
5. Syphilis
   • Caused by Treponema palladium
   • Types and features:
     
6. Scarlet Fever
   • Caused by streptococcus B-hemolytic
   • Systemic manifestations occur first
   • Skin rashes appear on 2nd and 3rd day and lasts for one week
   • On the face, skin rashes appear as sunburn with goose pimples
   • Oral manifestations
     • Initially, the tongue is covered with a white coat through which enlarged and reddened fungiform papillae project
     • This is strawberry tongue
     • Later, the coating is lost and the tongue appears beefy red with hyperplastic numerous fungiform papillae
     • This is called raspberry tongue
   • Scarlet Fever Complications:
     
     
7. Noma or Cancrum Oris
   • Caused by specific Vincent’s organism
   • Noma or Cancrum Oris is rapidly spreading mutilating, gangrenous stomatitis
   • Tire odor arising from gangrenous tissues is extremely foul
   • This leads to necrotizing ulcerative mucositis
   • Over skin, it leads to
     • Initially small, dark, reddish-purple area
     • This undergoes gangrenous necrosis
     • Due to the sloughing of tissues, a large hole develops on the cheek

Bacterial Infections Of Oral Cavity Long Essays

Question 1. Describe congenital and acquired syphilis
Answer:

1. Congenital Syphilis: It is an infection of the fetus established by the passage of spirochaetes from the mother through the placenta

Congenital Syphilis Clinical Features:

• Within the first 2 weeks of life, it leads to
  • Rhinitis
  • Chronic nasal discharge
  • Loss of weight
  • Bullae, vesicle formation
  • Superficial desquamation with cracking and scaling of reddened soles and palms
  • Petechiae, mucous patches
• After 2 years it leads to
  • Interstitial keratitis
  • Vascularization of cornea
  • Eight nerve deafness
  • Arthropathy
  • Neurosyphilis
  • Anterior tibial bowing

Read And Learn More: Oral Pathology Questions and Answers

Congenital Syphilis Oral Manifestations:

• Postrhagadic scarring
  • These are linear lesions found around oral and anal orifices
  • These are seen from 3rd-7th week after birth
  • They appear as red or copper-colored linear areas covered with soft crush
• Syphilitic rhagades
  • They are radially arranged and perpendicular to the mucocutaneous junction
• Teeth
  • Retarded root resorption of deciduous teeth
  • Sparing of permanent incisors
  • Spacing between cuspid and incisors
  • Malocclusion
  • Open bite
  • The crown of the molar is irregular- mulberry-shaped
  • Incisors are screwdriver-shaped
  • Rounding of mesial and distal incisal line angle
• Hypoplastic maxilla
• Frontal bossing
• Saddle nose

2. Acquired Syphilis

• Primary syphilis
  • Incubation period- about 21 days
  • Chancre develops
  • It is a solitary, painless, indurated, non-tendered, ulcerated, or eroded lesion
  • Initially, it was a dull red macule
  • Later it becomes ulcerated
  • Regional lymphadenopathy
• Secondary syphilis
  • Appears about 6-8 weeks
  • Skin lesions appear as macules, papules, follicles, or papulosquamous patches
  • Circinate lesions develop on the face
  • Headache
  • Fever, anorexia
  • Joint and muscle pain
  • Laryngitis, pharyngitis
  • Generalised lymphadenopathy
  • Lesions develop over the mucocutaneous junction
• Tertiary syphilis
  • Develops about 5-10 years after primary infection
  • Affects the skin, central nervous system, CVS, mucous membrane
  • Lesions are called gumma
  • It is a localized, chronic granulomatous lesion with a nodular or ulcerated surface
  • Causes generalized paresis, dementia, and strokes
  • Bone lesions cause osteomyelitis and destruction of joints

Question 2. Classify aphthous ulcers and describe its etiology, clinical features, and differential diagnosis
Answer:

Aphthous Ulcers: Aphthos ulcer is a non-traumatic ulcerative condition of the oral mucosa

Aphthous Ulcers Classification:

1. Minor aphthous ulcers
2. Major aphthous ulcers
3. Herpetiform ulcers

Aphthous Ulcers Etiology:

• Genetic predisposition
• Exaggerated response to trauma
• Immunological factors- immunosuppression
• Microbiologic factors- herpes simplex virus
• Nutritional deficiency
• Systemic condition- Behcet’s syndrome, Crohn’s disease
• Hormonal imbalance
• Nonsmoking
• Allergy and chronic asthma
• Stress and anxiety

Aphthous Ulcers Clinical Features:

• Develops over movable, non-keratinized oral mucosa
• Produces burning or tingling sensation
• Recurs in about 3-4 weeks
  • Minor Aphthous Ulcer
    • Occurs either single or in clusters
    • It is painful, shallow, round, or elliptical
    • Size-2-3 mm in diameter
    • It is surrounded by an erythematous halo
    • Covered by yellowish fibrinous membrane
    • Lasts for 7-10 days
    • Heals without scarring
  • Major Aphthous Ulcer
    • Size- larger, 0.5 cm in diameter
    • More painful lesion
    • Makes the patient ill
    • Appears crateriform
    • Heals with scar formation
    • Transforms into malignancy
  • Herpetiform ulcers
    • Extremely painful, small ulcers
    • Number-few dozen to hundred
    • An ulcer is surrounded by a zone of erythema
    • Size-1-2 mm in diameter
    • Lasts for several weeks or months
    • Heals within 1-2 weeks

Aphthous Ulcers Differential Diagnosis:

• Herpetic ulcers
• Traumatic ulcers
• Pemphigus Vulgaris
• Cicatricial pemphigoid
• Ulcers due to neutropenia

Bacterial Infections Of Oral Cavity Shot Essays

Question 1. Difference Between major and minor aphthous ulcers
Answer:

Difference Between Major And Minor Aphthous Ulcers

Question 2. Tuberculous ulcer of the oral cavity
Answer:

Tuberculous Ulcer Of The Oral Cavity

Tuberculous lesions of the oral cavity occur secondary to pulmonary Infections

1. Chronic ulcers
   1. Present over tongue, palate, gingiva, lips, buccal mucosa, alveolar ridge and vestibules
   2. Superficially located
   3. Have Irregular edges and Induration
   4. The base Is granular and covered by pseudomembrane
   5. Presence of single or multiple nodules
   6. Size- pinhead size
   7. Color- green color
2. Tongue lesion
   • Seen over lateral borders
   • They are well-defined, painful, firm, and yellowish-grey In color
   • Surrounding mucosa appears Inflamed and edematous
3. Palatal lessons
   • Seen over the hard palate
   • They are small ulcers
4. Lip lesions
   • Produces small, nongendered, granulating ulcers at mucocutaneous junctions
5. Gingival lesions
   • Produces small granulating ulcers or erosive lesions
   • Gingival hyperplasia
   • Presence of diffuse, hyperactive, nodular, or papillary projections from the gingival margin
6. Salivary glands
   • Generalized glandular swelling or abscess formation along with pain
   • Facial nerve palsy
   • Fistula tract formation
7. Lesions of jawbones
   • Sinus or fistula formation
   • Osteomyelitis
   • Trismus
   • Paraeslhesla
   • Lymphadenopathy
   • Sinus or fistula formation
   • Pain and swelling of |aw bones

Question 3. Scarlet Fever
Answer:

Scarlet Fever

• Scarlet fever is caused by streptococcus B- hemolytic

Scarlet Fever Clinical Features:

• Age 3-12 years of age
• Fever
• Headache
• Vomiting
• Tonsilitis, pharyngitis, generalized lymphadenopathy
• Tonsils, soft palate, and pharynx become erythematous
• Diffuse, bright red skin rash appears over the chest and spreads to other parts of the body
• Skin rashes undergo desquamation

Scarlet Fever Oral Manifestations:

• Skin rash over the face refers to sunburn with goose pimples
• Face is flushed
• The oral cavity exhibits generalized edema, elongation of uvula, and diffuse petechiae over the soft palate
• Congested and inflamed palate
• Congestion of oral mucosa
• Hal Koala
• Strawberry tongue reddened fungiform papillae project like small, red knobs
• Later tongue appears beefy red with hyperplastic fungiform papillae called raspberry tongue

Scarlet Fever Complications:

• Cancrurnoris
• Ulceration with perforation of the palate
• Osteomyelitis
• Peritonsillar abscess
• Mastoiditis, rhinitis, sinusitis, arthritis, meningitis
• Pneumonia
• Rheumatic fever
• Acute glomerulonephritis
• Septicaemia

Question 4. Diphtheria
Answer:

Diphtheria Etiology:

• Diphtheria is caused by Corynebacterium diphtheria

Diphtheria Clinical Features:

• Diphtheria is insidious at the onset
• Moderate grade fever
• Tachycardia
• Sore throat
• Formation of greyish-greenish pseudomembrane on the tonsils
• Swollen neck- Bull neck
• Tender lymphadenopathy
• Nasal infection
• Hoarseness of voice
• Cough
• Respiratory obstruction
• Acute circulatory failure
• Myocarditis
• Nerve palsies
• Dysphagia
• Dysphonia
• Paraesthesia in the limbs

Diphtheria Management:

• Antitoxin diphtheric serum (ADS)
  • The dose varies from 20,000 to 1,00,000 units depending on the duration and severity of the disease
  • In mild cases, a lesser dose may be used
• Antibiotics
  • Penicillin G-6,00,000 units every 12 hourly intravenously or
  • Amoxycillin 500 mg 8 hourly for 7-10 days
  • Patient allergic to penicillin
    • Erythromycin- 500 mg 6 hourly or
    • Azithromycin 500 mg daily or
    • Rifampicin 600 mg daily
    • Tracheostomy

Question 5. Actinomycosis
Answer:

Actinomycosis

• Actinomycosis is a chronic granulomatous disease

Actinomycosis Causative Organisms:

Actinomycosis Forms:

Actinomycosis Clinical Features:

• Actinomycosis is characterized by
  • Multiple abscesses
  • Tissue destruction
  • Fibrosis
  • Formation of multiple sinuses
  • Painless indurated swelling
• Gingivitis
• Periodontitis

Actinomycosis Treatment:

• Draining of abscess
• Excision of sinus tract
• Use of antibiotics- penicillin and tetracyclines

Question 6. Pyogenic Granuloma
Answer:

Pyogenic Granuloma

• Pyogenic granuloma represents an over-exuberant tissue reaction to some known stimuli or Injuries

Pyogenic Granuloma Clinical Features:

• Age-at early age
• Sex- common in females
• Presence of small, pedunculated or sessile, painless, soft, tabulated growth on gingiva
• Pyogenic Granuloma gets ulcerated and bleeds profusely
• Covered by yellow fibrinous membrane
• Size-upto 1 cm in diameter
• This leads to fibro-epithelial polyp
• Pyogenic Granuloma is common in pregnancy, so it is known as a “pregnancy tumor”

Pyogenic Granuloma Histopathology:

• Pyogenic Granuloma consists of lobular masses of hyperplastic granulation tissue containing multiple proliferating fibroblasts, blood capillaries, and chronic inflammatory cells
• There is the proliferation of endothelial cells
• The overlying epithelium is thin and ulcerated
• Connective tissue shows intercellular edema
• There is the presence of areas of hemorrhage and hemosiderin pigments

Pyogenic Granuloma Treatment: Surgical excision

Bacterial Infections Of Oral Cavity Short Question And Answers

Question 1. Gumma
Answer:

Gumma

• Syphilitic gumma is a lesion caused by tertiary syphilis
• Gumma is a solitary, localized rubbery lesion with central necrosis seen in the original like the liver, testis, bone, and brain-associated scarring of hepatic parenchyma.
• Histologically, the structure of gumma shows the following:
• Qintral coagulative necrosis resembles caseation but is less destructive so that outlines of necrotic cells can still be seen.
• Surrounding zone of palisaded macrophages with lymphocytes, plasma cells, giant cells, and fibroblasts.

Question 2. Hutchison’s Triad
Answer:

Hutchison’s Triad

• Hutchison’s Triad is a feature of congenital syphilis
• Hutchison’s Triad includes:
  • Interstitial keratitis
    • Hutchison’s Triad results from opacification of the corneal surface with resultant loss of vision
  • Enamel hypoplasia of permanent incisors and 1st permanent molars
  • Eight nerve deafness

Question 3. Condyloma Lata
Answer:

Condyloma Lata

• Condyloma Lata is a feature of secondary syphilis
• Condyloma Lata is a skin lesion occurring in the form of nodular, flat, or papillary form
• Condyloma Lata resembles viral papilloma

Question 4. Treponema pallidum
Answer:

Treponema pallidum

• Treponema pallidum is a causative organism of syphilis
• Treponema pallidum is a thin, delicate spirochaete with tapering ends having about ten regular spirals
• Treponema pallidum is actively motile showing rotation around the long axis, backward and forward movements, and flexion of the whole body
• Treponema pallidum can be seen by dark ground microscopy
• Treponema pallidum enters the body through minute abrasions on the skin and mucosa

Question 5. Kveim-Siltzbatch test
Answer:

Kveim-Siltzbatch Test

• Kveim-Siltzbatch Test is an intracutaneous test for the diagnosis of sarcoidosis
• Kveim-Siltzbatch Test utilizes suspension of human-known sarcoid tissues test antigen
• Kveim-Siltzbatch Test has a high degree of specificity
• Kveim-Siltzbatch Test is important to aid in the early and accurate diagnosis of disease

Question 6. Noma or cancrum oris
Answer:

Noma Or Cancrum Oris

• Noma is a rapidly spreading and extremely severe granulomatous infection of orofacial tissues

Noma or Cancrum Oris Causative Organisms:

• Fusobacterium necrophorum
• F.nucleatum
• Prevotella intermedia

Noma Or cancrum Oris Clinical Features:

• Age-1-10 years of age
• There is a formation of painful, red, indurated papule over the gingiva
• It gets ulcerated and spreads to mucosal surfaces called necrotizing ulcerative mucositis
• A small, dark, reddish-purple area appears on the skin over the cheek
• Later large hole of a few inches develops on the cheek
• Severe sore mouth
• Increased salivation
• Diffuse edema of the face
• Foul smell from mouth

Question 7. Histopathology of Tuberculosis ulcer
Answer:

Histopathology of Tuberculosis Ulcer

• Tuberculosis ulcer consists of central areas of caseous necrosis surrounded by lymphocytes, epithelioid cells, and multinucleated Langerhans giant cells
• Epitheloid cells are altered macrophages
• Area of caseous necrosis appears eosinophilic
• Presence of tubercle bacilli
• Tuberculosis Ulcer is surrounded by fibrous tissue and lymphocytes

Question 8. Ghon’s Complex
Answer:

Ghon’s Complex

• Primary complex/Ghons complex/childhood tuberculosis/ is primary tuberculosis.
• Is the infection of an individual who has not been previously infected/immunized.
• Ghon’s Complex consists of 3 components:
  • Pulmonary component
  • Lymphatic vessel component
  • Lymph node component.
• The most commonly involved tissues for the primary complex are the lung and hilar lymph nodes.
• Tubercle bacilli, either free/within phagocytes drain the regional lymph nodes, which often causes.
• This combination of the parenchymal lesion and nodal involvement is referred to as Ghons complex

Question 9. Sarcoidosis
Answer:

Sarcoidosis

• Sarcoidosis is a multi-system chronic granulomatous disease

Sarcoidosis Clinical Features:

• Age- 20-40 years of age
• Sex- common in females
• The organs involved are:
  • Lymph nodes
  • Salivary glands
  • Skin
  • Bone
• Fever, malaise
• Dry cough
• Weight loss
• Chest pain, dyspnea
• The presence of multiple, slow-growing, red patches over the skin which may ulcerate

Sarcoidosis Oral Manifestations:

• Keratoconjunctivitis
• Enlargement of parotid gland
• Xerostomia
• Small nodular submucosal growth appears over soft palate, gingiva, floor of mouth, or cheek
• Multiple erythematous nodules develop over the cheek, labial mucosa, and hard palate

Question 10. Mantoux Test Or Tuberculin Test
Answer:

Mantoux Test Or Tuberculin Test

• It is a routinely used method for tuberculin testing

Mantoux Test Or Tuberculin Test Method:

• 0.1 ml of purified protein derivative/ PPD containing 51D, tuberculin unit is injected intradermally into the flexor aspect of the forearm
• Mantoux Test is given between layers of the skin
• The site is examined after 48-72 hours for induration

Mantoux Test Or Tuberculin Test Result:

Mantoux Test Or Tuberculin Test Significance:

Question 11. Lumpy Jaw
Answer:

Lumpy Jaw

• Lumpy Jaw is a cervicofacial form of actinomycosis
• Lumpy Jaw is caused by Actinomyces israelii
• It is soft tissue swelling developing in the mandibular anterior region
• Develops abscess with discharge of pus containing sulfur granules
• The skin overlying the abscess is purplish red, indurated, and fluctuant
• Abscess may perforate the skin surface

Question 12. Chancre
Answer:

Chancre

• Chancre is one of the clinical findings of primary syphilis
• Incubation period 3-90 days
• Site
  • Penis in males
  • Vulva or cervix in females
• Chancre is slightly raised over the surface
• Chancre becomes ulcerated
• Chancre is a non-tender, non-bleeding firm plaque
• Shape- round and indurated
• Size- varies from 5 mm to several centimeters
• Edges- rolled raised edges are seen
• Chancre disappears without treatment

Bacterial Infections Of Oral Cavity Viva Voce

1. The causative organism of syphilis is Treponema pallidum
2. DOTS therapy is used in tuberculosis patients
3. Clostridium tetani causes tetanus
4. Raspberry tongue and strawberry tongue are peculiar features of scarlet fever
5. Diphtheria is caused by Corynebacterium diphtheria
6. Scarlet fever is caused by streptococcus B- hemolytic
7. The Kim-Siltzbatch test is used for the diagnosis of Sarcoidosis
8. Bull neck is a condition -seen in diphtheria
9. Diphtheria may lead to death due to airway obstruction
10. Asteroid bodies or Schaumann bodies are a histological feature of Sarcoidosis
11. Pyogenic granuloma leads to fibroepithelial polyp
12. Intercellular edema is seen in connective tissue in the case of pyogenic granuloma.