Oral Pathology

Diseases Of Blood And Blood Forming Organs Important Notes

1. Plummer-Vinson syndrome

• Iron deficiency anemia
• Carcinoma of hypopharynx
• Koilonychias

2. Types of anaemia

3. Hair on-end appearance is seen in

• Thalassemia
• Sickle cell anemia

4. Anitschow cells

• They are modified epithelial cells with
  • Elongated nuclei
  • Linear bar of chromatin
  • Seen in
• Sickle cell anemia
  • Iron deficiency anemia
  • Aphthous ulcer
  • Rheumatic heart disease

5. Clotting factors

6. Types of leukemia

7. Agranulocytosis

• Mostly occurs due to the ingestion of drugs like
  • Amidopyrine
  • Barbiturates
  • Chloramphenicol
  • Quinine
    • Sulfonamides
• Features
  • Presence of infection in the oral cavity, GIT, genitourinary tract, respiratory tract, and skin
  • Oral manifestation
    • Necrotizing ulcerations of oral mucosa, pharynx, tonsils
    • Rapid destruction of supporting tissues of the teeth

8. Cyclic neutropenia

• It is characterized by periodic cyclic diminution of leukocytes
• Cycle commonly occurs every 3 weeks
• Loss of alveolar bone around the teeth is an important oral manifestation

Diseases Of Blood And Blood Forming Organs Short Question And Answers

Question 1. Describe leukemia
Answer:

Leukemia

Leukemia: Leukemia is a disease characterized by the progressive overproduction of white blood cells which usually appears in the circulating blood in an immature form

Leukemia Etiology:

• Chromosomal abnormality-presence of Philadelphia chromosome
• Exposure to high doses of radiation therapy
• Exposure to certain chemicals- benzene, phenyl butanone
• Following chemotherapy treatment
• Myeloproliferative disorders like polycythemia vera
• Congenital or genetic abnormalities- Down’s syndrome
• The presence of primary immune deficiency
• Infection with human leukocyte virus
• Hereditary

Leukemia Classification:

1. Acute leukemia
   • Acute lymphocytic leukemia
   • Acute myeloblastic leukemia
2. Chronic leukemia
   • Chronic myelogenous leukemia
   • Chronic lymphocytic leukemia

Read And Learn More: Oral Pathology Questions and Answers

Clinical Features:

• Acute type is more common in children and young adults while chronic is more common in adults of middle age
• Males are more affected than females
• Fatigue
• Generalised weakness, malaise
• Easy bruising
• Epitaxis
• Headache
• Vomiting
• Generalised pain
• Hepatosplenomegaly
• Anaemia
• Persistent fever
• Weight loss
• Heat intolerance
• Scattered petechiae, ecchymosis
• Generalised lymphadenopathy
• Shortness of breath
• Tachycardia
• Hyperuricaemia
• Cerebral hemorrhage
• Increased intracranial pressure
• Cranial nerve palsies

Leukemia Oral Manifestations:

1. Gingiva
   • Gingivitis
   • Gingival hyperplasia
   • Enlargement of interdental papillae
   • Gingival tissues become swollen
   • Cyanotic bluish discoloration of gingiva
   • Thrombosis of gingival vessels
2. Teeth
   • Rapid loosening of teeth
   • Alterations in developing tooth crypts
   • Destruction of lamina dura
   • Displacement of teeth
3. Oral mucosa
   • Thinning of oral mucosa
   • Petechiae and ecchymosis develop over oral mucosa
   • Multiple large irregular necrotic ulcers develop
4. Other
   • Large hematomas over the lower lip
   • Oral infections
   • Palatal ulcerations
   • Mental nerve neuropathy
   • Prolonged post-extraction bleeding
   • Osteomyelitis of jaw

Leukemia Diagnosis:

1. Blood
   • WBC count- reduced
   • Presence of abnormal leukocytes
   • Platelet count- low
   • Hemoglobin levels- reduced
2. Bone marrow aspiration
   • Detects increase in the number of bone marrow cells
3. Lumbar puncture
   • Determines the presence of blast cells in CNS
4. Radiographic appearance
   • Chest X-ray- detects mediastinal involvement
   • Skeletal X-ray- Detects skeletal lesions
   • MRI and CT scan- detects lesions and site of infection
5. Lymphangiogram
   • Locates malignant lesions

Leukemia Treatment:

• Chemotherapeutic drugs
• Radiation therapy
• Corticosteroids

Question 2. What is anemia? Classify anemia. Write about clinical features and treatment of pernicious anemia.
Answer:

Anaemia: It is defined as an abnormal reduction in the number of circulating red blood cells, the quantity of hemoglobin, and the volume of packed red cells in a given unit of blood

Anaemia Classification: Etiological classification

1. Loss of blood
   • Acute posthemorrhagic anaemia
   • Chronic posthemorrhagic anaemia
2. Excessive destruction of red cells
   • Extracorpuscular causes
     • Antibodies
     • Infections
     • Drugs
     • Chemicals
     • Trauma to RBC
   • Intracorpuscular causes
     • Hereditary
       • Disorders of glycolysis
       • Abnormalities of RBC membrane
     • Acquired
       • Lead poisoning
     • Impaired blood production
       • Iron deficiency anemia
       • Pernicious anemia
       • Megaloblastic anemia
       • Protein deficiency
       • Ascorbic acid deficiency
3. Inadequate production of mature erythrocytes
   • Deficiency of erythroblasts
   • Infiltration of bone marrow
   • Endocrine abnormality
   • Chronic renal disease
   • Chronic inflammatory diseases
   • Cirrhosis of liver

Pernicious Anaemia: Pernicious anemia is a relatively chronic hematological disease

Pernicious Anaemia Clinical Features:

• Occurs after the age of 30
• Males are commonly affected
• Triad of symptoms: generalized weakness, sore and painful tongue, and numbness or tingling of the extremities
• Easy fatigability
• Headache, dizziness
• Nausea, vomiting, diarrhea, loss of appetite
• Shortness of breath
• Loss of weight
• Pallor
• Abdominal pain

Pernicious Anaemia Oral Manifestations:

• Glossitis
• Painful ami burning lingual sensation
• Inflamed and beefy red tongue
• Hunter’s glossitis
• Presence of small and shallow ulcers
• Atrophy of papillae- bald tongue
• Dysphagia
• Pallor of oral mucosa
• Hyperpigmentation of oral mucosa
• Increased susceptibility to oral infections

Pernicious Anaemia Treatment: Administration of Vitamin B12 and folio acid

Question 3. Hemophilia
Answer:

Hemophilia

Hemophilia is a potentially fatal inherited bleeding disorder characterized by profound hemorrhage due to genetic deficiency of clotting factors

Hemophilia Etiology:

• Hereditary
• Se-linked recessive trait
• Spontaneous mutations

Hemophilia Types

Hemophilia Clinical features

• Persistent bleeding following mild injury or spontaneously
• Easy bruising
• Bleeding into muscles and joints causing pain
• Spontaneous bleeding into subcutaneous tissues or internal organs resulting in hematoma formation
• Epitaxis
• Haemarthrosis
• Gastric hemorrhage
• Spontaneous hematuria
• Intracranial hemorrhage

Hemophilia Oral Manifestations:

• Massive and prolonged gingival hemorrhage
• Internal blooding Into the glottis
• Recurrent subperiosteal hematoma
• Deep tissue blooding In the oropharyngeal region
• Severe periodontal disease

Laboratory Findings

Hemophilia Treatment:

• Immediate transfusion of factor 8 or 9
• Transfusion of packed red blood cells or white blood cells to replace blood volume
• Prophylactic transfusion of factor 8 to a level of 50% above normal
• Use of local hemostatic agents to control topical bleeding
• Analgesics and corticosteroids to reduce joint pain and swelling
• Joint immobilization
• Use of intravenous desmopressin

Question 4. Cyclic neutropenia
Answer:

Cyclic neutropenia

Cyclic neutropenia is a rare form of agranulocytosis characterized by periodic decrease in circulating neutrophils due to bone marrow maturation arrest

Cyclic neutropenia Clinical Features:

• Can affect any age group
• Fever, malaise
• Sore throat
• Stoamtitis
• Regional lymphadenopathy
• Headache
• Arthritis
• Cutaneous infection
• Conjunctivitis

Cyclic neutropenia Oral Manifestations:

• Severe gingivitis
• Stomatitis
• Aphthous tike ulceration
• Serve gingival recession
• Rapid alveolar bone loss
• Tooth mobility
• Cyclic neutropenia

Cyclic neutropenia Diagnosis

Question 5. Agranulocytosis
Answer:

Agranulocytosis

Agranulocytosis is a serious acute leukopenia characterized by a significant decrease in neutrophil count

Agranulocytosis Etiology:

• Toxic effects of drugs
• Ionizing radiation
• Tuberculosis
• Typhoid fever
• Malaria

Agranulocytosis Clinical Features:

• Occurs at any age- common in adult women
• High fever with chills and sore throat
• Malaise, weakness
• Pallor skin
• Regional lymphadenopathy
• Severe dysphagia
• Urinary tract infections
• Weak and rapid pulse

Agranulocytosis Oral Manifestation:

• Necrotizing ulcerations Involving gingiva, soft palate, tonsils, lips, pharynx, and check.
• Gingival Weeding
• Excessive salivation
• Dysphagia
• The halitosis-Excessive tendency for secondary Infections
• Acute necrotizing ulcerative gingivitis
• Opportunistic fungal infections

Agranulocytosis Treatment:

• Elimination of causative factors
• Antibiotics
• Vitamin
• Antipyretics
• High-caloric soft diet

Question 6. Iron deficiency anemia
Answer:

Iron deficiency anemia

Iron deficiency anemia is a chronic, microcytic, hypochromic anemia

Iron deficiency anemia Etiology:

• Chronic blood loss
• Inadequate dietary intake
• Faulty iron absorption
• Increased demand for iron

Iron deficiency anemia Clinical Features:

• Fatigue
• Palpitations
• Dizziness
• Sensitivity to cold
• Generalized weakness
• Lemon-tinted pallor skin
• Koilonychia- spoon-shaped nails

Iron deficiency anemia Oral Manifestations:

• Pallor of oral mucosa
• Loss of keratinization of gingiva
• Atrophic mucositis
• Atrophic glossitis
• The tongue appears smooth, bald, and red with a burning sensation
• Abnormal bleeding from ulcers
• Angular cheilitis
• Delayed wound healing

Iron deficiency anemia Diagnosis:

• Peripheral blood smear- shows microcytic, and pale RBCs
• Hemoglobin level- reduced
• RBC count- reduced
• Serum iron- reduced
• Total iron binding capacity- elevated
• MCV, MCH, and MCHC- reduced
• Hemosiderin- absent

Iron deficiency anemia Treatment:

• High protein diet
• Replacement of iron by 300 mg ferrous sulfate tablet, 3-4 tablets per day for 6 months

Question 7. Plummer-Vinson syndrome
Answer:

Plummer-Vinson syndrome

• It is a feature of iron deficiency anemia
• It mainly occurs in women in the 4th-5th decade of life
• It consists of a triad of symptoms
  • Angular cheilitis
    • Cracks or fissures at the corners of the mouth
  • Glossitis
    • Smooth, red, and painful tongue
    • Atrophy of filiform and fungiform papillae
  • Dysphagia
    • This leads to the limitation of diet to a soft diet
    • Such patients are susceptible to oral cancers and pre-cancers

Question 8. Sickle cell anemia
Answer:

Sickle cell anemia

Sickle cell anemia is a hereditary type of chronic hemolytic disease

Sickle cell anemia Clinical Features:

• More common in females younger than 30 years
• Fever
• Weakness, fatigue
• Shortness of breath
• Joint pain
• Abdominal pain
• Nausea, vomiting, loss of appetite
• Systolic murmur
• Cardiomegaly
• Jaundice
• Loss of consciousness-sickle cell crisis
• Increased susceptibility to infection
• Renal failure
• Hypoxia, hypothermia

Sickle cell anemia Diagnosis:

• Total RBC count-reduced
• Hemoglobin level-reduced
• Serum unconjugated bilirubin-raised
• Presence of Hb-S in blood

Question 9. Rh pump
Answer:

Rh pump

• Rh pump is the term by Waston
• It is seen in erythroblastosis fetalis
• Enamel hypoplasia involves the p[ortion of the deciduous cuspid and first molar crown
• This results in a characteristic ring-like defect
• This is called the Rh pump

Question 10. Eosinophilic granuloma

Answer:

Eosinophilic granuloma

• Eosinophilic granuloma was introduced by Lichtenstein
• It describes a lesion of bone which is primarily a histiocytic proliferation with an abundance of eosinophilic leukocytes

Eosinophilic granuloma Clinical Features:

• Initially asymptomatic
• Later causes local pain, swelling, and tenderness of the involved bone
• General malaise, weakness
• Fever
• Sites Involved are:
• Skull
• Mandible
• Femur
• Humerus
• Ribs

Eosinophilic granuloma Treatment:

• Surgical currettage
• Radiotherapy

Question 11. Polycythaemia
Answer:

Polycythaemia

It is a chronic stem cell disorder with an insidious onset

Polycythaemia Clinical Features:

• Headache
• Dizziness
• Weakness, lassitude
• Tinnitus
• Visual disturbances
• Mental confusion
• Slurring of speech
• Inability to concentrate
• Flushing or diffuse reddening of skin

Polycythaemia Oral Manifestations:

• Oral mucosa appears deep purplish red
• Cyanosis
• Gingiva are often engorged and swollen and bleed easily
• Submucosal petechiae
• Hematoma formation
• Increased susceptibility to infections

Question 12. Purpura
Answer:

Purpura

Purpura is defined as purplish discoloration of the skin and mucous membrane due to spontaneous extravasation of blood

Purpura Types:

• Non-thrombocytopenic purpura
• Thrombocytopenic purpura
• Primary purpura
• Secondary purpura

Purpura Clinical Features:

• Commonly occurs in females below 40 years of age
• Petechiae, ecchymosis
• Hematoma formation
• Purpuric spots
• Excessive gingival bleeding
• Blister formation over oral mucosa
• Excessive bruising
• Epitaxis
• Hematuria
• Melena and hematemesis
• Spontaneous bleeding
• Prolonged bleeding per surgery or injury
• lnlmerenlel bleeding

Question 13. Strawberry tongue
Answer:

Strawberry tongue

• It Is the oral manifestation of scarlet fever
• The tongue exhibits a white coating
• Fungiform papillae are edematous and by pernnomlc
• The project above the surface of the tongue as small red knobs
• So-called strawberry tongue

Question 14. Thalassaemia
Answer:

Thalassaemia

Thalassaemia is a genetically determined disorder of hemoglobin synthesis with decreased production of either alpha or beta polypeptide chain of the hemoglobin molecule

Thalassaemia Clinical Features:

• Jaundice
• Fever with chills
• Anaemia
• Malaise with generalized weakness
• Hepatosplenomegaly
• Bone marrow hyperplasia
• Leg Ulcers
• Severe infections in tissues
• Mongloid prominent forehead, depressed time bridge, prominent cheekbones, protrusion of maxillary anterior teeth, and slanting eyes
• High cardiac failure
• Xerostomia
• Severe malocclusion
• Retracted upper lip
• Discoloration of teeth

Question 15. Hair on-end appearance
Answer:

Hair on-end appearance

• It is a radiographical feature of the skull bone
• Appears as a thin, poorly defined inner and outer cortex of the bone
• Trabeculae between them are coarse, elongated and bristle-like
• This produces hair with an end appearance
• Seen in
  • Thalassemia
  • Sickle cell anemia

Question 16. Chloroma
Answer:

Chloroma

• It is a solid collection of leukemic cells occurring outside of bone marrow
• Seen in
  • Acute myeloid leukemia
  • Myeloproliferative
  • syndrome
  • Eosinophilic leukemia

Chloroma Clinical features

• Skin lesions appear as raised, nontender plaques or nodules
• Oral lesions appear as swollen and painful gingiva that bleeds profusely

 

Diseases Of Blood And Blood Forming Organs Viva Voce

1. Rh hump is seen in erythroblastosis fetalis
2. The bald tongue of the sandwich is a feature of pernicious anemia
3. Howell Jolly bodies are seen in pernicious anemia
4. Safety pin cells are seen in thalassemia
5. Sickle cell anemia occurs due to the substitution of valine for glutamic acid of the sixth position of the beta globulin chain
6. Philadelphia chromosome is seen in chronic myeloid leukemia
7. Most common form of leukemia in children is acute lymphocytic leukemia
8. Splenomegaly of moderate grade is seen in acute leukemia
9. Massive splenomegaly is seen in chronic leukemia
10. Purplish discoloration of skin occurs in purpura
11. The presence of Hb-S is seen in sickle cell anemia
12. Hunter’s glossitis is seen in pernicious anemia

 

Allergic And Immunological Diseases Of Oral Cavity Important Notes

1. Recurrent aphthous stomatitis
   • It is a common disease characterized by the development of painful recurring solitary or multiple ulceration of the oral mucosa
   • Recurrent aphthous stomatitis Etiology
     • Bacteria – alpha-hemolytic streptococci, strep. Sanguis
     • Genetic factors
     • Immunologic abnormality
     • Iron, vitamin B12, folic acid deficiency
     • Allergic factors
     • Trauma
     • Endocrine factors
     • Psychic
     • Systemic disease – Behcet’s syndrome, cyclic neutropenia, HIV infection
   • Recurrent aphthous stomatitis Classification
     • Recurrent aphthous minor
     • Recurrent aphthous major
     • Recurrent Herpetiform ulceration
     • Recurrent ulcers associated with Behcet’s syndrome
   • Recurrent aphthous stomatitis Clinical features
     • Presence of small nodules
     • Burning sensation
     • Erythema
     • General edema of the oral cavity
     • Paraesthesia
     • Malaise
     • Low-grade fever
     • Local lymphadenopathy
     • Vesicle-like lesions containing mucus
     • Ulcer-presenting features
       • Single/multiple erosions
       • Covered by grey membrane
       • Has necrotic center with clearly defined raised margins surrounded by erythematous halo
       • Painful
       • Interferes with eating and speech
       • f.No -1-100
       • Size – 2-3 mm to 10 mm in diameter

Allergic And Immunological Diseases Of Oral Cavity Short Question And Answers

Question 1. Contact Stomatitis
Answer:

Contact Stomatitis

• Contact stomatitis is an allergic reaction due to local application or contact with certain drugs, foods, restorative materials, gentrifies, etc.
• It can be acute or chronic

Contact Stomatitis Cause:

• Antigen-antibody reaction at the site of contact

Contact Stomatitis Treatment:

1. In mild cases
   • Removal of suspected allergens
   • Antihistamines along with topical anesthetic agents
2. In chronic cases
   • Removal of the antigenic source
   • Application of topical corticosteroids like fluocinonide or dexamethasone elixir

Question 2. Histamines
Answer:

Histamines

• Histamine is an amine of the tissues present in all the tissues of the body in an inactive or bound form
• It is liberated as active histamine during
  • Injury to tissues
  • Antigen-antibody reaction
• It is destructed by antihistaminic drugs

Contact Stomatitis Actions:

• Vasodilatation
• Increases vascular permeability
• Causes itching and pain
• Constricts the smooth muscles of the bronchi

Question 3. Immunoglobulin
Answer:

Immunoglobulin

Immunoglobulin is defined as a protein of animal origin endowed with known antibody activity

Immunoglobulin Synthesis:

• They are synthesized by plasma cells and lymphocytes

Immunoglobulin Structure: Immunoglobulin consists of

1. Two heavy chains
2. Two light chains

• Variable mg ion Is present at the amino terminus while constant region is present at the carboxy-terminal
• Rased on heavy chains, immunoglobulins are deed filed Into 5 classes
• Light chains In all classes are Kappa and Lambda

Question 4. Anitschkow cells
Answer:

Anitschkow cells

• Wood and his associates have described characteristic changes In the nuclei of epithelial cells taking cytological smears from around recurrent aphlhousulers
• These are referred to as Anitschkow cells
• It consists of cells with elongated nuclei containing a linear bar of chromatin with radiating processes of chromatin extending toward the nuclear membrane
• Its Ultrastructure has been described by Haley and his associates
• They found that the nuclear chromatin was made up of pleomorphic masses forming an irregular band along the long axis of the nucleus
• Anitschkow cells are also found in patients with
  • Sickle cell disease
  • Megaloblastic anemia
  • Iron deficiency anemia
  • In children receiving chemotherapy for cancer
  • Normal persons

Read And Learn More: Oral Pathology Questions and Answers

Question 5. Delayed hypersensitivity
Answer:

Delayed hypersensitivity

• Delayed hypersensitivity reaction is mediated by sensitized T-lymphocytes
• It cannot be passively transferred by serum but can be transferred by lymphocytes or the transfer factor

Delayed hypersensitivity Pathogenesis:

Delayed hypersensitivity Types:

1. Tuberculin type
2. Contact dermatitis type

Question 6. Antischkow cell
Answer:

Antischkow cell

• Present in recurrent aphthous ulcer
• Characteristic features are
• Elongated nuclei
• Linear bar of chromatin
• Few radiating processes extend toward the nuclear membrane

Allergic And Immunological Diseases Of Oral Cavity Viva Voce

1. Anitschkow cells are characteristic cells of recurrent aphthous ulcer
2. Behcet’s syndrome consists of oral and genital ulceration, ocular lesions, and skin lesions
3. Reiter’s syndrome is associated with urethritis, Balanitis, conjunctivitis, and mucocutaneous lesions
4. Sarcoidosis is a multisystem granulomatous disease of unknown origin characterized by the formation of uniform, discrete, compact, noncaseating epithelioid granuloma
5. Angioedema is a diffuse oedematous swelling of the skin, mucosa, and submucosal connective tissue
6. The allergic reaction of the skin is called dermatitis medicamentosa
7. Contact stomatitis is a type of reaction in which a lesion of the skin or mucous membrane occurs at a localized site after repeated contact with the causative agent
8. Wegener’s granulomatosis is a disease with urn known etiology that involves the vascular, renal, and respiratory systems.

Oral Aspects Of Metabolic Diseases Important Notes

1. Normal serum levels

2. Total values of elements In the body

3. Daily requirements

4. Deficiencies of different minerals cause

5. Types of calcium in plasma

• Ionized form
• Protein-bound
• Complex form

6. Selenium-containing amino adds

• Selenomethionine
• Selenocysteine
• Selenocysteine

7. Progeria

• Described by Hutchison in 1886
• Characterised by dwarfism and premature senility
• Clinical features
  • Manifestations begins within 1st few years
  • Alopecia
  • Pigemented areas of trunk
  • Atrophic skin
  • Prominent veins
  • Loss of subcutaneous fat
  • High-pitched squeaky voice
  • Beak like nose
  • Hypoplastic mandible
  • Coxa valga
  • Exophthalmos
  • Muscular atrophy
  • Joint deformities
  • Intelligence is normal or above normal
  • Patient resembles wizened little old person at a very early age
  • No patient lives beyond the age of 27 years
• Oral manifestations
  • Accelerated formation of irregular dentin
  • Delayed eruption of teeth

Read And Learn More: Oral Pathology Question And Answers

8. Vitamins

 

Oral Aspects Of Metabolic Diseases Short Question And Answers

Question 1. Hypopituitarism
Answer:

Hypopituitarism

Hypopituitarism is a condition of deficiency of pituitary hormone

Hypopituitarism Causes:

• Tumour of pituitary
• Hypophyseal fibrosis
• Supracellar cyst
• Destruction of pituitary gland

Hypopituitarism Clinical Features:

• Short stature of the body
• Presence of fine, silky, sparse hair over body
• Wrinkled atrophic skin
• Hypogonadism
• Extreme weight loss
• Coma and death in severe cases

Hypopituitarism Oral Manifestations:

• Small face
• Delayed exfoliation of deciduous teeth
• Delayed root completion
• Delayed eruption of permanent teeth
• Hypofunction of salivary gland
• Decreased salivary flow
• Increased caries activity and periodontal disease
• Crowding of teeth
• Underdevelopment of maxilla, mandible, and 3rd molars
• Smaller crown size and root length of teeth

Hypopituitarism Diagnosis:

• Hypoglycaemia
• Decreased serum growth hormone levels
• Skull X-ray- reveals tumour in cellar region
• CT scan and MRI- detects brain tumour

Hypopituitarism Treatment:

• Correction of skeletal and dental malocclusion
• Fluoride application
• Corticosteroids

Question 2. Hyperpituitarism
Answer:

Hyperpituitarism

• Hyperpituitarism is an increased production of growth hormone
• It results in gigantism in infants and acromegaly in adults

Hyperpituitarism Etiology:

• Pituitary adenoma
• Increased function of anterior pituitary

Hyperpituitarism Clinical Features:

1. Gigantism
   • Overgrowth of body
   • Excessive perspiration
   • Headache
   • Lassitude
   • Fatigue
   • Muscle and joint pain
   • Defective vision
   • Genital underdevelopment
   • Hypertension
2. Acromegaly
   • Thick bones with larger hands and feet
   • Increase in ribs size
   • Barrel shaped chest
   • Temporal headache
   • Increased intracranial tension
   • Photophobia
   • Blurred vision
   • Hepatomegaly, cardiomegaly
   • Osteoporosis
   • Arthralgia, myalgia
   • Bowing of legs

Hyperpituitarism Oral Manifestations:

1. Gigantism
   • Broad, enlarged nose
   • Enlarged maxilla and mandible
   • Large siae of teeth and root
   • Macroglossia
   • Class 3 malocclusion
   • Interdental spacing
   • Hypercementosis
2. Acromegaly
   • Anterior open bite
   • Class 3 xnalocclusion
   • Macroglossia
   • Thick lips
   • Prodinaiion of teeth
   • Hypercementosis
   • Enlargement of maxillary air anuses
   • Large nose, ears, and prominent eyebrows
   • Increase in thickness of jaw bones
   • Increased incidence of periodontitis

Hyperpituitarism Diagnosis:

• Increased serum inorganic phosphorous level
• GlyCosuria
• Hypercaldnuria
• T4 level- reduced or normal
• Serum growth hormone level-increased
• Hyperphosphatemia

Question 3. Addison’s disease
Answer:

Addison’s disease

Addison’s disease is a debilitating and potentially fatal condition occurring due to chronic insufficiency of the adrenocortical hormone

Addison’s disease Clinical Features:

• Lethargy, fatigue, muscular weakness
• Vomiting, diarrhea
• Severe anaemia
• Irregular menstruation
• Loss of bdy hair
• Dehydration
• Hypertension
• Postural dizziness
• Brownish discoloration of skin and oral mucosa
• Small and feeble pulse
• Chronic mucocutaneous candidiasis

Addison’s disease Diagnosis:

• Acanthosis with silver-positive granules in epithelial cells
• Low diurnal plasma cortisol level
• ACTH level reduced
• Serum potassium elevated

Question 4. Diabetes mellitus
Answer:

Diabetes mellitus

Diabetes mellitus is metabolic disorder due to glucose intolerance

Diabetes mellitus Clinical Features:

• Polyuria
• Glycosuria
• Polydipsia
• Nocturia
• Weakness
• Weight loss
• Tiredness
• Increased susceptibility to infections Pain and paraesthesia in limbs

Diabetes mellitus Oral Amnrfestations:

• Gingival hyperplasia
• Dry mouth
• Multiple carious lesion
• Candidiasis
• Delayed wound healing
• Dry socket formation
• Burning mouth syndrome
• Painless, recurrent swelling of salivary gland
• Erosive lichen planus
• Loss of taste sensation
• Enamel hypoplasia
• Atypical tooth pain
• Benign migratory glossitis

Diabetes mellitus Diagnosis:

• Blood sugar estimation
• Glucose tolerance test- above 130 mg/dl
• Urinary glucose estimation-above 10-20 mg/dl
• Presence of ketone bodies in urine

Diabetes mellitus Treatment:

• Diet control
• Oral hypoglycaemic drugs
• Insulin therapy

Question 5. Scurvy
Answer:

Scurvy

Deficiency of vitamin C leads to scurvy

Scurvy Clinical Features:

• Fatigue
• Bruising
• Premature loss of hair
• Joint pain and swelling
• Intrabony haemorrhage
• Hematoma formation
• Disturbed bone growth
• Follicular hyperkeratosis
• Retardation of wound healing
• Swelling in legs

Scurvy Oral Manifestations:

• Petechiae and echymosis of oral mucosa
• Color of gingiva- bright red
• Surface of gingiva- swollen, smooth, shiny
• Gingiva becomes boggy, ulcerated, and bleeds
• Foul breath
• Loss of bone
• Loosening of teeth
• Difficulty in taking food
• Premature exfoliation of deciduous teeth
• Weak attachment between bone and periosteum

Question 6. Oral manifestations of hyperparathyroidism
Answer:

Oral manifestations of hyperparathyroidism

• Loosening and mobility of teeth
• Fracture of jawbones
• Swelling of the jaw
• Development of brown tumour

Question 7. Rickets
Answer:

Rickets Clinical Features:

• The gross skeletal changed depend on the severity of the rachitic process, its duration, and in particular the stresses to which individual bones are subjected.
• Craniotabes, the earliest bony lesion occurring due to small round unossified areas in the membranous bones of the skull.
• Harrisons sulcus which occurs due to in drawing of soft ribs on inspiration.
• Pigeon chest deformity
• Bow legs occur in ambulatory children due to weak bones of lower legs.
• Knocked knees may occur due to enlarged ends of the femur, tibia, and fibula.
• Lower epiphyses of radius may be enlarged.
• Lumbar lordosis due to involvement of the spine and pelvis.

Question 8. Pellagra
Answer:

Pellagra

• Niacin deficiency causes Pellagra i.e. naught skin.
• The cardinal manifestations of pellagra are referred to as three Ds i.e., dermatitis, diarrhea, and dementia and if not treated may lead to 4th D i.e, death.
• Dermatitis: Sun-exposed areas of skin developed erythemia resembling sunburn which may progress to chronic type with blister formation.
• Diarrhea: This is seen along with stomatitis, glossitis, enteritis, nausea, and vomiting.

Dementia: Degeneration of neurons of the brain of spinal tract results in neurological symptoms such as dementia, peripheral neuritis, ataxia, visual and auditory disturbances.

• Oral findings include:
  • Bald tongue of sandwich,
  • Raw beefy tongue
  • Mucosa becomes fiery red and painful
  • Profuse salivation.
• Chronic alcoholics tire at high risk of developing pellagra because in addition to dietary deficiency, niacin absorption is impaired in them.

Question 9. Amyloidosis
Answer:

Amyloidosis

• Amyloidosis is the term used for a group of diseases characterised by the extracellular deposition of a fibrillar proteinaceous substance called amyloid having a common morphological appearance, staining properties, and physical structure but with variable protein composition.

Amyloidosis Features:

• Smooth surfaces, waxy papules over lips, eyelids and neck
• Macroglossia
• Gingival swelling
• Formation of ulcers
• Surface of lesion- pale and purplish
• Petechiae and ecchymosis of oral mucosa
• Claudication
• Xerostomia
• Dryness of mouth

Question 10. Hyperthyroidism
Answer:

Hyperthyroidism

Hyperthyroidism is caused by the excessive production of the thyroid hormone

Hyperthyroidism Clinical Features:

• Tremors
• Tachycardia
• Sweating
• Weight loss
• Nervousness
• Muscle weakness
• Heat intolerance
• Exophthalmia
• Alveolar atrophy
• Hypertension
• Excitability, anxiety, and irritability
• Photophobia
• Premature eruption of permanent teeth
• Early exfoliation of deciduous teeth
• Increased susceptibility to oral infections

Question 11. Pituitary dwarfism
Answer:

Pituitary dwarfism Clinical Features:

• Short stature of the body
• Presence of fine, silky, sparse hair over body
• Wrinkled atrophic skin
• Hypogonadism
• Extreme weight loss
• Coma and death in severe cases

Pituitary dwarfism Oral Manifestations:

• Small face
• Delayed exfoliation of deciduous teeth
• Deayed root completion
• Delayed eruption of permanent teeth
• Hypofunction of salivary gland
• Decreased salivary flow
• Increased caries activity and periodontal disease
• Crowding of teeth
• Underdevelopment of maxilla, mandible, and 3rd molars
• Smaller crown size and root length of teeth

Question 12. Eosinophilic granuloma
Answer:

Eosinophilic granuloma

Eosinophilic granuloma is a chronic, localized form of bone disorder

Eosinophilic granuloma Clinical Features:

• Fever, malaise
• Headache
• Anorexia
• Local pain, swelling, and tenderness in jaw bones
• Swelling of gingival tissues
• Halitosis
• Mobility of teeth
• Eosinophilic granuloma Radiographic Features:
• Appears ns irregular radiolucent areas
• Cortex is destroyed
• Pathologic fractures occur
• Single or multiple areas of destruction appear as hanging in the air

 

Oral Aspects Of Metabolic Diseases Viva Voce

1. Magnesium is 4th most abundant element in body
2. Calcium is 5th most abundant element in body
3. Bantu sideroses results from ingestion of homemade beer fermented in iron pots
4. Bronze diabetes occurs due to iron overload
5. Protein-energy malnutrition is kwashiorkor and marasmus
6. Lack of adequate bone matrix causes osteoporosis
7. Porphyria is inborn error of porphyrin metabolism
8. Vitamins is defined as an organic substance not made by the body which is soluble in either fat or water and is ordinarily needed in only minute quantities to act as a cofactor in a variety of metabolic reactions.

 

Healing Of Oral Wounds Important Notes

1. Types of healing
   • Healing by 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 apposed
     • 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 – wound in area with 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 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 healing of extraction wound and mention about 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
   • 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
   • Treatment
     • Excision of lesion
     • Bony repair

Question 2. Dry socket
Answer:

Dry socket

It 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

Exfoliaive 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 healing of oral wound
Answer:

Factors affecting 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- speeds 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

It 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 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 Replantation 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
• Nonaccessible 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
     • It 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
     • It 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:

• They 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
• They 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

Resorption of Teeth Complications:

• Loss of vitality of 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

Read And Learn More: Oral Pathology Questions and Answers

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

It 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

• It is a narrow band of dentin bordering the pulp
• It represents continued, slower deposition of dentin by odontoblasts
• There is greater deposition on the roof and floor of the chamber than on other parts
• It 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.
   • It 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
   • 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
   • It is a diffuse inflammation of soft tissues that tends to spread through tissue spaces and along fascial planes
   • Causative organisms – streptococci and anaerobes
   • 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
   • It is an acute or chronic inflammation of 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
   • It 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
   • 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

It 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
• It 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:

• It 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
   • Definition
     • Osteomyelitis is defined as inflammation of bone and bone marrow along with surrounding periosteum
   • 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:

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

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

Read And Learn More: Oral Pathology Questions and Answers

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 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
• It involves teeth with large, open carious lesions
• It 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
• It contains desquamated cells from buccal mucosa, gingiva, and salivary gland carried by the saliva
• There is hyperaemia 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

• It 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
• It 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
• It 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
• 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

It 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

It 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
• It 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
• It 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

It 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
   • It 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
   • 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
   • It is characterized by sharp pain on chewing without any obvious reason
   • Causes
     • Attrition
     • Bruxism
     • Trauma
     • Accidental biting on a hard object
     • Presence of large restoration
     • Improper endodontic treatment
   • 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:

• It 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
• It 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

It 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 gingival third of buccal and lingual surfaces
     • Cervical caries
       • Extends from area opposite to the gingival crest occlusal to 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 bottle 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
   • It is a suspension of an attenuated or killed micro-organism administered for the prevention, amelioration, or treatment of infectious diseases

Route Of Administartion

• 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
• It leads to weakening of tooth structure, cavity formation, and eventual loss of tooth

Dental caries Classification:

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

Dental caries Clinical Features:

• It occurs on pit and fissures/smooth surfaces and roots of teeth
• 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

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 of odontoblastic processes
   • It is capable of remineralizalion
   • 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 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 decakiified 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
   • It is outermost zone of carious dentin
   • Characterised by complete destruction of dentinal tubules
   • Areas of decomposition of dentin occurs 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
   • It 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
   • It 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, process of caries involves four factors
         • Dietary carbohydrates
         • Micro-organisms
         • Acids
         • Dental plaque
2. Proteolytic chelation theory
   • It 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
   • It releases the positively charged calcium ions from the enamel or dentin
3. Sucrose chelation theory
   • It proposes the sucrose itself and not the acid derived from it can cause dissolution of enamel by forming ionized calcium saccharate
4. Autoimmune theory
   • It suggests that few odontoblast cells at some specific sites within pulp are damaged by an autoimmune mechanism

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 dissolution of hydroxyapatite crystals of enamel
• Risk of caries occurrence increases if dietary sugar is sticky and adheres to the tooth surface for longer time
• Following its ingestion, 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 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

Read And Learn More: Oral Pathology Question And Answers

• Advanced enamel caries
  • It presents several zones in tissues
    • Zone 1- Translucent Zone
      • It is deepest zone
      • It 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 translucent zone
      • Excessive demineralization of enamel occurs
      • It is narrow in rapidly advancing caries and wide in slowly advancing caries
      • Contains 2-4% pore volume
      • Pores are smaller than that of the translucent zone
      • There is some degree of remineralization present
    • Zone 3- Body of lesion
      • Present between dark zone and surface layer of enamel
      • Represents 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
      • It remains unaffected
      • It 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 tooth from oral pathogenic bacteria by acting as specific agglutinin
  • It binds and agglutinates specific oral bacteria
  • Prevents their adherence to tooth
  • Removes it from 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
• It 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 readon pH meter

Swab test Interpretation:

4. Salivary reductase test

Salivary reductase test Procedure:

• Paraffin-stimulated saliva is collected in collection tube
• It 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 pathogenesis of dental caries
Answer:

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

Role of Plaque:

• It 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 on to the tooth surface for a long duration
• Increased thickness of plaque does not allow the salivary buffers to enter into it to neutralise the acids produced by the cariogenic bacteria
• Plaque protects the acids produced by the cariogenic bacteria from getting neutralized in two ways
  • It 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 netralization of acids
    • Continued sugar production from bacterial intracellular polysaccharides helps to maintain a low pH and facilitates more tooth decay

Question 2. Describe about 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
     • Increase in mineral content leads to increased resistance to caries
   • Morphology
     • 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
     • Rise in pU neutrally adds attacks on the tooth surface during carle progression
   • Composition
     • Bicarbonateionscauses neutrailiftalton
     • Ammonia- causes rise in pH
   • Quantity
     • Reduction of saliva leads to
     • Rampant caries
     • Exacerbation of caries
   • Viscocity
     • Extremely viscous saliva leads to Carles free mouth
     • Abundant, thin, watery saliva exhibit 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 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. It 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. It 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 carles 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 oral cavity
• They gets accumulate In plaque and ferments carbohydrate present In diet
• Produces add and results in dissolution of enamel to cause cavity formation
• Microorganisms Involved in caries process are
  • Streptococcus mutans
    • Streptococcus mutans are catalase-negative, gram-positive cocci forming short or medium chains
    • It synthesizes Insoluble polysaccharides from sucrose
    • It results in production of lactic acid
    • This causes drop in pH favoring carles
    • It also has the ability to stora intracellular glycogen amylopectin
    • Provides a reservoir of substrate and enables prolonged periods of increased metabolic activity
  • Lactobacillus
    • It long and thin, non-motile
    • It may occur singly or in palm or in chain
    • It could multiple in low-pH of plaque and carious lesions
    • Hence it is important etiologic agent of dental caries
    • It is present in deep fissures and in deep dentinal caries
    • It causes progress of carles
    • Actinomycosis
    • It cause root caries

Question 5. Preventive measures for carles control
Answer:

Preventive measures for carles control

Preventive measures for caries control include

1. Chemical measures
   • It includes sublances that
     • Alter tooth surface or tooth structure
     • Interfere with carbohydrate degradation
     • interfere with bacterial growth and metabolism
   • They are
   • 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 caries Invasion pathway
   • Vitamin K
     • Prevents acid formation
2. Nutritive measures
   • Diet rich in fag low in carbohydrate and free of sugar have low caries activity
   • Phosphate rich diet causes 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 carles
Answer:

Clinical types of carles

1. Pit and fissure caries
   • It develops on occlusal surfaces of molars and promoters, buccal and lingual surfaces of motel’s and palatal surfaces of maxillary Inch sors
   • 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 cartes
   • 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
• Enamel surrounding the caries is bluish-white
• It extends both buccally and lingually
• There is formation of cavity

Question 10. Theories of dental caries
Answer:

Acidogenic theory

• Postulated by WD Miller
• It 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

• It 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

• It proposes that the sucrose itself and not the acid derived from it can cause dissolution of enamel by forming ionized calcium saccharates

Autoimmune theory

• It 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
• It is long and thin, non-motile
• It may occur singly or in pairs or in chains
• It could multiple in low-pH of plaque and carious lesion
• Hence it is important etiologic agent of dental caries
• It is present in deep fissures and in deep dentinal caries
• It 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
• It synthesizes insoluble polysaccharides from sucrose
• It results in production of lactic acid
• This causes drop in pH favoring caries
• It 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, Niesseria, 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
• It 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
• 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

• It 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 mineralised 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 anteriors are affected
• They are protected by the position of tongue
• Initially caries appears as the dull, white area along gingival margin
• This progresses to cervical margin to form ring-like lesion
• Finally, whole crown of 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 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
   • 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

It 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 effected
• It involves all teeth including mandibular incisors
• Rapidly new lesions develop in addition to the present old lesions
• Carious tooth are with pulpal involvement

Rampant caries Treatment: Pulpotomy is done

Question 18. Pit and fissure caries
Answer:

Pit and fissure caries

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

• It explains the process of dental caries
• According to it
  • Initially all proteolytic breakdown of the organic portion of 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. Most cariogenic carbohydrate is sucrose
2. Clinical significance of sclerotic dentin is that it is resistant to caries
3. Most significant organism for pit and fissure caries is Strep. Mutans and lactobacillus
4. Most significant organism for root surface caries is A. Viscosus
5. Lingual surface of maxillary lateral incisor is more susceptible to caries
6. pH below 5.5 causes demineralization of 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
   • Functions
     • Attaches tooth to the jaw bone
     • Maintains integrity of masticatory system
2. 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
   • It is inflammation of the soft tissue surrounding the osseointegrated implant in function and progressive bone loss
   • It begins at the coronal portion of the implant.
   • 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

Acute Necrotizing Ulcerative Gingivitis:

• It 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

Read And Learn More: Oral Pathology Questions and Answers

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:
   • 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
   • 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
   • 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
   • 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

• It 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 gingivitis Clinical Features:

Question 10. Scorbutic gum
Answer:

Scorbutic gum

• Scorbutic gum is seen in scurvy, vitamin C deficiency

Desquamative gingivitis 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.