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Determination Of Prognosis

Determination Of Prognosis Important Notes

1. Factors determining prognosis

1. Prognosis

• It is a prediction of the probable course, duration, and outcome of a disease based on general knowledge of the pathogenesis of the disease and the presence of risk factors for the disease.
• It is established after the diagnosis is made and before the treatment plan is established

2. For a younger patient with rapid bone destruction, the prognosis is considered poor because of the shorter period in which the bone loss has occurred in spite of greater bone reparative capacity

Determination Of Prognosis Long Essay

Question 1. Define Prognosis. Describe in detail the factors determining prognosis.
Answer:

Overall:

1. Patient age:

• Old age- Better prognosis
• Young age – Not good

2. Disease severity:

1. Pocket depth:
   • Deep pocket – Better prognosis
2. Level of attachment:
   • The extent of disease to the root surface
3. Pulpal involvement:
   • Endodontic involvement – Poor prognosis
4. Degree of bone loss:
   • Height of remaining bone determining prognosis
5. Type of bony defects:
   • Vertical bone defect – Good prognosis
   • Good regeneration

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3. Plaque control:

• Effective plaque removal – Good prognosis

4. Patient compliance and cooperation:

• Cooperative patients – Good prognosis
• Unwilling patients – Poor prognosis

5. Economic consideration:

• Patients having low income try to avoid expensive treatment
• Thus have a poor prognosis

6. Knowledge and ability of dentist: Dentists should know different modalities of treatment of a specific case.

Systemic Factors:

1. Type 1 and type 2 diabetes:

• The prognosis depends on the patient’s compliance

2. Uncontrolled diabetes:

• Questionable prognosis

3. Parkinson’s disease:

• Improved prognosis by use of automated oral hygiene devices

4. Genetic factors:

• Defects – Genetic polymorphism
• Increased production of IL1-ẞ

Stage:

• Early detection of patients at risk
• Identification of risk during the course of treatment
• Identification of young patients at risk
• Alterations in treatment improve prognosis

Respective Measures:

• Early implementation of therapy
• Adjunctive antibiotic therapy
• Early intervention

5. Environmental factors:

• Smokers – Fair to poor prognosis
• Patient having quit smoking – Fair to good progress

6. Local Factors:

• Plaque/calculus – Efficient removal-good prognosis
• Subgingival restoration – Poor prognosis
• Anatomic variations/factors

Types:

• Short tapered roots
• CEP
• Enamel pearls
• Poor concavities
• Developmental grooves
• Poor prognosis due to reduced periodontal support

Determination Of Prognosis Short Essays

Question 1. Types of Prognosis.
Answer:

Question 2. Anatomic Variations.
Answer:

1. Cervical enamel projections:

• Flat, ectopic extensions of enamel
• Extend: Beyond CEJ furcations
• Site: Buccal surfaces of maxillary 2nd molars

2. Enamel pearls:

• Large round deposits of enamel
• Extend – Furcation and root surfaces
• Effect – Interferes with attachment
• Prevent regeneration

3. Root concavities:

• Shallow flutings to deep depressions
• Resistant to torquing forces
• Inaccessible areas

4. Developmental grooves:

• Palato gingival grooves
• Extend – Enamel to the root surface

5. Other:

• Root proximity
• Furcation areas
• Difficult to access

Determination Of Prognosis Viva Voce

1. The prognosis is considered poor if the base of the pocket is close to the root apex
2. In the case of supra bony pocket, the prognosis depends on the height of the existing bone
3. In the case of infrabony pockets, the contour of existing bone and the number of remaining osseous walls influ- ences prognosis

 

Diagnosis

Diagnosis Important Notes

1. Radiographs

• They reveal only about the amount of bone present
• Do not give any information about the morphology of bone defects and the number of walls involved
• Do not reveal the presence of pockets or soft tissue lesions

2. DNA probe

• It identifies the species-specific sequences of nucleic acids that make up DNA
• Helps in the identification of organisms

3. Dark field microscopy

• It is used as an alternative to cultural methods
• It has the ability to assess directly and rapidly the morphology and motility of bacteria in a plaque sample

Diagnosis Long Essays

Question 1. Define diagnosis. Describe microbiological in-investigations used. Add a note on the limitations of radiographs in periodontal diseases.
Answer:

Definition:

• It may be defined as identifying a disease from an evaluation of the history, signs and symptoms, laboratory tests, and procedures

Microbiological Investigations:

1. Direct microscopy

• Specimens are viewed directly under a light
  1. Light microscopy
     • Gram staining is done to differentiate Gram-positive and Gram-negative organisms
  2. Darkfield microscopy
     • Fresh, unstained samples are examined by it

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2. Culture methods:

• Used for cultivation and identification of organisms
• It determines its susceptibility or resistance to various antimicrobial agents

Specimens Obtained:

• Blood samples
• Mucosal surfaces
• Periodontal pockets

Sampling Methods:

• Nickel-plated curettes
• Scalers
• Paper points
• Irrigation
• Surgical excision

Types Of Media:

1. Supportive media:

• Allows growth of only specific organisms

2. Enriched media:

• Encourages the growth of organisms

3. Nonselective media:

• Permits growth of most oral micro-organisms

4. Selective media:

• Contains dyes, antibiotics that are inhibitory to specific organisms

Culture Techniques:

• Jar technique
• Pre-reduced anaerobically sterilized roll tubes
• Anaerobic chamber techniques
• Enzyme reduction technique

Speciation Techniques:

1. Gas-liquid chromatography

• In it, various metabolic products of anaerobes are studied

2. DNA probes:

• Identifies periodontal pathogens

Limitations Of Radiograph In Periodontics:

• 30-60% of the mineral content of the bone must be lost to visualize the change
• Lacks sensitivity
• Actual damage is more extensive
• It is a two-dimensional view of a three-dimensional object
• It does not reveal current cellular activity
• Reflects effects of past cellular experience on bone and roots

Diagnosis Short Essays

Question1. Importance of radiographs in periodontal diseases
Answer:

• Importance Of Radiograph In Periodontics:
• Estimates severity
• Determines prognosis
• Evaluates treatment outcomes
• Demonstrates changes in calcified tissues
• Shows visual image of bone support around tooth or implant
• It detects
  • Periodontal bone level
  • The pattern of bone destruction
  • PDL space width
  • Radiodensity
  • Trabecular pattern
  • The marginal contour of interdental bone
• Compares pretreatment and post-treatment results

Radiographic Features Of Periodontal Diseases:

1. Periodontitis:

• Disruption of lamina dura
• Widening of PDL space
• Reduced height of interdental bone

2. Interdental craters:

• Seen as irregular areas of reduced density

3. Furcation involvement:

• Widening of PDL space

4. Periodontal abscess:

• The extent of bone destruction is seen
• Detects morphological changes in bone

5. Localized aggressive periodontitis:

• Vertical arc-like bone destruction

6. Trauma from occlusion:

• Thickening of lamina dura
• Morphological changes of the alveolar crest
• Widening of PDL space
• Change in the density of surrounding cancellous bone

Diagnosis Short Question and Answers

Question 1. Methods of probing.
Answer:

1. Walking probing method:

• In it, the probe is inserted at the distalmost surface of the tooth and walked or stepped towards the mesial surface. of the tooth at a 1 mm distance without taking out the probe completely from the gingival sulcus
• Measurement is recorded at each millimeter

2. Transgingival probing:

Uses:

• To detect alveolar bone loss
• Confirms the extent and configuration of infrabony component of the pocket and the furcation defects

Method:

• Before flap reflection locally anesthetize the area
• Next probe is walked along the tissue tooth interface

Question 2. Subtraction radiography.
Answer:

• Subtraction radiography relies on the conversion of serial radiographs into digital images
• These images are then superimposed and the composite is viewed on a video screen
• Changes in bone density and volume can be seen
• Bone gain is seen as lighter areas and bone loss as darker areas
• Computer-assisted subtraction radiography helps in detecting changes from baseline images
• It helps in the detection of minor changes in the bone by removing the unchanged anatomic structures from the image
• It increases the sensitivity

Question 3. Periotemp.
Answer:

• These are thermal probes used to measure early in-inflammatory changes in gingival tissues
• It enables calculation of the temperature differential be- tween the probed pocket and subgingival temperature
• This allows consideration of differences in core temperature between individuals
• Individual temperature differences are compared with those expected for each tooth and higher temperature pockets are signaled with a red-emitting diode

Question 4. Identification of furcation involvement.
Answer:

• Naber’s probe is used to assess the furcation involve- ment clinically
• If the pocket depth is >5 mm, there are more chances of furcation involvement
• The probe is inserted parallel to the long axis of the tooth at the mid-buccal surface of the tooth and approximately 5 mm from the CEJ
• It is angulated to find out the possible bone loss in the furcation area
• If there is minimal bone loss, furcation can be felt like a groove between

Question 5. Enumerate the criteria for the ideal probe
Answer:

• The precision of 0.1 mm
• Range of 10 mm
• Constant and standardized probing force
• Non-invasive, lightweight, and easy to use
• Easy to access any location around all teeth
• A guidance system to ensure proper angulation
• Complete sterilization of all portions entering the mouth
• No biohazard from material
• Direct electronic reading and digital output

Diagnosis Viva Voce

1. Computer-assisted densitometer image analysis system offers an objective method for following alveolar bone density changes quantitatively
2. Transgingival probing and visual examination by sur- gical exposure are definitive ways of knowing bone morphology
3. Definitive diagnosis of furcation involvement, pocket depth, and periodontal abscess is made by clinical examination only
4. In subtraction radiographs, the lighter areas indicate bone gain
5. The disadvantage of subtraction radiography is it re- quires an identical projection in serial radiographs
6. Periotemp probe is used to measure subgingival temperature
7. Florida probe is an automated probe for recording pocket depth
8. The diameter of the Florida probe tip is 0.4 mm
9. Foster-Miller probe detects CEJ
10. The bacterial culture technique is used to assess the antibiotic susceptibility of the microbes
11. Evalusite is chairside membrane immunoassay
12. Periotron is used to measure gingival crevicular fluid volume
13. Periogard is a chairside test kit for aspartate aminotransferase
14. Periocheck is a chairside test kit to detect neutral pro-tease in GCF

Aids And The Periodontium Important Notes

1. Gingival and periodontal diseases in HIV Linear gingival erythema

• Necrotizing ulcerative gingivitis
• Necrotizing ulcerative periodontitis

2. Oral hairy leukoplakia

• Primarily occurs in persons with HIV infection
• Found chiefly on the lateral borders of the tongue bilaterally
• The lesions do not rub off and resemble other keratotic oral lesions

Necrotizing Ulcerative Gingivitis Short Essays

Question 1. HIV periodontitis.
Answer:

1. HIV-associated gingivitis:

• Linear inflammation around the gingival margin occurs
• Presence of punctuate erythema
• The lesion extends throughout the width of the attached gingiva
• This occurs even in the presence of excellent oral hygiene

2. HIV-associated periodontitis:

• Rapid loss of attachment
• Tissue destruction
• Deep pain

3. HIV necrotizing gingivitis:

• Sudden onset
• Bleeding on toothbrushing
• Pain
• Characteristic halitosis
• Gingiva appears fairly red and swollen
• Presence of yellow to grayish necrosis
• Common in anterior gingival

4. Necrotizing stomatitis:

• Sequestration of interdental bone
• Soft tissue necrosis
• It is the most severe form of periodontal infection

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Question 2. Oral manifestations of AIDS.
Answer:

Oral Manifestations Of Aids:

1. Oral hairy leukoplakia:

• Found on lateral borders of the tongue
• Caused by human papillomavirus
• Keratotic, asymptomatic area with vertical stria- tions giving a corrugated appearance
• When dried appears hairy

2. Oral candidiasis:

• Manifested as
• Pseudomembranous candidiasis
• Erythematous candidiasis
• Hyperplastic candidiasis
• Angular chelitis

3. Kaposi’s sarcoma:

• Multifocal, vascular neoplasm manifested as nodules, papules, or non-elevated macules

4. Bacillary angiomatosis:

• It is an infectious vascular proliferative disease
• It appears red, purple, or blue edematous soft tissue lesion

5. Oral hyperpigmentation:

6. Atypical ulcers and delayed healing:

Aids And The Periodontium Short Question and Answers

Question 1. Periodontal disease associated with HIV.
Answer:

1. HIV-associated gingivitis (HIV-G):

• Linear inflammation around the gingival margin
• Punctuate erythema

2. HIV-associated periodontitis (HIV-P):

• Rapid loss of attachment
• Tissue destruction
• Deep pain

3. HIV- necrotizing gingivitis (HIV-NG) – ANUG:

4. Necrotizing stomatitis (NS):

• Sequestration of interdental bone
• Soft tissue necrosis

Question 2. Tests for HIV
Answer:

1. ELISA(Enzyme-Linked Immunosorbent Assay):

• It is a color reaction test

Method:

• A serum containing antibodies is developed from the patient’s blood sample
• It is added to the ELISA plate
• Wash off the inactive antibodies
• A second layer of antibodies called conjugate is added
• Excess antibodies are again washed off
• A substrate is added to it

Result:

• Color becomes darker- positive test
• No color change- negative test

2. Western blot test:

Method:

• Viral proteins from the patient’s blood sample are passed through a gel
• The separated proteins are then passed through an electric current
• Human serum is added
• A chromogen is added to it

Result:

• A specific band of viral protein is detected

Question 3. Linear Gingivitis.
Answer:

Gingiva:

• Color – Bright red
• Site – Marginal and attached gingiva
• Bleeding on probing – present
• Progression – Involves entire gingiva

Negative Features:

• No ulceration
• No attachment loss
• No response to treatment
• No relation with plaque accumulation

Treatment:

• Medical consultation
• Scaling
• Irrigation with 10% povidone-iodine
• Mouth rinse-0.12% chlorhexidine Antifungal agents
• daily

Recalls:

• Next day
• After one week
• Every 4 weeks
• Every 3-6 months

Aids And The Periodontium Viva Voce

1. Candidiasis is found in 90% of AIDS patients
2. In linear gingival erythema, the erythematous, easily bleeding gingiva may be limited to marginal gingiva or may be diffuse extending into attached gingiva
3. CD4+ T lymphocyte levels less than 200/mm3 are de- finitive for AIDS and indicate severe immunogenic- science

 

Necrotizing Ulcerative Periodontitis Refractory Periodontitis

Necrotizing Ulcerative Periodontitis Refractory Periodontitis Important Notes

1. AIDS-associated necrotizing ulcerative periodontitis

Features:

• Severe soft tissue necrosis with rapid destruction of bone leading to its exposure
• Destruction may extend to the vestibular area and palate
• May result in necrotizing stomatitis

Necrotizing Ulcerative Periodontitis Refractory Periodontitis Short Essays

Question 1. Necrotizing ulcerative periodontitis (NUP).
Answer:

• When ulcerative gingivitis extends deeper into the periodontal structures, it results in loss of attachment and bone loss

Types:

• AIDS-associated
• Non-AIDS type NUP

Clinical Features:

• Ulceration and necrosis of the gingival margin
• Presence of pseudo-membranous slough
• Pain
• Bleeding spontaneously
• Deep pockets
• Osseous craters, Gingival recession

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General Features:

• Localized lymphadenopathy
• Fever
• Malaise

Question 2. Refractory Periodontitis.
Answer:

Definition:

• According to AAP, it is defined as those cases which do not respond to any treatment provided, whatever the thoroughness or frequency

Etiology:

• Abnormal host response
• Resistant strains of microorganisms
• Failure to treat plaque retentive factors Smoking
• Systemic diseases
• Micro-organisms
  • B.forsythus, F.nucleatum, C.rectus
  • S.intermedius, P.gingivalis

Clinical Features:

• Failure to restrict the progression of the disease
• No response of treatment on
  • Plaque accumulation
  • Attachment loss
• Persistent bleeding on probing
• Development of new areas of attachment loss

Treatment:

• Scaling and root planning
• Followed by antibiotic therapy
  • Tetracycline 250 mg QID
  • Amoxicillin 250 mg + 125 mg TID
  • Clindamycin 150 mg QID for 1 week
  • Metronidazole 400 mg TID
  • Local drug delivery – gels, fibers, or chips
  • Sub-antimicrobial dose of doxycycline SDD – 20 mg BID for 3 months

Question 3. Differentiate between Recurrent and Refractory Periodontitis.
Answer:

Question 4. Retrograde periodontitis.
Answer:

• Periodontitis caused by pulpal infections that have entered the periodontal ligament either through the apical foramen or through lateral canals is termed retrograde periodontitis

Pathways Of Communications

1. Pathways of developmental origin:

• Apical foramen
• Accessory canals and lateral canals
• Developmental grooves
• Enamel projections and pearls

2. Pathways of pathologic origin

• Tooth fracture
• Idiopathic resorption
• Loss of cementum

3. Pathways of iatrogenic origin

• Exposure of dentinal tubules following root planning
• Accidental lateral perforation during an endodontic procedure
• Root fracture due to endodontic procedure

Pathogenesis:

Necrotizing Ulcerative Periodontitis Refractory Periodontitis Viva Voce

Cases that do not respond to therapy or recur soon after adequate treatment are referred to as refractory periodontitis

 

Aggressive Periodontitis

Aggressive Periodontitis Important Notes

1. Signs of aggressive periodontitis

• Mobility
• Pathological migration of first molars and incisors
• Distolabial migration of maxillary incisors with diastema formation
• Lack of inflammation
• Presence of deep periodontal pockets

2. Aggressive periodontitis is differentiated from chronic periodontitis by

• Age of onset
• The rapid rate of disease progression
• Nature and composition of the associated subgingival microflora
• Alterations in the host’s immune response
• Familial aggregation of diseased individuals
• Racial influence

3. Periodontal diseases associated with neutrophils disorder

• Aug
• Localized juvenile periodontitis
• Various forms of aggressive periodontitis

4. Types of juvenile periodontitis

1. Localized
   • Characterized by a distribution of lesions in the first molars and incisors with the least destruction in the cuspid-premolar
2. Generalized
   • There is generalized involvement of teeth

5. Juvenile periodontitis

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• Also known as periodontosis
• Microflora are composed of gram-negative bacteria, including cocci, rods, filaments, and spirochaetes
• Microbes identified are
  • Actinobacillus actinomycetemcomitans
  • Capnocytophaga
  • Mycoplasma and spirochaetes

Aggressive Periodontitis Long Essays

Question 1. Describe clinical features, diagnosis, and management of localized juvenile periodontitis. (or) Describe the etiology, clinical features, and treatment of localized aggressive periodontitis.
Answer:

Localized Aggressive Periodontitis:

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

Clinical Features:

• Age- 20 years
• Sex- common in females
• The site involves incisors and the first molar
• 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

Treatment:

• Extraction of 1st molar and transplantation of 3rd molar in its position
• Scaling and root planning
• Curettage
• Root amputation
• Hemisection
• Antibiotic therapy
• Tetracycline-250 mg QID for 14 days Doxycycline-100 mg/day
• Chlorhexidine rinses

Question 2. Define and classify plaque. Describe the plaque-host interaction in juvenile periodontitis.
Answer:

Definition:

• It is soft deposits that form biofilm adhering to the tooth surface or other hard surfaces in the oral cavity including removable and fixed restoration

Classification:

• Dental plaque is classified into

1. Supragingival plaque
2. Subgingival plaque

• • It is further divided into

1. 1. Tooth associated
   2. Epithelium associated

Plaque-Host Interaction:

Aggressive Periodontitis Short Essays

Question 1. Aggressive Periodontitis.
Answer:

Definition:

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

Types:

• Localized Aggressive Periodontitis
• Generalized Aggressive Periodontitis

Microbiology:

• A.actinomycetem contains
• Capnocytophaga

Virulence Factors:

• Leukotoxin – Destroys leukocytes
• Endotoxins – Activates host cells
• Secretes inflammatory mediators
  • Bacteriocin – Inhibit IgG and IgM production
  • Collagenase-Degradation of collagen
  • Chemotactic Inhibiting factors Inhibit neutrophil chemotaxis

Risk Factors:

• Microbiologic Factors – A.a.comitans
• Immunologic Factors – Neutrophil defect
• Genetic factors
• Environmental factors – Smoking

Question 2. Localized Aggressive Periodontitis (LAP).
Answer:

Clinical Features:

• Age – 20 years
• Sex – common in females
• The site involves – Incisors and the first molar

Reason-Production Of Antibodies:

• Bacteria antagonist
• Losing of leukotoxin-producing ability
• Defect in cementum formation

Associated Features:

• 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 formation
• 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

Microbiology:

• A.a. contains
• Capnocytophaga

Treatment Modalities:

• Extraction of 1st molar and transplantation of 3rd molar in its position
• Scaling and root planning
• Curettage
• Root amputation
• Hemisection
• Antibiotic therapy
  • Tetracycline 250 mg QID for 14 days
  • Doxycycline 100 mg/day
  • Chlorhexidine rinses

Question 3. Generalized Aggressive Periodontitis.
Answer:

• Characterized by generalized interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors

Microbiology:

• P.gingivalis
• A.actinomycetem contains
• Bacteroids forsythias

Gingival Response:

General Features:

• Weight loss
• Mental depression
• General malaise

Clinical Features:

• Age Between puberty and 35 years
• Sex-both sex

Aggressive Periodontitis Short Question and Answers

Question 1. Define Aggressive Periodontitis/Juvenile Periodontitis.
Answer:

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

Question 2. Microbiologic of LAP.
Answer:

• Causative organisms of LAP are
• A.a. contains
• Capnocytophaga

Question 3. Risk factors for Aggressive Periodontitis.
Answer:

Risk Factors

• Microbiologic factors- A.a. contains
• Immunologic factors- Neutrophil defect
• Genetic factor
• Environmental factors-smoking

Question 4. Virulence factors.
Answer:

Virulence Factors:

• Leukotoxin- Destroys leukocytes
• Endotoxin
  • Activates host cells
  • Secretes inflammatory mediators
• Bacteriocin- Inhibits IgG and IgM production
• Collagenase- degrades collagen
• Chemotactic inhibiting factors- inhibits neutrophil chemotaxis

Question 5. Stages in Development of Disease.
Answer:

Stage 1:

• Degeneration of principal fibers
• Cessation of cementum formation
• Bone resorption
• Absence of inflammation
• Tooth migration

Stage 2:

• Loss of periodontal fibers
• The rapid proliferation of JE
• Initiation of inflammation

Stage 3:

• Progressive inflammation
• Deep, infra bony pockets

Question 6. Burn-out Phenomenon.
Answer:

• Concept explaining localization of aggressive periodontitis
• Localized aggressive periodontitis is confined to incisors and first molars
• Micro-organisms responsible for it A.a. contains
• The reason for localization is the production of opsonizing antibodies against it.

Question 7. Radiographic features of LAP.
Answer:

• 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

Question 8. Differences between localized and generalized aggressive periodontitis.
Answer:

Aggressive Periodontitis Viva Voce

1. Periodontosis is the old name for juvenile periodontist- tis or aggressive periodontitis
2. Gingivosis is the old name for desquamative gingivitis
3. Vertical bone loss around incisors and molars is diag- nostic of localized juvenile periodontitis
4. Arc-shaped bone loss extending from the distal surface of the second premolar to the mesial surface of the second molar creating a mirror image is characteristic of juvenile periodontitis

 

Chronic Periodontitis Long Essay

Question 1. Chronic Periodontitis.
Answer:

Chronic Periodontitis Definition:

• An infectious disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment loss, and bone loss.

Chronic Periodontitis Clinical Features:

• Age-30-35 years
• Distribution – Generalized
• Gingival
• Color – pale red to magenta
• Size – swollen
• Surface texture-Loss of stippling
• Margins-blunt or rolled
• Papillae-flattened/cratered

Chronic Periodontitis Associated symptoms:

• Spontaneous bleeding
• Exudation from pockets
• Plaque accumulation
• Deep-seated, dull pain
• Tooth mobility
• Foul odor

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Chronic Periodontitis Micro-Organisms Involved:

• P.gingival is
• P.intermedia
• A.a. contains
• C.rectus
• Capnocytophaga

Chronic Periodontitis Radiographic Features:

• Infrabony pockets – Vertical bone loss
• Supra bony pockets – Horizontal bone loss

Chronic Periodontitis Short Answers

Question 1. Classification of Chronic Periodontitis.
Answer:

Question 2. Models explaining Chronic Periodontitis.
Answer:

1. Continuous Paradigm:

• Implies slow, continuous, and progressive destruction of the periodontics

2. Random burst theory:

• Progression of disease at short periods of active destruction
• Followed by periods of remission

3. Asynchronous multiple burst model:

• Tissue destruction occurs at a definite time

Question 3. Risk factors of Chronic Periodontitis.
Answer:

1. Chronic Periodontitis Local Factors:

• Plaque and plaque retentive factors
• Micro-organisms

2. Chronic Periodontitis Systemic Factors:

• Type 2 diabetes mellitus
• Hypertension

3. Chronic Periodontitis Environmental/Behavioral factors:

• Smoking
• Emotional stress

4. Chronic Periodontitis Genetic factors:

• Genetic predisposition

Osseous Defects In Periodontic Disease

Osseous Defects In Periodontic Disease Important Notes

1. Angular defects

• They are classified according to the number of walls remaining
• The fewer the number of walls remaining the poor is the prognosis

Types:

• One wall defect – One wall is present
  • Also called hemiseptum
  • The prognosis is poor regenerative procedures cannot be carried out in it
• Two walls defect-Two walls are present
• Three wall defect – Three walls are present
  • Also called intrabody defect
  • Prognosis is better
  • Regenerative procedures can be easily carried out
  • Appears most frequently on the mesial aspects of second and third maxillary and mandibular molars
• Combined osseous defect – No. of walls present in the apical portion are greater than that in the coronal portion

2. Osseous craters

• They are concavities in the crest of interdental bone confined within facial and lingual walls
• They make up about one-third of all defects and two third of all mandibular defects

3. Pathways of inflammation

• Interproximal from gingiva to bone, from bone to periodontal ligament
• Facially and lingually from gingiva to bone along the outer bone and from gingiva into the periodontal ligament

Osseous Defects In Periodontic Disease Short Essays

Question 1. Various Bone Destruction patterns.
Answer:

1. Horizontal bone loss:

• Reduction in bone height
• Bone margins are perpendicular to the tooth surface
• The common pattern of bone loss

2. Vertical/Angular Defects:

• Bone loss in an oblique direction
• The hallow trough in bone alongside the root
• The base of the defect apical to the surrounding bone
• Seen in trauma from occlusion
• Juvenile periodontitis

Types:

1. One wall defect: One wall is present
2. Two wall defects: Two walls are present
3. Three wall defect: Three walls are present
4. Combined osseous defect: No. of walls present in the apical portion is greater than that in cor- the a portion

2. Osseous Craters:

• Concavities in a crest of interdental bone confined Answer: within facial and lingual walls
• Seen in TFO

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3. Bulbous Bony Contours:

• Bony enlargements due to exostoses

4. Reversed bone architecture:

• Interdental bone loss without loss of radicular bone
• Seen in food impaction

Osseous Defects In Periodontic Disease Short Answers

Question 1. Reversed Architecture.
Answer:

• Interdental bone loss without loss of radicular bone
• Common in maxilla
• Seen in food impaction

Question 2. Osseous Craters.
Answer:

• Concavities in the crest of the interdental bone are confined within facial and lingual walls

Site:

• Mandibular teeth
• Common in posteriors

Reason For Occurrence:

• Prone for plaque accumulation
• Difficult to clean
• Vascular patterns from gingiva

Question 3. Ledges.
Answer:

• Bone defect
• Plateau-like bone margins

Cause: Resorption of thickened bony plates

Question 4. Angular Defects.
Answer:

• Bone loss in the oblique direction
• A hallow trough in bone alongside root
• The base of the defect apical to the surrounding bone
• Seen in trauma from occlusion
• Juvenile periodontitis

Types

1. One wall defect- one wall is present
2. Two wall defects – Two walls are present
3. Three wall defect – Three walls are present
   • Common in mesial surfaces of upper and lower molars
4. Combined osseous defect
   • The number of walls present in the apical portion is greater than that in the coronal portion

Question 5. Enumerate bone destructive patterns in periodontal disease.
Answer:

Bone Destructive Patterns In Periodontal

Disease:

1. Horizontal bone loss
2. Angular defects
   • One wall defect
   • Two wall defect
   • Three wall defect
   • Combined osseous defect
3. Osseous craters
4. Bulbous bony contours
5. Reversed bone architecture

Osseous Defects In Periodontic Diseaseviva Voce

1. Osseous craters are the most occurring defect in mandible
2. The pathway of the spread of inflammation affects the pattern of bone destruction in periodontal disease
3. When inflammation spreads directly from PDL to gin- give and from gingiva to PDL, it results in angular bone loss
4. Angular defects are classified according to the number of walls remaining.
5. Ledges are plateau-like bone margins caused by re- sorption of thickened bony plates.
6. Combined osseous defect refers to the combination of angular defect with varying numbers of walls at the cervical and apical part
7. Three walls are destroyed in one wall defect
8. 50 gms of probing force is required to diagnose a periodontal osseous defect

 

Bone Loss And Patterns Of Bone Destruction

Bone Loss And Patterns Of Bone Destruction Important Notes

1. Radius of action.

• States that local resorbing factors must be present in close proximity of bone, to exert their effect.
• According to Waerhaug range of effectiveness is 1.5-2.5 mm
• Beyond 2.5 mm, there is no effect and are thus unable to cause bone resorption
• Large def effect far exceeding 2.5mm from tooth surface is caused by the presence of bacteria in the tissues

Bone Loss And Patterns Of Bone Destruction Short Essays

Question 1. Mechanism of bone.
Answer:

1. Bone formation:

2. Bone destruction:

1. Local factors:

Replacement of fatty bone marrow with fibrous type

2. Trauma from occlusion

Read And Learn More: Periodontics Question and Answers

3. Combination

• Systemic factors:
  • Osteoporosis
  • Hyperparathyroidism
  • Leukemia

Bone Loss And Patterns Of Bone Destruction Short Answers

Question 1. Bone factor concept.
Answer:

• By Glickman
• Explains the role of Systemic factors in bone resorption
• States that when there is a generalized tendency towards bone resorption, bone loss initiated by local inflammation gets magnified.

Example:

• Osteoporosis in post-menopausal women
• Hyperparathyroidism
• Leukemia

Question 2. Agents of Bone resorption.
Answer:

1. Complement

2. Flurbiprofen

Question 3. The radius of action.
Answer:

• States that local resorbing factors must be present in close proximity of bone, to exert their effect.
• According to Waerhaug range of effectiveness is 1.5-2.5 mm
• Beyond 2.5 mm, there is no effect and are thus unable to cause bone resorption

Periodontal Pocket

Definitions

1. Periodontal pocket

• Pathological deepening of the gingival sulcus

Periodontal Pocket Important Notes

1. Classification of pocket

• Depending upon its morphology
  • Gingival/false pocket
  • Periodontal/true pocket
  • Combined pocket
• Depending upon its relationship to crustal bone
  • Suprabony pocket
  • Infrabony pocket
• Depending upon the no. of surfaces involved
  • Simple
  • Compound
  • Complex
• Depending upon the nature of the soft tissue wall
  • Edematous
  • Fibrotic
• Depending upon disease activity
  • Active
  • Passive

Depending on depth:

• Deep pocket
• Shallow pocket

2. Suprabony and infrabony pockets

3. Periodontal cyst

• It is an uncommon lesion occurring most often in the mandibular canine-premolar region
• It may develop from a dentigerous cyst, a primordial cyst of supernumerary tooth germ from stimulation of epithelial rests f periodontal ligament

Read And Learn More: Periodontics Question and Answers

4. Simple, compound, and spiral pocket

5. Acute periodontal abscess

• Purpose of treatment
  • To alleviate pain
  • Control the spread of infection
  • Establish drainage
  • Drainage can be establish
  • Through pocket
  • Through incision from the external surface

6. Types of pocket depth

1. Biologic/histologic depth
   • The distance between the gingival margin and the base of the pocket
   • Can be measured only in carefully prepared histologic sections
2. Clinical/probing depth
   • The distance to which the probe penetrates into the pocket
   • The probing force is 25 pounds or 0.75 N.

7. Pus

• It is a common feature of periodontal disease
• It is not an indication of the depth of pocket or severity of periodontal destruction
• It reflects the nature of inflammatory changes in the pocket wall

Periodontal Pocket Long Essay

Question 1. Define and classify pocket. Describe its clinical features pathogenesis and treatment.
Answer:

Definition: Pathological deepening of the gingival sulcus

Classification:

1. Depending upon its morphology:

1. Gingival/false pocket:
   • Due to the bulk of gingiva
   • No destruction of underlying periodontal tissues
2. Periodontal/true pocket:
   • Leads to loosening and exfoliation of tissues
3. Combined pocket:

2. Depending upon its relationship to the crustal bone:

1. Suprabony pocket:
   • The bottom of the pocket is coronal to the underlying bone
2. Infrabony pocket:
   • The bottom of the pocket is apical to the underlying bone

3. Depending upon the no. of surfaces involved:

1. Simple: Involving one tooth surface
2. Compound: Involving two/more tooth surfaces
3. Complex: The base of the pocket is not in direct communication with the gingiva margin

4. Depending upon the nature of the soft tissue wall:

1. Edematous: Due to inflammation
2. Fibrotic

5. Depending upon disease activity:

• Active
• Passive

6. Depending on depth:

• Deep pocket
• Shallow pocket

Features:

Gingiva:

• Color – bluish red
• Size – enlarged
• Surface – shiny, discolored
• Consistency-puffy
• Bleeding – Positive
• Purulent exudates – positive
• Bluish red vertical zone extending from marginal gingiva to alveolar mucosa
• Break in faciolingual continuity of gingiva

Teeth:

• Mobility
• Extrusion from socket
• Pathological migration
• Toothache
• Sensation of pressure
• Foul taste
• Radiating pain, gnawing feeling
• Thermal sensitivity
• Stickness of food
• Urge to dig

Pathogenesis:

• Collagenase released by bacteria, phagocytes, and fibro-blast
• Forces by bacteria
• Exudation

Treatment:

1. Gingival pocket/False pocket:

• Scaling and root planning
• Recall
• If required gingivectomy/gingivoplasty

2. Periodontal pocket:

• Scaling and root planning
• Removal of pocket wall-Gingivectomy
• Hemisection

3. Suprabony pockets:

• Scaling and root planning
• Flap surgery

4. Infrabony pockets:

• New attachment procedures
• Nongraft associated
• Graft associated
• Combinations

Question 2. Discuss the contents of the periodontal pocket.
Answer:

Contents:

• Micro-organisms and their product sections
  • Enzymes
  • Endotoxins
  • Metabolic products
• Dental plaque, food remnants
• Gingival fluid
• Salivary mucin
• Serum
• Fibrin
• Cells
  • Desquamated epithelial cell
  • Leukocytes
  • Degenerated and necrotic PMNs
  • Pus formation

Question 3. Describe histopathology and sequels.
Answer:

Histopathology:

1. Changes in soft tissue wall:

• Blood vessels are engorged and dilated
• Connective tissue is edematous and densely infiltrated with plasma cells, lymphocytes, and PMNs
• Degeneration and necrosis of epithelium leading to ulceration of epithelium
• Bacterial invasion along the lateral and apical areas of the pocket
• The epithelial projection extends deep into the connective tissue

2. Microtopography of a gingival wall of the pocket:

• 7 areas are identified
  • Area of relative quiescence
  • Area of bacterial accumulation
  • Area of leukocytes
  • Area of bacterial leukocyte interaction
  • Area of epithelial desquamation – Area of ulceration
  • Area of hemorrhage

3. Periodontal pocket as healing lesion:

• Characterized by destructive and constructive tissue changes
• Destructive changes are characterized by fluid and cellular inflammatory exudates

4. Changes in root surface wall:

• Structural changes:
  • Presence of pathogens
  • Areas of increased mineralization
  • Areas of root caries
• Chemical changes:
  • Increased calcium, magnesium, phosphate, and fluoride
• Cytotoxic changes:
  • Bacterial penetration
  • Presence of endotoxins

Sequel:

• Inflamed gums with damaged fibers
• Bone destruction
• Exposed root surfaces

Question 4. Define periodontal pocket. Classify periodontal pockets. Discuss briefly the root surface wall of the pocket.

Root Surface Wall Changes:

Structural:

• Presence of pathogens
• Areas of increased mineralization
• Areas of root caries
• Chemical – Increased Calcium, Magnesium, Phosphate,
• Cytotoxic – Bacterial penetration, Presence of endotoxin-ins

Zones:

• Cementum
• Attached plaque
• Unattached plaque
• Junctional epithelium
• Partially lysed CT fibers
• Intact CT fibers
• Constant probing depth with different levels of attachment loss

Periodontal Pocket Short Essays

Question 1. Differentiate supra bony and inf ebony pockets.
Answer:

Question 2. Periodontal Cyst.
Answer:

• Localized destruction of the periodontal tissues along the lateral root surface
• Site: Common mandibular canine premolar area

Etiology:

• Odontogenic cyst
• Dentigerous cyst
• Primordial cyst
• The proliferation of epithelial cell rest of molasses

Features:

• Asymptomatic
• Localized
• Tenderness

Radiographic Feature:

• Radiolucent lesion bordered by a radiopaque line

Treatment:

• Scaling and root planning
• Drainage

Question 3. Changes of root surface wall of the pocket.
Answer:

• Structural
• Presence of pathogens
• Areas of increased mineralization
• Areas of root caries

Chemical: Increased Calcium, Magnesium, Phosphate, and Fluoride

Cytotoxic: Bacterial penetration, Presence of endotoxins

Zones:

• Cementum
• Attached plaque
• Unattached plaque
• Junctional epithelium
• Partially lysed CT fibers
• Intact CT fibers

Question 4. Classify periodontal pockets. Treatment of pseudopockets.
Answer:

Treatment:

• Scaling
• Oral hygiene instructions are given
• Patients on antiepileptic drugs, calcium channel blockers or immune suppressants should consult a physician for alternative drugs
• Procedures like gingivectomy and gingival curettage are done

Question 8. Correlation of clinical and histopathological features of a periodontal pocket
Answer:

Periodontal Pocket Short Answers

Question 1. Periodontal disease activity
Answer:

• According to the concept of periodontal disease activity, periodontal pockets go through periods of exacerbation and quiescence.

1. Period of quiescence:

• Characterized by a reduced inflammatory response
• There is little or no loss of bone and connective tissue attachment
• Presence of unattached plaque with gram-negative bacteria

2. Period of exacerbation:

• Bone and connective tissue attachment loss Pocket deepens
• It lasts for days, weeks, or months
• It is followed by a period of quiescence
• These periods of quiescence and exacerbation are known as periods of inactivity and periods of activity

Question 2. Methods of pocket therapy.
Answer:

1. Gingival pocket/false pocket:

• Scaling and root planning
• Recall
• If required gingivectomy/gingivoplasty

2. Periodontal pockets:

• Scaling and root planning
• Gingivectomy
• Hemisection

3. Suprabony pockets:

• Scaling and root planning
• Flap surgery

4. Infrabony pockets:

• New attachment procedures
• Nongraft associated
• Graft associated
• Combination

Question 3. Treatment of pseudo/edematous/false pocket.
Answer:

• Scaling and root planning
• Recall
• If required gingivectomy/gingivoplasty

Question 4. Complex pocket.
Answer:

• It is also known as a spiral pocket
• It originates on one tooth surface and twisting around the tooth involves one or more additional surfaces
• Here the base of the pocket is not in direct communication with the gingival margin
• It is most common in furcation areas

Question 5. Long junctional epithelium.
Answer:

• During the healing of the periodontal pocket, the area is in- vaded by cells from 4 different sources.

1. Oral epithelium.
2. Gingival connective tissue
3. Bone
4. Periodontal ligament

• If epithelium proliferates along the tooth surface before the cells from other tissues reaches the area, it results in the long junctional epithelium

Question 6. Suprabony pockets.
Answer:

• Also known as suprarenal or supra-alveolar pocket
• In it, the bottom of the pocket is coronal to the underlying alveolar bone
• A horizontal pattern of bone loss is seen
• Interproximal, trans-septal fibers that are restored during progressive periodontal disease are arranged horizontally in the space between the base of the pocket and the alveolar bone
• On facial and lingual surfaces, periodontal ligament fi- bres beneath the pocket follow their normal horizontal-oblique course between tooth and bone

Question 7. Infrabony pockets.
Answer:

• Also known as subcrustal or intra-alveolar pocket In it the bottom of the pocket is apical to the underlying alveolar bone
• An angular pattern of bone loss is seen
• Interproximal, trans-septal fibers are oblique and extend- ing from the cementum beneath the base of the pocket along also- lar bone and over the crest to the cementum of the adjacent tooth
• On facial and lingual surfaces, periodontal ligament fi- bres beneath the pocket follow an angular pattern of adjacent bone
• They extend from the cementum beneath the base of the pocket along the alveolar bone and over the crest to join with the outer periodontium

Periodontal Pocket Viva Voce

1. In a pseudo or gingival pocket, there is no attachment loss
2. The pocket depth is due to the coronal movement of the gingival margin
3. In a true pocket there is apical movement of the junc- tional epithelium due to the destruction of the sup- porting tissues
4. In suprabony pocket the base of the pocket is coronal to the alveolar bone
5. Periodontal abscess is usually formed in the support- ing periodontal tissues along the lateral aspect of root or in the soft tissue wall
6. The most severe destruction occurs in the lateral sur- face of pocket
7. The normal distance between junctional epithelium and alveolar bone is about 1.07-1.97 mm
8. The normal distance between the apical extent of cal- culus and the alveolar crest is 1.97 mm
9. The pattern of bone destruction in infrabony pockets is angular
10. The pocket formed by gingival enlargement is re- ferred to as pseudo pocket
11. Periodontal abscess is also known as parietal abscess
12. Periodontal cyst is commonly seen in mandibular ca- nine and premolar
13. The only reliable method of detecting periodontal pockets is probing

Desquamative Gingivitis Short Essays

Question 1. Desquamative Gingivitis.
Answer:

• A peculiar condition characterized by intense erythema, defamation, and ulceration of the free and attached gingival.
• Coined by Prinz in 1932

Structure of Desquamative Gingivitis:

Associated Diseases:

• Lichen planus
• Cicatricial pemphigoid Pemphigus vulgaris
• Linear IGA dermatitis
• Dermatitis herpetiformis
• Drug reactions

Clinical examination:

• Examine the distinct clinical features
• Presence of Sikorsky’s Sign

Biopsy:

• Tissue culturing with Michelles buffer

Read And Learn More: Periodontics Question and Answers

Treatment:

• Local – Oral prophylaxis
• Administration of soft brush and mouthwash
• Topical application of corticosteroids
• Systemic-Systemic antibiotic
• Example: Prednisolone – 30-40 mg daily

Desquamative Gingivitis Short Answers

Question 1. Management of Chronic Desquamative gingivitis.
Answer:

• Local Treatment:
• Plaque control
• Oxidizing mouthwashes
• Topical corticosteroid ointments

Systemic Therapy:

• Systemic corticosteroid
• Prednisolone 30-40 mg daily
• Reduce the dose gradually