NEET MDS Periodontology Syllabus

Periodontology syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Periodontology in NEET MDS, not a summary of it.

1. 1

   Introduction to Periodontology

   2 topics

   • History of Periodontology
     • Early Discoveries
     • Modern Developments
   • Periodontal Anatomy
     • Gingiva
     • Periodontal Ligament
     • Cementum
     • Alveolar Bone
2. 2

   Periodontal Diseases

   4 topics

   • Gingivitis
     • Etiology
     • Pathogenesis
     • Clinical Features
     • Diagnosis
     • Treatment
   • Periodontitis
     • Etiology
     • Pathogenesis
     • Clinical Features
     • Diagnosis
     • Treatment
   • Aggressive Periodontitis
     • Etiology
     • Pathogenesis
     • Clinical Features
     • Diagnosis
     • Treatment
   • Periodontal Abscesses
     • Etiology
     • Pathogenesis
     • Clinical Features
     • Diagnosis
     • Treatment
3. 3

   Periodontal Treatment Modalities

   4 topics

   • Non-Surgical Therapy
     • Scaling and Root Planing
     • Antimicrobial Therapy
     • Host Modulation Therapy
   • Surgical Therapy
     • Flap Surgery
     • Gingivectomy
     • Osseous Surgery
     • Guided Tissue Regeneration
     • Soft Tissue Grafts
   • Laser Therapy
     • Types of Lasers
     • Indications and Contraindications
     • Clinical Applications
   • Periodontal Maintenance
     • Importance of Maintenance
     • Maintenance Protocols
     • Patient Education
4. 4

   Periodontal-Systemic Interrelationships

   4 topics

   • Cardiovascular Disease
     • Pathophysiological Links
     • Clinical Evidence
     • Implications for Treatment
   • Diabetes Mellitus
     • Bidirectional Relationship
     • Clinical Evidence
     • Implications for Treatment
   • Pregnancy
     • Pregnancy Gingivitis
     • Preterm Birth and Low Birth Weight
     • Clinical Management
   • Respiratory Diseases
     • Pneumonia
     • Chronic Obstructive Pulmonary Disease (COPD)
     • Clinical Management
5. 5

   Advanced Periodontal Techniques

   3 topics

   • Implantology
     • Implant Placement
     • Bone Grafting
     • Peri-Implantitis
   • Periodontal Plastic Surgery
     • Crown Lengthening
     • Esthetic Crown Lengthening
     • Gingival Augmentation
   • Microsurgery
     • Principles of Microsurgery
     • Clinical Applications
     • Outcomes and Benefits

Periodontology flashcards for NEET MDS

23 of 61 cards from the Periodontology deck — real questions with worked answers.

1. Who is regarded as the "Father of Modern Periodontology" and is known for promoting tissue-conserving, non-surgical maintenance therapy?

   Bernhard Gottlieb is often cited for foundational histology, but Paul Riggs popularized "Riggs' disease" (pyorrhea); the title "Father of Modern Periodontology" is most commonly given to Bernhard Gottlieb / and clinically to Paul R. Stillman. The widely accepted answer for organized clinical periodontics is Dr. Robert Neumann and Dr. Leonard Widman (flap surgery), while Dr. R. Earl Robinson and especially Dr. Sigurd Ramfjord shaped maintenance.

2. What landmark classification system replaced the 1999 Armitage classification of periodontal diseases?

   The 2017 World Workshop classification (AAP/EFP), which introduced staging (I-IV) and grading (A-C) of periodontitis and a separate category for peri-implant diseases.

3. In the 2017 classification, what three parameters determine the STAGE of periodontitis?

   Severity (interdental clinical attachment loss, radiographic bone loss, tooth loss), complexity (probing depth, furcation, defects, need for rehabilitation), and extent/distribution (localized, generalized, molar-incisor).

4. In the 2017 classification, how is the GRADE of periodontitis primarily determined?

   By the rate of progression: Grade A (slow), B (moderate), C (rapid), estimated from bone loss/age ratio, direct evidence over 5 years, and risk factors such as smoking and diabetes (HbA1c).

5. What are the four major tissues that make up the periodontium?

   Gingiva, periodontal ligament (PDL), cementum, and alveolar bone.

6. What is the normal width of the periodontal ligament space?

   Approximately 0.15-0.38 mm (average about 0.2 mm), being narrowest in the middle (fulcrum) and wider at the crest and apex.

7. What is the biologic width (supracrestal tissue attachment), and what are its average component dimensions?

   It is the dimension of soft tissue attached to the tooth coronal to the alveolar bone, averaging about 2.04 mm total: junctional epithelium ~0.97 mm + connective tissue attachment ~1.07 mm (Gargiulo, 1961).

8. Which collagen fiber group of the gingiva connects the cementum to the gingiva and resists gingival displacement?

   The dentogingival fibers of the gingival fiber apparatus (part of the supra-alveolar/gingival fiber group, mainly type I collagen).

9. Name the principal fiber groups of the periodontal ligament.

   Alveolar crest, horizontal, oblique (most numerous, resist masticatory/vertical forces), apical, and interradicular fibers.

10. What is the predominant cell type and its function in the periodontal ligament?

    Fibroblasts, which synthesize and remodel collagen; the PDL also contains epithelial cell rests of Malassez, cementoblasts, osteoblasts, and osteoclasts.

11. What are the four clinical signs of gingival inflammation used to diagnose gingivitis?

    Redness (erythema), swelling/edema, bleeding on probing, and change in contour/consistency, with no attachment or bone loss.

12. According to the 2017 classification, what probing depth and bleeding-on-probing thresholds define gingival health on an intact periodontium?

    Probing depths ≤3 mm and bleeding on probing at <10% of sites, with no attachment loss.

13. What histologic stages did Page and Schroeder describe in the development of periodontal disease?

    Initial lesion (2-4 days), early lesion (4-7 days, T-cell dominated), established lesion (2-3 weeks, plasma cell/B-cell dominated, chronic gingivitis), and advanced lesion (periodontitis, bone loss).

14. What is necrotizing ulcerative gingivitis (NUG) and its classic triad of clinical features?

    An acute, painful, often Fusobacterium/spirochete-associated gingival infection presenting with the triad of punched-out, ulcerated interdental papillae; pain; and spontaneous bleeding (often with pseudomembrane and fetor oris).

15. What is the fundamental difference between gingivitis and periodontitis?

    Gingivitis is reversible inflammation confined to the gingiva with no loss of attachment or bone; periodontitis involves irreversible loss of connective tissue attachment and alveolar bone.

16. What is the difference between a suprabony and an infrabony (intrabony) pocket?

    In a suprabony pocket the base of the pocket is coronal to the alveolar crest (horizontal bone loss); in an infrabony pocket the base is apical to the crest (vertical/angular bone loss).

17. How are infrabony defects classified by the number of remaining bony walls?

    By walls: three-wall, two-wall, one-wall (hemiseptum), and combined defects; three-wall defects have the best prognosis for regeneration.

18. What is the Glickman classification of furcation involvement?

    Grade I: incipient/early, suprabony; Grade II: cul-de-sac, partial bone loss but not through-and-through; Grade III: through-and-through but soft-tissue covered; Grade IV: through-and-through and clinically open/visible.

19. Which keystone pathogen is most strongly associated with chronic periodontitis as part of the "red complex"?

    Porphyromonas gingivalis, together with Tannerella forsythia and Treponema denticola (Socransky's red complex).

20. What is the key microbiological marker associated with localized aggressive (juvenile) periodontitis?

    Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans), particularly the JP2 clone with leukotoxin production.

21. What is the classic clinical/radiographic pattern of localized aggressive periodontitis?

    Rapid attachment and bone loss localized to first molars and incisors in otherwise healthy young patients, with relatively little plaque/calculus and a familial pattern; arc-shaped (vertical) bone loss around molars.

22. In the 2017 classification, how is what was formerly called aggressive periodontitis now categorized?

    It is no longer a separate entity; it is incorporated into "periodontitis" and typically captured as Grade C (rapid progression), often molar-incisor pattern, Stage III/IV.

23. What host defect involving neutrophils is commonly associated with aggressive periodontitis?

    Neutrophil (PMN) chemotaxis and phagocytosis defects, leading to impaired bacterial clearance.

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