BDS 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 BDS, 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 BDS

23 of 51 cards from the Periodontology deck — real questions with worked answers.

1. Who is regarded as the "father of modern periodontology" and is credited with founding the specialty in the early 20th century?

   Dr. John M. Riggs is historically associated with periodontal disease (once called "Riggs' disease"), but Bernhard Gottlieb and later the American Academy of Periodontology (founded 1914) shaped modern periodontology. Gottlieb's histological studies of the periodontium are considered foundational.

2. What are the four components of the periodontium?

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

3. What is the biologic width (supracrestal tissue attachment) and its average total dimension?

   The dimension of soft tissue attached to the tooth above the alveolar crest, comprising junctional epithelium (~0.97 mm) plus connective tissue attachment (~1.07 mm), totaling approximately $2.04\ \text{mm}$ (Gargiulo).

4. Which type of collagen predominates in the periodontal ligament, and what is the main cell type?

   Type I collagen predominates (with some type III); the fibroblast is the main cell of the PDL.

5. Name the principal fiber groups of the gingival (free gingival) fibers.

   Dentogingival, dentoperiosteal, alveologingival, circular (circumferential), and transseptal fibers.

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

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

7. What is the normal probing depth of a healthy gingival sulcus?

   Approximately $1\text{–}3\ \text{mm}$.

8. Define gingivitis and state its key reversible feature.

   Gingivitis is plaque-induced inflammation confined to the gingiva with no loss of connective tissue attachment or alveolar bone. It is reversible with plaque control.

9. According to the 1976 Page & Schroeder model, what are the four stages of gingival/periodontal inflammation?

   Initial lesion (2–4 days), early lesion (4–7 days), established lesion (2–3 weeks, chronic gingivitis), and advanced lesion (periodontitis).

10. Which inflammatory cell predominates in the established gingivitis lesion versus the advanced (periodontitis) lesion?

    Plasma cells predominate in both the established and advanced lesions; the early lesion is dominated by T-lymphocytes, and the initial lesion by neutrophils.

11. Define periodontitis and its distinguishing feature from gingivitis.

    Periodontitis is inflammation of the periodontium with irreversible loss of connective tissue attachment and alveolar bone, forming true periodontal pockets. The distinguishing feature is clinical attachment loss (CAL).

12. How is Clinical Attachment Level (CAL) calculated from probing depth (PD) and gingival margin position?

    $\text{CAL} = \text{PD} + \text{gingival recession}$ (distance from CEJ to gingival margin). If the margin is coronal to the CEJ, that overgrowth is subtracted instead.

13. In the 2017 classification, how is periodontitis staged and graded?

    Staging (I–IV) is based on severity/complexity (using interdental CAL, radiographic bone loss, tooth loss). Grading (A–C) reflects rate of progression, estimated by bone loss / age ratio, and risk factors such as smoking and diabetes.

14. In the 2017 grading, how is the primary criterion (bone loss relative to age) calculated and interpreted?

    $\text{Grade} = \dfrac{\%\ \text{bone loss}}{\text{age}}$. $<0.25$ = Grade A (slow), $0.25\text{–}1.0$ = Grade B (moderate), $>1.0$ = Grade C (rapid).

15. What bacteria form the "red complex" (Socransky) most associated with periodontitis?

    Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola.

16. Which organism is the key pathogen classically associated with localized aggressive periodontitis?

    Aggregatibacter actinomycetemcomitans (formerly Actinobacillus actinomycetemcomitans), particularly the JP2 clone, producing leukotoxin.

17. What are the classic clinical features of localized aggressive periodontitis (LAP)?

    Onset around puberty in otherwise healthy patients; rapid attachment/bone loss localized to first molars and incisors; amount of destruction inconsistent with (relatively small) plaque deposits; often familial aggregation and neutrophil (PMN) dysfunction.

18. What distinguishes generalized aggressive periodontitis (GAP) from the localized form?

    GAP typically affects patients under ~30, involves at least three permanent teeth other than first molars and incisors, shows a pronounced episodic (burst) pattern of attachment loss, and poor serum antibody response to infecting agents.

19. What is a periodontal abscess and its typical clinical presentation?

    A localized purulent infection within the periodontal tissues, presenting as a smooth shiny swelling on the gingiva, pain, tenderness to percussion, deep pocket, and often suppuration; the tooth is usually vital.

20. How do you differentiate a periodontal abscess from a periapical (endodontic) abscess?

    Periodontal abscess: tooth usually VITAL, associated with a deep periodontal pocket, swelling near the gingival margin/lateral aspect. Periapical abscess: tooth usually NON-VITAL, pain on percussion, apical radiolucency, sinus tract near the apex.

21. What is the goal and mechanism of non-surgical periodontal therapy (scaling and root planing)?

    To remove supra- and subgingival plaque, calculus, and endotoxin-laden cementum, disrupting the biofilm to resolve inflammation and allow reattachment/long junctional epithelium formation. It reduces probing depth and bleeding on probing.

22. What probing depth threshold is often cited as the limit of effective closed root planing efficiency?

    Instrumentation efficacy declines markedly in pockets deeper than $5\ \text{mm}$; residual calculus increases substantially in pockets $>5\text{–}6\ \text{mm}$, favoring surgical access.

23. What is the role of systemic sub-antimicrobial dose doxycycline (SDD) in periodontal therapy?

    At $20\ \text{mg}$ twice daily it acts as a host-modulating agent by inhibiting matrix metalloproteinases (collagenase), reducing tissue breakdown without an antibacterial effect.

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