MJDF Periodontology Fundamentals 2 — Questions and Answers

Question 1: According to the 2017 World Workshop classification, which of the following BEST describes Stage III Grade C periodontitis?

Mild bone loss, slow progression, no complexity factors, associated with local factors only
Severe bone loss or tooth loss with complexity factors such as masticatory dysfunction, and a rapid rate of progression possibly associated with systemic factors or risk factors like smoking (Correct answer)
Moderate bone loss with no systemic disease association and moderate rate of progression
Gingivitis only, reversible, no bone loss

Correct answer: Severe bone loss or tooth loss with complexity factors such as masticatory dysfunction, and a rapid rate of progression possibly associated with systemic factors or risk factors like smoking

Stage III indicates severe periodontitis with significant bone/tooth loss and complexity factors (like vertical bone defects, furcation involvement). Grade C indicates rapid progression and/or risk factors (smoking, poorly controlled diabetes, systemic disease).

The 2017 World Workshop on the Classification of Periodontal and Peri-implant Diseases and Conditions (Tonetti, Greenwell & Kornman 2018) introduced a new staging and grading system for periodontitis that replaced the older classification system (chronic vs. aggressive periodontitis). Staging (I-IV) describes severity and complexity: Stage I: Initial bone loss (1-2mm), probing depths ≤4mm, no tooth loss, no complexity factors. Stage II: Moderate bone loss (15-33%), probing depths ≤5mm, no tooth loss due to periodontitis, no complexity factors. Stage III: Severe bone loss (>33% or involving middle or apical third), probing depths ≥6mm, tooth loss ≤4 teeth, complexity factors (vertical bone loss ≥3mm, furcation class II/III, masticatory dysfunction, root proximity). Stage IV: Like Stage III but with additional severe complexity factors including masticatory dysfunction requiring complex rehabilitation, bite collapse, flaring, drifting, <20 remaining/opposing teeth (10 opposing pairs). Grading (A, B, C) describes rate of progression and modifying/risk factors: Grade A: Slow progression rate (no radiographic bone loss over 5 years, low biofilm load for bone destruction, no risk factors like smoking or diabetes). Grade B: Moderate progression rate. Grade C: Rapid progression rate (>2mm bone loss in 5 years), high biofilm-to-bone-loss ratio, heavy smoker, poorly controlled HbA1c >7%, other systemic influences. The staging and grading are determined at presentation and may be modified as additional information becomes available. This classification guides treatment planning and prognosis.

Question 2: What is the primary cause of chronic periodontitis?

A genetic predisposition independent of plaque levels
Subgingival dental plaque (biofilm) and the host's inflammatory response to it (Correct answer)
Mechanical trauma from occlusal forces
Systemic disease alone without local plaque accumulation

Correct answer: Subgingival dental plaque (biofilm) and the host's inflammatory response to it

Periodontitis is fundamentally caused by the host inflammatory response to subgingival bacterial plaque biofilm. The destruction of periodontium results from this immune-inflammatory response rather than direct bacterial destruction alone.

Periodontitis is an inflammatory disease of the supporting tissues of the teeth (gingiva, periodontal ligament, alveolar bone, cementum) caused by specific pathogenic bacteria within the dental biofilm (dental plaque). However, the tissue destruction is not caused directly by bacterial products alone — rather, it results from the host's immune-inflammatory response to the subgingival bacterial challenge. The pathogenesis: subgingival biofilm accumulates and matures, with a shift towards a more dysbiotic (pathogenic) microbial community including species such as Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola (the 'red complex' pathogens), and many others in polymicrobial community. These bacteria and their products (LPS, proteases, fimbriae) stimulate the local innate and adaptive immune response. Cytokines (IL-1β, TNF-α, IL-6, PGE2) activate osteoclasts, which resorb alveolar bone; matrix metalloproteinases (MMPs) degrade collagen in the periodontal ligament and connective tissue. This results in the progressive tissue destruction characterising periodontitis. The key insight: susceptible hosts develop more severe disease for a given bacterial challenge. Host factors (genetic polymorphisms in cytokine genes, immune function) and systemic factors (diabetes, smoking — which impairs neutrophil function and vascularity) modify the host's inflammatory response, explaining why some patients with heavy plaque have mild disease while others with moderate plaque have severe disease. Treatment rationale follows from pathogenesis: removing the bacterial trigger (supragingival and subgingival debridement) reduces the inflammatory response, allowing resolution and repair of the periodontal tissues.

Question 3: In periodontal assessment, a 'bleeding on probing' (BOP) score is important because:

BOP only occurs in advanced periodontitis and indicates imminent tooth loss
BOP indicates the presence of gingival inflammation and is used to monitor disease activity and treatment response (Correct answer)
BOP is a normal finding in healthy gingiva and requires no action
BOP indicates infection with a specific periodontopathogen and guides antibiotic selection

Correct answer: BOP indicates the presence of gingival inflammation and is used to monitor disease activity and treatment response

Bleeding on gentle probing (BOP) indicates inflamed gingival tissues and is the primary clinical marker used to monitor the success of plaque control and periodontal treatment — healthy gingiva does not bleed.

Bleeding on probing (BOP) is assessed during periodontal examination by inserting a periodontal probe to the base of the sulcus/pocket and recording whether bleeding occurs within 30 seconds. It is one of the key parameters in periodontal charting alongside probing pocket depths, attachment levels, recession, mobility, furcation status, and BOP. Clinical significance of BOP: BOP indicates the presence of subgingival inflammation — an inflamed pocket lining (junctional epithelium and surrounding connective tissue) has increased vascularity, dilated, fragile capillaries, and ulceration of the pocket wall. Even gentle probing causes bleeding of these fragile vessels. Healthy gingiva (with a non-inflamed pocket lining) does not bleed. BOP as a clinical tool: BOP percentage is used to assess disease activity — a BOP score of <10-20% after active periodontal therapy is associated with periodontal stability and low risk of further attachment loss; persistent high BOP indicates residual inflammation and active disease risk; a reduction in BOP from baseline (after treatment) is a primary outcome measure of periodontal therapy effectiveness; sites with persistent BOP at reassessment are target sites for additional treatment. Limitations of BOP: positive BOP is sensitive for inflammation but not highly specific for periodontitis (BOP without bone loss = gingivitis); false negatives can occur in smokers (smoking causes vasoconstriction, reducing gingival vascularity — smokers may have less BOP despite significant inflammation, masking disease extent); technical factors (probe force, angulation) affect BOP recording. For MJDF candidates, understanding BOP interpretation within the full periodontal assessment context is essential for both examination and clinical scenarios.

Question 4: What is the purpose of subgingival debridement (root surface debridement/RSD) in the non-surgical treatment of periodontitis?

To remove all cementum from the root surface to expose clean dentine
To mechanically disrupt and remove the subgingival biofilm and calculus from root surfaces, reducing the bacterial load causing periodontal inflammation (Correct answer)
To surgically remove the inflamed periodontal pocket lining
To apply fluoride to exposed root surfaces to prevent caries

Correct answer: To mechanically disrupt and remove the subgingival biofilm and calculus from root surfaces, reducing the bacterial load causing periodontal inflammation

Root surface debridement aims to mechanically disrupt and remove the subgingival bacterial biofilm and calculus, eliminating the primary cause of periodontal inflammation and allowing the host's tissues to heal.

Root surface debridement (RSD), also called subgingival debridement, scaling and root planing (SRP), or non-surgical periodontal therapy (NSPT) is the cornerstone of active periodontal treatment. It is the primary, evidence-based non-surgical intervention for periodontitis. Rationale: since periodontitis is caused by subgingival bacterial biofilm and the host's inflammatory response to it, treatment must disrupt and remove the biofilm (and calculus, which serves as a retentive surface for biofilm) from root surfaces within the periodontal pocket. Reducing the bacterial load below the threshold that sustains chronic periodontal inflammation allows the host's inflammatory response to resolve and periodontal tissues to repair. Clinical outcomes of RSD (supported by strong evidence): reduction in pocket depth (combination of tissue shrinkage/recession and slight gain of attachment); reduction in BOP (resolution of inflammation); gain of clinical attachment level (1-2mm on average in moderate pockets); improvement in bone levels in some cases (though bone regeneration is not reliably achieved by RSD alone). Older terminology (root planing) referred to aggressive planing of the root surface to achieve physical smoothness. Modern evidence and terminology has shifted to 'debridement' — emphasising biofilm removal rather than excessive cementum removal. Cementum contains growth factors and is valuable for healing; removing excessive cementum is not necessary and may be counterproductive. Systematic reviews confirm that manual (curettes) and ultrasonic (piezoelectric/magnetostrictive) instruments are equally effective for RSD. Adjuncts to RSD: local antimicrobials (subgingivally delivered chlorhexidine, doxycycline, minocycline); systemic antibiotics (metronidazole ± amoxicillin — recommended as adjunct to RSD for Stage III-IV Grade C periodontitis in younger patients; antibiotic stewardship considerations apply); photodynamic therapy; other host modulation therapies.

Question 5: Which furcation classification system grades furcation involvement using a probe measurement, and what does Class II indicate?

Ramfjord classification — Class II means bone loss is present but less than 50% of the buccal/lingual width
Hamp classification — Class II means the probe penetrates >3mm horizontally into the furcation but does not pass through (Correct answer)
Nabers probe system — Class II means the tooth requires immediate extraction
BSP Basic Periodontal Examination — Class II means the tooth has a 4-5mm pocket with furcation exposure

Correct answer: Hamp classification — Class II means the probe penetrates >3mm horizontally into the furcation but does not pass through

Hamp's classification grades furcation involvement by horizontal probe penetration: Class I (<3mm), Class II (>3mm but not through-and-through), Class III (through-and-through furcation — probe passes completely from one side to the other).

Furcation involvement describes the degree of bone loss in the furcation area (the area between the roots of a multi-rooted tooth where the roots diverge from the trunk). Furcation assessment is an essential part of periodontal charting for all multi-rooted teeth (upper molars with three roots; lower molars and upper premolars with two roots). Hamp's classification (1975) is the most widely used system for recording furcation involvement in periodontal practice: Class I: Horizontal probing penetration <3mm. There is bone loss in the furcation but the probe does not penetrate ≥3mm. Typically manageable with subgingival debridement. Class II: Horizontal probing penetration ≥3mm but does not pass through to the other side of the furcation. Significant furcation involvement; debridement is more difficult; may require surgical access. Tunnelling (in lower molars with good anatomy) or root resection may be options in advanced cases. Class III: Probe passes completely through the furcation from one aspect to the other (through-and-through). Very poor prognosis; root resection, tunnelling, or extraction often considered. Assessment technique: use a curved Nabers probe (specifically designed for furcation exploration) along the buccal, lingual, mesial, and distal aspects of each multi-rooted tooth. For upper first molars, assess the buccal furcation (between MB and DB roots), mesial furcation (often under contact area), and distal furcation. Furcation involvement is a complexity factor in the 2017 Classification (Stages III and IV include Class II/III furcation involvement). Furcation-involved teeth have a reduced periodontal prognosis — Class III furcation involvement is associated with significantly higher tooth loss rates.

Question 6: Which systemic condition has the STRONGEST evidence for bidirectional association with periodontitis?

Rheumatoid arthritis
Diabetes mellitus (Correct answer)
Cardiovascular disease
Chronic kidney disease

Correct answer: Diabetes mellitus

Diabetes mellitus has the strongest and most well-established bidirectional link with periodontitis — diabetes increases the risk and severity of periodontal disease, and periodontitis adversely affects glycaemic control in diabetic patients.

The relationship between diabetes mellitus (DM) and periodontitis is the best-documented example of a bidirectional systemic-periodontal disease association and is the most relevant for clinical dental practice. Diabetes → Periodontitis: diabetic patients have a 2-3 fold increased risk of periodontitis. Mechanisms include: impaired neutrophil function (reduced chemotaxis and phagocytosis); advanced glycation end products (AGEs) accumulating in periodontal tissues, promoting inflammation and impairing collagen synthesis; altered vascular function (microangiopathy reduces tissue perfusion and healing capacity); altered wound healing; increased susceptibility to infection. Poorly controlled diabetes (high HbA1c) has more severe periodontitis than well-controlled diabetes. Periodontitis → Diabetes: chronic systemic inflammation from periodontal disease can worsen insulin resistance and glycaemic control. Multiple studies and meta-analyses demonstrate that successful periodontal treatment (RSD) is associated with a reduction in HbA1c of approximately 0.4% in diabetic patients — clinically significant, comparable to adding a second oral hypoglycaemic drug. This positions periodontal dentists as partners in systemic disease management. Clinical implications: all diabetic patients should have regular periodontal assessment; HbA1c should be known/checked for periodontal patients with diabetes; patients with severe periodontitis and no known diabetes should be screened (opportunistic screening with HbA1c or random blood glucose); periodontal treatment should be offered as part of holistic diabetic management; patients should be informed of the bidirectional relationship. While associations with cardiovascular disease (strongest epidemiological evidence), rheumatoid arthritis (shared inflammatory mechanisms and potential bidirectionality), and other systemic conditions exist, the diabetes relationship has the most robust evidence and clearest mechanisms for bidirectionality.

MJDF Periodontology Fundamentals 2

According to the 2017 World Workshop classification, which of the following BEST describes Stage III Grade C periodontitis?