9.1 2018 Periodontal Staging, Grading & Risk Factor Assessment
Key Takeaways
- The 2018 AAP/EFP World Workshop Classification categorises periodontitis by Stage (I-IV, reflecting disease severity and complexity) and Grade (A-C, reflecting rate of progression and risk modifiers).
- Periodontitis Staging is determined primarily by interdental clinical attachment loss (CAL) at the site of greatest loss, radiographic bone loss (RBL), and tooth loss due to periodontitis.
- Periodontitis Grading utilizes indirect evidence (% bone loss / age ratio) and is modified by key systemic risk factors: smoking status (<10 vs ≥10 cigarettes/day) and diabetes status (HbA1c <7.0% vs ≥7.0%).
- Basic Periodontal Examination (BPE) or PSR screening guides clinical management in Australian practice, mandating full-mouth periodontal charting when BPE Code 3 or 4 is recorded.
- Drug-induced gingival overgrowth is caused by calcium channel blockers (e.g., Nifedipine), anticonvulsants (Phenytoin), and immunosuppressants (Cyclosporine), requiring biofilm control and medical substitution.
9.1 2018 Periodontal Staging, Grading & Risk Factor Assessment
Accurate diagnosis, staging, and grading of periodontal and peri-implant conditions form the cornerstone of evidence-based periodontics in contemporary Australian dental practice. Adopted worldwide following the 2018 AAP/EFP World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions, this diagnostic framework is fully endorsed by the Australian Society of Periodontology (ASP) and tested extensively in the Australian Dental Council (ADC) Written Examination.
1. Diagnostic Categorisation: Health, Gingivitis & Periodontitis
The 2018 classification establishes clear physiological and pathological boundaries between periodontal health, plaque-induced gingivitis, and periodontitis, accounting for both intact and reduced periodontium clinical presentations.
| Diagnostic Category | Periodontal Status | Probing Depths (PD) | Bleeding on Probing (BOP) | Clinical Attachment Loss (CAL) & Bone Loss |
|---|---|---|---|---|
| Periodontal Health | Intact Periodontium | PD ≤ 3 mm | BOP < 10% of sites | No CAL or Radiographic Bone Loss (RBL) |
| Periodontal Health | Reduced Periodontium (Non-Periodontitis) | PD ≤ 3 mm | BOP < 10% of sites | CAL present (e.g. recession, crown lengthening); no RBL |
| Periodontal Health | Reduced Periodontium (Stable Periodontitis) | PD ≤ 4 mm (no 4 mm site with BOP) | BOP < 10% of sites | CAL & RBL present; disease successfully treated and stable |
| Plaque-Induced Gingivitis | Intact Periodontium | PD ≤ 3 mm | BOP ≥ 10% of sites | No CAL or RBL |
| Plaque-Induced Gingivitis | Reduced Periodontium (Non-Periodontitis or Stable) | PD ≤ 3 mm | BOP ≥ 10% of sites | Pre-existing CAL present; no active attachment loss |
| Periodontitis | Periodontal Breakdown | Pockets ≥ 4 mm with BOP or CAL | BOP variable | Interdental CAL detectable at ≥2 non-adjacent teeth, or buccal/lingual CAL ≥3 mm with pockets >3 mm at ≥2 teeth |
2. 2018 Periodontitis Staging Framework (Severity & Complexity)
Staging reflects the severity of clinical attachment loss and bone destruction at presentation, as well as the complexity of clinical management. Staging is assigned based on the site of greatest destruction across the dentition.
A. Severity Matrix by Stage
- Stage I (Initial Periodontitis):
- Interdental CAL (site of greatest loss): 1 to 2 mm.
- Radiographic Bone Loss (RBL): Coronal third (<15% of root length).
- Tooth Loss due to Periodontitis: 0 teeth.
- Stage II (Moderate Periodontitis):
- Interdental CAL: 3 to 4 mm.
- RBL: Coronal third (15% to 33% of root length).
- Tooth Loss due to Periodontitis: 0 teeth.
- Stage III (Severe Periodontitis with Potential for Additional Tooth Loss):
- Interdental CAL: ≥ 5 mm.
- RBL: Extending to middle or apical third of root (>33%).
- Tooth Loss due to Periodontitis: ≤ 4 teeth lost.
- Stage IV (Advanced Periodontitis with Extensive Tooth Loss & Potential for Dentition Collapse):
- Interdental CAL: ≥ 5 mm.
- RBL: Extending to middle or apical third of root (>33%).
- Tooth Loss due to Periodontitis: ≥ 5 teeth lost.
B. Complexity Factors
- Stage I: Maximum probing depth ≤ 4 mm; horizontal bone loss predominant.
- Stage II: Maximum probing depth ≤ 5 mm; horizontal bone loss predominant.
- Stage III: Probing depths ≥ 6 mm; vertical bone loss ≥ 3 mm; furcation involvement Class II or III; moderate alveolar ridge defect.
- Stage IV: In addition to Stage III criteria: masticatory dysfunction, secondary occlusal trauma (tooth hypermobility Grade 2 or 3), severe ridge defect, bite collapse, drifting/flaring of teeth, and fewer than 20 residual teeth (fewer than 10 opposing pairs).
3. 2018 Periodontitis Grading Framework (Rate of Progression & Risk Modifiers)
Grading indicates the biologic rate of disease progression, responsiveness to standard therapy, and potential impact on systemic health. A patient is initially assigned Grade B by default and modified up or down based on direct/indirect evidence and risk factors.
| Grading Criteria | Grade A: Slow Rate | Grade B: Moderate Rate | Grade C: Rapid Rate |
|---|---|---|---|
| Direct Evidence | No loss of CAL or RBL over 5 years | < 2 mm CAL or RBL loss over 5 years | ≥ 2 mm CAL or RBL loss over 5 years |
| Indirect Evidence (% RBL / Age) | Ratio < 0.25 | Ratio 0.25 to 1.0 | Ratio > 1.0 |
| Case Phenotype | Heavy biofilm deposits with low levels of destruction | Destruction commensurate with biofilm deposits | Destruction exceeds expectations given biofilm; early-onset pattern |
| Grade Modifier: Smoking | Non-smoker | Smoker < 10 cigarettes / day | Smoker ≥ 10 cigarettes / day |
| Grade Modifier: Diabetes | Normoglycaemic / No diabetes | Diabeteic with HbA1c < 7.0% | Diabetic with HbA1c ≥ 7.0% |
Note on ADC Examination Rules: If a patient has multiple grade modifiers (e.g. non-smoker but HbA1c is 8.2%), the highest severity modifier dictates the final grade (Grade C).
4. Screening Protocols: BPE & PSR in Australian Practice
In Australian clinical practice, the Basic Periodontal Examination (BPE) (or Periodontal Screening and Recording - PSR) is a rapid screening tool performed on all new patients and regular check-ups using a WHO dentate probe (featuring a 0.5 mm ball tip and a black band between 3.5 mm and 5.5 mm).
BPE / PSR Scoring Codes & Required Clinical Actions:
Code 0: Black band completely visible; no BOP; no calculus/overhangs.
Action: Routine preventive care; re-screen at recall.
Code 1: Black band completely visible; BOP present; no calculus/overhangs.
Action: Oral hygiene instruction (OHI); supragingival plaque control.
Code 2: Black band completely visible; supragingival/subgingival calculus or overhangs present.
Action: OHI; removal of calculus and restoration overhangs.
Code 3: Black band partially obscured by gingival margin (Probing depth 3.5 mm to 5.5 mm).
Action: Detailed periodontal charting of the affected sextant; Step 1 & 2 therapy.
Code 4: Black band completely disappears into pocket (Probing depth > 5.5 mm).
Action: Full-mouth detailed periodontal charting; comprehensive Step 1 & 2 therapy +/- specialist referral.
Code *: Furcation involvement (Class I-IV), tooth mobility Grade 2-3, or recession >3.5 mm.
Action: Detailed recording of specific defect regardless of depth code.
5. Systemic Risk Factors & Drug-Induced Gingival Overgrowth
Systemic factors significantly influence periodontal pathogenesis, immune response, and treatment prognosis.
A. Major Systemic Risk Factors
- Smoking: Primary environmental risk factor. Induces peripheral vasoconstriction (masking clinical signs of inflammation like BOP), impairs neutrophil chemotaxis and phagocytosis, suppresses IgG antibody production, and increases prevalence of Porphyromonas gingivalis and Tannerella forsythia.
- Diabetes Mellitus: Bidirectional relationship. Uncontrolled hyperglycaemia leads to accumulation of Advanced Glycation End-products (AGEs), which interact with RAGE receptors on monocytes and endothelial cells, hyper-amplifying pro-inflammatory cytokine release (IL-1β, TNF-α, IL-6) and accelerating alveolar bone resorption.
B. Drug-Induced Gingival Overgrowth (DIGO)
Three major pharmacological classes cause gingival enlargement, typically originating at the interdental papillae within 1 to 3 months of drug initiation:
- Anticonvulsants: Phenytoin (prevalence ~50%). Fibroblastic hyperplasia with dense collagen accumulation.
- Immunosuppressants: Cyclosporine (prevalence ~30%). Highly vascular enlargement; exacerbated by concomitant calcium channel blocker use.
- Calcium Channel Blockers (CCBs): Nifedipine, Amlodipine, Diltiazem, Verapamil (prevalence ~10-20%).
Management in Dental Practice: Rigorous professional and self-performed plaque control; surgical gingivectomy if functional/aesthetic impairment occurs; medical consultation with the patient's physician to consider drug substitution (e.g., swapping Nifedipine to an ACE inhibitor or Tacrolimus instead of Cyclosporine).
A 52-year-old non-smoker presents with interdental clinical attachment loss of 5 mm at multiple posterior sites, radiographic bone loss reaching the middle third of the root (40%), probing depths of 6-7 mm, and Class II furcation involvement on tooth 46. He has lost 2 molars due to periodontitis. His HbA1c is 6.2%. What is the correct 2018 periodontal staging and grading?
A 45-year-old female taking Nifedipine for hypertension presents with fibrous, lobulated gingival enlargement covering the coronal third of her anterior teeth. Probing reveals 5 mm pseudo-pockets without interdental clinical attachment loss or radiographic bone loss. What is the definitive diagnosis and primary initial management step?
During a routine examination of a 38-year-old patient, a WHO dentate probe is placed in the mesio-buccal pocket of tooth 16. The black band (3.5 mm to 5.5 mm) completely disappears into the pocket, and Bleeding on Probing is noted. What is the correct Basic Periodontal Examination (BPE) Code and required clinical follow-up?