Созылмалы периодонтит
Prevalence: Affects ~46% of adults over 30; severe form in ~8–9% of the global population
Overview
Тістің тіреуіш аппаратының прогрессивті қайтымсыз бұзылуы
Etiology and Risk Factors
Chronic periodontitis is initiated by subgingival dental biofilm (plaque dysbiosis) but its extent and severity are modulated by the host immune-inflammatory response, genetic susceptibility, and systemic risk factors.
KEY PATHOGENS — the 'red complex' (Socransky 1998): Porphyromonas gingivalis (key virulence: gingipains, LPS, fimbriae — subverts complement via C3 cleavage, classified as a 'keystone pathogen'), Treponema denticola (motile spirochete, dentilisin protease), Tannerella forsythia (BspA surface protein). The orange complex (Fusobacterium nucleatum, Prevotella intermedia) bridges early colonisers to red complex.
SYSTEMIC RISK FACTORS: Diabetes mellitus (HbA1c >7% correlates with 3× more severe periodontitis — bidirectional relationship); smoking (nicotine impairs neutrophil function, reduces gingival blood flow masking BOP — a critical diagnostic pitfall); stress (elevated cortisol → immunosuppression); genetic polymorphisms (IL-1α/β positive genotype = 2–4× more severe disease).
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Pathogenesis
Pathogenic cascade: subgingival biofilm dysbiosis → innate immune activation (complement, TLRs on sulcular epithelium) → pro-inflammatory cytokines (IL-1β, TNF-α, IL-6, IL-17) → matrix metalloproteinases (MMP-8, MMP-13) and RANKL/OPG imbalance → collagen degradation → osteoclast activation → alveolar bone resorption.
Classification
Stage I
Initial periodontitis
Stage II
Moderate periodontitis
Clinical Manifestations
CLASSIC SIGNS: Bleeding on probing (BOP); increased probing depths (>3mm pathological); clinical attachment loss (CAL = distance from CEJ to pocket base); alveolar bone loss on radiographs; gingival recession.
Diagnosis
Full-mouth periodontal charting at 6 sites per tooth: probing depth, BOP, CAL, recession, furcation, mobility. Establishes disease severity map.
Treatment Protocol
Phase 1 — Cause-Related Therapy
Non-surgical periodontal therapy
Prognosis
With comprehensive treatment and SPT, Stage I–II: ~0.06–0.1 teeth lost/year. Stage III–IV: 0.3–0.5 teeth/year. Untreated: 1–3 teeth/year. Regular SPT reduces tooth loss by 90% vs. no maintenance.
Prevention
- Daily interproximal cleaning (floss or interdental brushes)
- Twice-daily toothbrushing with modified Bass technique
Interactive Quiz
Test your understanding of Созылмалы периодонтит.
Q1.
3D Pathology Description
3D mandibular molar with advanced chronic periodontitis: angular alveolar bone defect on mesial surface (cross-section showing infrabony defect); Class II furcation involvement on buccal aspect (probe penetrating >3mm through furcation); subgingival calculus deposits (dark mineralised) on root surface; deepened pocket (7mm); intact vs degraded PDL fibres (some absent in destroyed zones); junctional epithelium migrated 5mm apically from CEJ; osteoclasts at alveolar bone margin; root surface biofilm layer. Colour coding: red inflamed gingiva, brown calculus, orange bone loss zone, blue intact PDL, yellow migrated junctional epithelium.