What is periodontitis, and how does it differ from gingivitis?
Periodontitis is a chronic infectious disease of the periodontium—the tissues that support the teeth (gums, periodontal ligament, alveolar bone, and root cementum). Unlike gingivitis (a reversible inflammation limited to the gums), periodontitis involves the progressive and irreversible destruction of the alveolar bone and periodontal ligament. The teeth remain stable for a long time, but once the bone is destroyed, it does not regenerate on its own. All cases of periodontitis require monitoring by a dental health professional—a dentist or periodontist—to halt its progression.Oral hygiene care products and suitable dental floss are available in the store.
- Mechanism of destruction: anaerobic bacteria in periodontal pockets (Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola—the “red complex”) trigger an excessive immune response—pro-inflammatory cytokines (IL-1β, TNF-α, PGE₂) activate osteoclasts → bone resorption—it is the host’s immune system, rather than the bacteria themselves, that destroys the bone
- 2017 International Classification: Grade A (slow progression, few risk factors) — Grade B (moderate progression) — Grade C (rapid progression, major risk factors—smoking, diabetes) — Stages I through IV based on the severity of bone loss and treatment complexity
- Clinical signs: bleeding on probing (early sign—see the page on bleeding gums) — periodontal pockets > 4 mm — gingival recession (gums “pulling back”) — progressive tooth mobility — diastemas (spaces between teeth widening) — persistent bad breath
- Prevalence: Severe periodontitis affects 10–15% of adults — moderate periodontitis affects approximately 50% of adults over 30 years of age — it is the leading cause of tooth loss after age 40 in developed countries
What are the risk factors and links to overall health?
- Tobacco — a major risk factor: increases the risk of severe periodontitis by 3 to 7 times — masks gum bleeding (vasoconstriction = false sign of health) — reduces the effectiveness of periodontal treatment — periodontitis in smokers progresses more rapidly and responds less well to scaling and root planing — quitting smoking significantly improves the prognosis
- Diabetes — bidirectional relationship: poorly controlled diabetes increases the risk of severe periodontitis threefold (glycation of tissue proteins, local immunosuppression) — periodontitis, in turn, increases insulin resistance and impairs glycemic control — treating periodontitis can lower HbA1c by 0.3 to 0.5% — a link recognized by the International Diabetes Federation
- Cardiovascular links: periodontal bacteria (particularly P. gingivalis) can enter the bloodstream and contribute to atherosclerosis — epidemiological studies linking periodontitis to an increased risk of myocardial infarction, stroke, and heart failure—mechanism: chronic systemic inflammation + transient bacteremia during chewing
- Other associations: pregnancy (periodontitis associated with preterm birth and low birth weight—screening recommended)—respiratory diseases (aspiration of oral bacteria → bacterial pneumonia in frail individuals) — rheumatoid arthritis (P. gingivalis produces enzymes that citrullinate proteins — common antigen)
How is periodontitis diagnosed and treated?
- Diagnosis: periodontal probing (measuring pocket depth with a graduated probe around each tooth—depth, bleeding, pus) — panoramic and periapical X-rays (bone level, affected furcations) — plaque and bleeding index — comprehensive periodontal evaluation = essential first step before any treatment
- Etiological treatment (phase 1) — scaling and root planing (SRP): mechanical removal of subgingival calculus and pathogenic biofilm adhering to the root — sonic or ultrasonic instrument + curettes — under local anesthesia (quadrant by quadrant) — standard procedure recognized by the HAS — maximum effectiveness if followed by a phase of regular maintenance
- Periodontal surgery (Phase 2 if necessary): access flap (surgical access to the roots for deep, inaccessible root planing) — guided bone regeneration (GBR — membranes + bone substitutes) — gingival grafts (to cover recessions) — indicated in cases of DSR failure or very deep pockets (> 6 mm) — performed by a periodontist
- Maintenance phase: long-term success depends on follow-up — professional checkups every 3–6 months — assessment of residual pockets and re-instrumentation if necessary — without regular maintenance, periodontitis recurs in 70–80% of cases within 5 years — daily oral hygiene using a toothbrush and interdental brushes is essential
What can be done on a daily basis to slow the progression of periodontitis?
- Rigorous daily plaque control: brush twice a day (soft-bristled toothbrush — modified Bass technique to reach the gingival sulcus) — appropriately sized interdental brushes (larger than dental floss for periodontally compromised spaces) — tongue scraper (reduces bacterial load) — without daily care, any professional periodontal treatment is futile
- Chlorhexidine mouthwashes: the gold standard antibacterial agent (0.12–0.2%) — limited-time use (2–4 weeks) as an adjunct to active treatment — maintenance possible with milder formulations (0.06%) or stannous fluoride — avoid chronic use (staining + dysgeusia)
- Smoking cessation: improves response to treatment within the first few weeks — gradually normalizes gingival blood flow — is an integral part of the periodontal treatment plan according to HAS recommendations
- Diabetes control: in patients with diabetes, glycemic control (HbA1c < 7%) improves response to periodontal treatment—and vice versa—coordination between the dentist and the patient’s primary care physician is recommended in cases of diabetes and periodontitis—in cases of periodontal abscess, immediate consultation is essential
