Gum disease, explained

What gum disease actually is

Gum disease is not "having sensitive gums". It is a chronic infection. Bacteria that accumulate at the gum line form a biofilm called plaque. Plaque that is not removed daily hardens into calculus (tartar) — a calcified deposit that brushing cannot dislodge. Once calculus forms below the gum line, the body's immune response to it begins to destroy the tissue around the tooth.

There are two stages:

Gingivitis — the gums are inflamed. They are puffy, may bleed when brushed, and have changed colour from coral pink to dusky red. No permanent damage has been done. A thorough cleaning and a daily oral hygiene routine reverses it.

Periodontitis — the inflammation has spread below the gum line. The body's response has begun to destroy the periodontal ligament (the fibres that hold the tooth to the bone) and the alveolar bone itself. Pockets form between the tooth and the gum. The teeth, eventually, become loose.

Periodontitis is not reversible. The bone that has been lost does not regrow on its own. It is, however, very treatable — meaning the disease can be stopped, the tissue around the tooth stabilised, and the tooth kept in service. With good ongoing maintenance, a tooth diagnosed with moderate periodontitis can comfortably last another two decades.

How common is it

Periodontitis is one of the most common chronic conditions of adulthood. Large epidemiological studies consistently report that:

• In the United States adult population, periodontitis (in any stage) was found in around 42% of adults aged 30 and over in the NHANES 2009–2014 surveys, with severe periodontitis in 7.8%.⁴
• A 2020 Global Burden of Disease analysis identified severe periodontitis as the sixth most prevalent disease globally.⁵
• Worldwide, periodontitis and dental caries are established as the two leading causes of tooth loss in adults (Frencken et al., 2017).⁶

We have not yet published a South African epidemiological figure here because population data for SA is fragmented; we will add a SA-specific figure when an authoritative source is available. In our own Pretoria practice, gum-disease referrals are routinely among the most common reasons general dentists send patients to a specialist.

What causes it

Plaque bacteria are the proximate cause. But why some patients develop severe periodontitis and others do not, despite similar oral hygiene, has been the subject of half a century of research. The strongest contributors:

• Genetics — family history of tooth loss to gum disease is a significant predictor.
• Smoking — smoking is one of the strongest established risk factors for periodontitis. Tomar and Asma's analysis of US national data found that nearly half of periodontitis cases were attributable to current or former smoking, with current smokers approximately four times more likely than non-smokers to have periodontitis.⁷ Treatment outcomes in smokers are measurably less favourable.
• Diabetes — uncontrolled diabetes both increases the risk of periodontitis and is worsened by it (the relationship is bidirectional).
• Stress and immune suppression — periods of high cortisol or impaired immunity correlate with periodontal flares.
• Hormonal changes — pregnancy, menopause, and oral contraceptive use can amplify gingival response.
• Poor oral hygiene — necessary but not sufficient. Many patients with exemplary brushing still develop disease because of one or more of the factors above.

How a specialist diagnoses it

Periodontal diagnosis is not a matter of looking at the teeth. It requires:

1. Pocket charting — measuring, with a calibrated probe, the depth of the gum sulcus at six points around every tooth. Pockets deeper than 4 mm are abnormal.
2. Bleeding indices — recording at how many sites the gum bleeds on probing. Bleeding is the most sensitive early sign of active disease.
3. Recession measurement — recording how far the gum has receded from its original position.
4. Mobility assessment — testing each tooth for looseness.
5. Furcation involvement — checking whether disease has tracked between the roots of multi-rooted teeth.
6. Radiographs — periapical x-rays and a panoramic view to see bone levels around the roots.

A periodontist will then assign a stage (I to IV, based on the severity of damage) and a grade (A to C, based on the rate of progression). This staging-and-grading framework was formalised in 2018 by the AAP/EFP World Workshop and is now the international standard.

How it is treated

Treatment for gum disease has four sequential phases:

Phase 1 — Cause control

The foundation. This is what most patients think of as "deep cleaning":

• Non-surgical periodontal therapy (also called scaling and root planing) is staged in two steps. First the oral hygienist removes the tartar and bacteria above the gums and tailors an oral hygiene regime specifically for your mouth. The specialist then cleans below the gum line, using ultrasonic and hand instruments, under local anaesthetic (intraoral injections) — usually one quadrant at a time, across 2–4 visits.²
• Oral hygiene instruction — interdental brushing technique, electric toothbrush technique, sometimes specific aids for the patient's anatomy.
• Smoking cessation support for smokers.
• Liaison with the GP for diabetic patients to optimise glycaemic control.

Many patients with moderate periodontitis respond well enough to Phase 1 alone that they progress directly to maintenance without surgery. The EFP S3 clinical practice guideline summarises the evidence on this step and the criteria for re-evaluation.² After approximately 6 to 8 weeks, the periodontist re-charts the pockets to decide whether surgical phases are needed.

Phase 2 — Surgical treatment

For sites where pockets remain deep after Phase 1, or where bone architecture is so altered that the patient cannot clean effectively, surgery is indicated:

• Open-flap debridement — the gum is reflected back to give direct access to clean the root surfaces and reshape the bone.
• Regenerative surgery — using collagen membranes, bone grafts, enamel matrix derivative (Emdogain), or growth factors to regenerate lost bone in well-defined defects. The collagen membrane is the key component: it keeps the soft tissue out of the defect so bone can fill it.
• Resective surgery — reshaping the bone to a contour the patient can maintain.

Phase 3 — Restorative integration

Once the gums are stable, missing teeth can be replaced (implants, bridges) and damaged teeth can be restored. This is the phase in which we coordinate closely with your general dentist.

Phase 4 — Periodontal maintenance

The phase nobody likes to hear about but every patient with a history of periodontitis needs. Every 3 to 4 months, a periodontal hygienist removes the early calculus that has reformed and updates the pocket chart. Long-term observational research is unusually strong on the value of this step: Axelsson and colleagues' 30-year follow-up of a well-motivated Swedish cohort showed very high tooth retention and stable periodontal health in patients who attended regular maintenance, in contrast to substantial attachment and tooth loss in patients who did not.⁸ The cohort was not representative of all patient populations, but the direction of effect — that compliance with maintenance is decisive for the long-term outcome — is consistent across other studies.

What it costs

See the detailed L3 page on gum-disease treatment costs in South Africa for current ranges. Treatment is sequenced (initial therapy, possible surgical phase, then maintenance), and an itemised estimate is provided in writing after the first consultation so each phase is costed separately. Practice fees are reviewed annually and are current at the date stated on the estimate, not at the date this page was last reviewed.

Gum disease and the rest of your health

This is the area of periodontology that has expanded most over the last two decades. Bacteria from inflamed periodontal pockets can enter the bloodstream through the ulcerated pocket lining during everyday activities such as chewing and brushing, and the resulting low-grade systemic inflammation is the leading hypothesis for the associations described below.

Current expert consensus reports describe the following associations:

• Cardiovascular disease — the EFP/World Heart Federation 2020 consensus identified periodontitis as a modifiable risk factor for atherosclerotic cardiovascular disease, although a causal relationship has not been proven.³
• Type 2 diabetes — a two-way relationship: poorly controlled diabetes worsens periodontitis, and severe periodontitis is associated with worse glycaemic control.
• Adverse pregnancy outcomes — the evidence here is more contested; some studies show an association with pre-term birth and low birth weight, but treatment trials have not consistently improved outcomes.
• Rheumatoid arthritis — shared inflammatory pathways are biologically plausible and the association is observed, but causality is not established.

In short: the associations are real and reflected in the published literature, but "associated with" does not mean "causes". The pragmatic point for patients is that treating periodontitis is unlikely to harm general health and may help — particularly for diabetic patients in whom periodontal treatment is associated with modest improvement in glycaemic control.

The dedicated L3 page on whether gum disease affects overall health goes through the evidence study by study.