Periodontitis is the most advanced form of gum disease and can potentially have an impact on a systemic level, with a prevalence of 35.4% in adults between the ages of 35 and 44, and 38% in people between 35 and 74 years.
Gingivitis can remain stable for years; however, this may become a risk factor for periodontitis and tooth loss. In such cases, gingival inflammation spreads to the periodontal ligament, connective tissue and alveolar bone. The gingival epithelium migrates on root surfaces in a destructive process that causes the formation of subgingival pockets and bone and connective tissue resorption, and ultimately ends in tooth loss.
Several factors predispose patients to periodontitis and have a direct impact on disease progression:
- Bacterial plaque: biofilm is a key factor in the inflammation of periodontal tissues, although the transformation of gingivitis into periodontitis is governed greatly by individual risk factors. The main bacteria responsible for periodontitis belong to the red cluster (Porphyromonas gingivalis, Tannerella forsythia and Treponema denticola) and the orange cluster (Prevotella intermedia and Campylobacter rectus), causing moderate and severe periodontal disease, while the green cluster bacteria (streptococci) are less virulent.
- Aggregatibacter actinomycetemcomitans and Prevotella spp, as well as many other bacterial species, have also been detected in the subgingival pocket.
Age: ageing itself does not increase one’s susceptibility to periodontitis, but the cumulative effect of plaque and calculus deposits, as well as the greater number of spaces where these deposits can be held, and loss of bone and attachment, all explain the greater prevalence of this disease in older people.
- Smoking: smoking is a risk factor for chronic periodontitis, and it also reduces periodontal treatment response. The main signs and symptoms of periodontitis (gingival redness and bleeding on probing) are more difficult to detect in people who smoke.
- Systemic diseases: haematological defects, leukaemia, diabetes mellitus, certain medications and genetic traits may predispose individuals to developing periodontal disease.
- Stress: daily life tension and negative emotions regulate several physiological systems, including the endocrine and immune systems. Several studies link periodontitis to psychosocial variables that act as promoters of gingivitis expression. Even so, there are insufficient data to support the hypothesis relating psychosocial factors to the aetiology of chronic periodontitis.
- Genetics: Convincing evidence does not exist on periodontal disease susceptibility. Numerous studies have tried to identify the genes and polymorphisms involved in the different forms of periodontal disease.
This is known to be the most common form of periodontitis, characterised by pocket formation and/or gingival recession.
It is classified according to its extent, in number of sites affected:
- Localised: number of sites affected is less than or equal to 30%
- Generalised: number of sites affected is greater than 30%
It can also be classified according to severity:
- Mild: attachment loss 1-2mm
- Moderate: attachment loss 3-4mm
- Severe: attachment loss greater than or equal to 5mm
Aggressive periodontitis is characterised by rapid destruction of alveolar bone and attachment loss. It can be classified as follows:
Localised Aggressive Periodontitis: high prevalence in pubertal patients, affecting the first molars and incisors, with interproximal attachment loss in at least two permanent molars.
Generalised Aggressive Periodontitis: affects people under 30 years of age, with generalised attachment loss affecting at least three different permanent teeth.
Periodontitis associated with systemic diseases
Since 1999, periodontitis stemming from certain systemic diseases is considered as a separate category within periodontitis.
|Associated with haematological disorders||Associated with genetic disorders|
|Acquired neutropenia||Cyclic congenital neutropenia|
Leukocyte Adhesion Deficiency Syndrome
Papillon Lefevre Syndrome
Glycogen Storage Syndromes
Infantile Genetic Agranulocytosis
Ehlers-Danlos syndrome (types IV and VIII)