Periodontitis: Causes

Pathogenesis (development of disease)

Periodontitis is a disease with multiple causes, which include plaque with its resident bacteria (Agregatibacter actinomycetemcomitans – facultatively anaerobic, common in aggressive periodontitis; Porphyromonas gingivalis – strictly anaerobic, in aggressive and advanced periodontitis; Prevotella intermedia – strictly anaerobic, in large numbers in aggressive periodontitis) count and the associated defense reactions as well as incorrect stresses on the periodontium and the time available to the bacteria living in the plaque, during which periodontal destruction can develop. Other marker germs in periodontitis are: Tanerella forsythesis and Treponema denticola. Periodontitis usually results from untreated gingivitis (inflammation of the gums). As the inflammation progresses, the body’s defense mechanisms against the subgingival bacteria (bacteria that accumulate under the gums) break down over time. We can now clearly speak of subgingival plaque flora. Pocket formation and pathological changes in the root cementum occur as a result of the bacterial infestation. Factors that favor plaque formation include:

  • Mouth breathing – leads to gingivitis in the anterior region, probably as a result of decreased wetting with saliva and consequent drying of the gingiva.
  • Salivary flow – protective mechanism of saliva is impaired when saliva is too viscous or salivary flow is too low.
  • Tartar – plaque can adhere better to the rough surface.
  • Tooth anatomy – enamel beads, enamel tongues, retractions of the crown (“palatal groove”).
  • Tooth gap – provides settlement opportunities for the plaque, which are difficult to clean.
  • Restorative margins – provide niches for the accumulation of bacteria.
  • Caries – bacterial reservoir from which pathogenic plaque can quickly develop again.
  • Orthodontic appliances – complicate cleaning.
  • Diet – the more chewable and fibrous the food, the more likely it is to have a mechanical cleaning effect, food that gets stuck in spaces favors plaque

In systemic diseases such as diabetes mellitus, serum levels of inflammatory molecules (e.g., C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), and interleukin-6 (Il-6)) in plasma are elevated in periodontitis. Thus, a (subclinical) chronic systemic inflammatory state is present. The amoeba Entamoeba gingivalis (E. gingivalis), a common oral unicellular parasite, is involved in tissue destruction and severe inflammatory response in severe periodontitis. While the bacterial diversity of the oral cavity is decreasing, the frequency of Entamoeba gingivali is increasing. Inflamed gingival pockets showed amoebae in about 80 percent of patients, but were detectable in only 15 percent of healthy subjects. Periodontal disease is primarily caused by a pathogenic microbial biofilm and chronic inflammation.

Etiology (Causes)

Biographic causes

  • Genetic Bealstung
    • Genetic risk is dependent on genetic variants that also increase the risk of atherosclerosis (arteriosclerosis, hardening of the arteries) (ANRIL, PLG, VAMP3/CAMTA1) or are related to cholesterol and glucose metabolism ( ANRIL, VAMP3/CAMTA1, NPY)
    • Genetic diseases
      • Chediak-Higashi syndrome (CHS) – metabolic disease with poor prognosis; destructive periodontitis, cause lysomal defects, especially in neutrophils (granulocytes are a subset of white blood cells (leukocytes)) and chemotaxis (release or formation of chemokines (messenger substances) induced attraction of cells of the immune system).
      • Cohen syndrome (synonyms: English : Pepper syndrome or Cervenka syndrome) – rare disease due to a mutation; extensive alveolar bone loss.
      • Ehlers-Danlos syndrome (EDS) – connective tissue disease, genetic; impaired collagen synthesis, increased susceptibility to periodontitis.
      • Glycogen storage syndrome – autosomal recessive inherited diseases of glycogen degradation or glycogen synthesis with pathologically increased glycogen storage in many organs; decreased numbers and impaired function of neutrophil leukocytes, thereby increased occurrence of periodontitis.
      • Haim-Munk syndrome (HMS) – autosomal recessive inherited syndrome described only in a Jewish population in India. Symptoms: palmoplantar hyperkeratosis and aggressive course periodontitis.
      • Histiocytosis syndrome (synonym: eosinophilic granuloma) – Langerhans cell histiocytosis (LCH) is a generic term for reactive-proliferative disorders with proliferation of histiocytes (tissue macrophage) of the Langerhans cell phenotype; lesions clinically resembling necrotizing, ulcerative periodontitis
      • Hypophosphatasia (HPP; synonyms: Rathbun syndrome, phosphatase deficiency rickets; phosphatase deficiency rickets) – rare, autosomal recessive inherited, inborn error of metabolism with decreased alkaline phosphatase activity; disturbances of skeletal structure as well as other body functions, such as digestion and nerve function; typical is premature loss of both primary teeth and second dentition (tooth eruption from the jaw into the oral cavity); almost complete absence of cementum formation leads to rapid periodontal collapse
      • Infantile genetic agranulocytosis – genetic deficiency of leukocytes; associated with severe aggressive periodontitis.
      • Leukocyte Adhesion Deficiency Syndrome (LADS) – a rare congenital, autosomal recessive inherited defect of the adhesion cascade; patients suffer from various bacterial infections, such as recurrent skin infections, otitis media (middle ear infection), septicemia (blood poisoning), delayed wound healing, and very aggressive periodontitis
      • Papillon-Lefèvre syndrome (PLS) – rare, autosomal recessive hereditary palmoplantar keratosis with prepubertal periodontitis, associated with neutrophil defects.
      • Trisomy 21 (Down syndrome; mode of inheritance: mostly sporadic) – special genomic mutation in humans in which the entire 21st chromosome or parts of it are present in triplicate (trisomy). In addition to physical features considered typical for this syndrome, the cognitive abilities of the affected person are usually impaired; about half of those affected develop a cataract; severe destructive periodontitis in young adults, is probably based on deficient neutrophil function.

Behavioral causes

  • Nutrition
    • Malnutrition – low energy and low protein (low protein) diet.
    • Micronutrient deficiency (vital substances) – see prevention with micronutrients.
  • Consumption of stimulants
  • Drug use
  • Psycho-social situation
    • Emotional stress
  • Inadequate oral hygiene
  • Overweight (BMI ≥ 25; obesity)

Disease-related causes

  • Bacterial infection of the oral cavity such as gingivitis.
  • Diabetes mellitus – increased periodontal breakdown and periodontal abscesses, possibly due to deficient neutrophil function
  • Leukemia (blood cancer) – severe destructive periodontitis associated with neutropenia.
  • HIV infection – severe destructive periodontitis.
  • Bekhterev’s disease (synonym: ankylosing spondylitis) – chronic inflammatory disease of the spine, which can lead to joint stiffness (ankylosis) of the affected joints (about 7 times the risk of periodontitis).
  • Crohn’s disease – chronic inflammatory bowel disease; it usually runs in relapses and can affect the entire digestive tract; characteristic is the segmental affection of the intestinal mucosa, that is, it may affect several intestinal sections that are separated by healthy sections of each other; mild to moderate course of periodontitis (possibly due tohigh prevalence of periodontitis-associated anaerobes, especially of the genus Campylobacter)
  • Neutropenia (→ increased susceptibility to infection) – associated with ulceration, necrosis, hemorrhage, deep pockets and bone resorption.
  • Osteoporosis (bone loss)
  • Rheumatoid arthritis – chronic inflammatory multisystem disease that usually manifests itself in the form of synovitis (inflammation of the synovial membrane).It predominantly affects the joints (polyarthritis, i.e. arthritis of ≥ 5 joints), more rarely other organs such as eyes and skin.

Laboratory diagnoses – laboratory parameters that are considered independent risk factors.

  • C-reactive protein (CRP)

Medication

Environmental exposure – intoxications (poisonings).

  • Heavy metal poisoning (including, lead).

Other causes

  • Pregnancy