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Gum disease or periodontitis is a common oral disease and causes damage to supporting tissues of the teeth. There may be initial gingivitis or inflammation and infection of the gums that leads to inflammation of the marginal periodontium and finally periodontitis.
Not every gingivitis case, however, goes on to become periodontitis. The cause lies in the microorganisms and their virulence plays a role in the disease.
Periodontitis also plays an important role in causation of other problems such as heart disease, cerebrovascular disease, diabetes, respiratory disease and poor pregnancy outcome (miscarriage or preterm labour).
There have been studies that show an association with rheumatic diseases, especially rheumatoid arthritis (RA).
Long term plaque formation along with inflammation of the periodontium is among the most common oral diseases and occurs in 80 to 90% of the population. This leads to destruction of both the soft and hard periodontal tissue leading to loss of the tooth.
The virulence of the microbes causing the inflammation as well as the host immune system is responsible for the severity of the condition.
Tissue injury and weakened immunity leads to infection with the normally existing microorganisms in the mouth. Gram-negative anaerobic bacteria that form the bacterial plaque or biofilm over the tooth surface is said to initiate this tissue-destroying process.
There are over 20 species of bacteria that may cause periodontal disease. One of the most studied organisms is the Porphyromonas gingivalis.
The immune system has two phases of response to the inflammation. The initial immune response refers to the constant immunologic interaction between periodontal-pathogenic bacteria and the cells of the immune system. If the initial response is inadequate a more widespread immune response is stimulated.
RA is a chronic inflammatory joint disease that has similar pathogenic processes as those seen in periodontitis.
It has been reported that patients with longstanding active RA have a raised risk of developing periodontitis compared to healthy individuals. In addition, patients with periodontitis have a higher prevalence of RA than patients without the condition.
The hypothesis that oral infections may play a role in pathogenesis of RA is strengthened by the detection of bacterial DNA of anaerobes and high antibody titers against these bacteria in both the serum and the synovial fluid of RA patients in the early and later stages of the disease.
Furthermore P. gingivalis that causes periodontitis has the ability to destroy epithelium, invade human endothelium cells and affect protein synthesis. Thus they can cause wide spread damage and antibodies and the DNA of these bacteria are found in blood and synovial joint fluid in RA patients.
Rheumatoid factor may be positive in RA as well as periodontitis. RF may be found in the gingiva, in the subgingival plaque as well as in the blood of patients with periodontitis.