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Chronic periodontitis is initiated by Gram-negative tooth-associated microbial biofilms that elicit a host response, which results in bone and soft tissue destruction. In response to endotoxin derived from periodontal pathogens, several osteoclast-related mediators target the destruction of alveolar bone and supporting connective tissue such as the periodontal ligament.
Aggressive periodontitis is distinguished from the chronic form mainly by the faster rate of progression. Loss of attachment may progress despite good oral hygiene and in the absence of risk factors such as smoking. Aggressive periodontitis may occur in younger persons and there may a genetic aspect, with the trait sometimes running in families ...
[1] [2] At least 16 systemic diseases have been linked to periodontitis. These systemic diseases are associated with periodontal disease because they generally contribute to either a decreased host resistance to infections or dysfunction in the connective tissue of the gums , increasing patient susceptibility to inflammation-induced destruction.
To complete the diagnosis, the extent of the disease must be assessed. This is defined as: mild (1-2mm), moderate (3-4mm) or severe (≥ 5mm) depending on the amount of attachment loss present. Radiographs such as bitewings, intra-oral periapicals or a panoramic radiograph can be taken to help assess the bone loss and aid in diagnosis.
Periodontal disease, also known as gum disease, is a set of inflammatory conditions affecting the tissues surrounding the teeth. [5] In its early stage, called gingivitis , the gums become swollen and red and may bleed. [ 5 ]
Strictly speaking, Vincent's angina is not a necrotizing periodontal disease. However, Vincent's angina is widely confused with necrotizing gingivitis (previously also called "Vincent's gingivitis"). Vincent's angina is tonsillitis and pharyngitis, [3] and does not typically involve the gums. Many publications using the term "Vincent's angina ...
Porphyromonas gingivalis is a Gram-negative anaerobe associated with the pathogenicity of periodontal disease, [10] and aggressive periodontitis is no exception. Greater numbers of both Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans were found in active, destructive periodontal lesions in comparison to non-active sites.
Periapical periodontitis of some form is a very common condition. The prevalence of periapical periodontitis is generally reported to vary according to age group, e.g. 33% in those aged 20–30, 40% in 30- to 40-year-olds, 48% in 40- to 50-year-olds, 57% in 50- to 60-year-olds and 62% in those over the age of 60. [13]
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