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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]
Consequently, a new classification was developed at the International Workshop for a Classification of Periodontal Diseases and Conditions in 1999. This covered in much more detail the full range of periodontal diseases. "Adult periodontitis" was reclassified "chronic periodontitis" and "early-onset periodontitis" to "aggressive periodontitis". [1]
Periodontal abscesses may be difficult to distinguish from periapical abscesses. Since the management of a periodontal abscess is different from a periapical abscess, this differentiation is important to make (see Dental abscess#Diagnostic approach) For example, root canal therapy is unnecessary and has no impact on pain in a periodontal abscess.
Periodontal disease is the most common disease found in dogs and affects more than 80% of dogs aged three years or older. Its prevalence in dogs increases with age, but decreases with increasing body weight; i.e., toy and miniature breeds are more severely affected.
In 1890, W.D. Miller, considered the father of oral microbiology, was the first to associate pulpal disease with the presence of bacteria. [11] This was confirmed by Kakehashi, who, in 1965, proved that bacteria were the cause of pulpal and periradicular disease in studies using animal models; pulpal exposures were initiated in both normal and germ-free rats, and while no pathologic changes ...
Irreversible pulpitis progresses to pulp necrosis, wherein the nerves are non-functional, and a pain-free period following the severe pain of irreversible pulpitis may be experienced. However, it is common for irreversible pulpitis to progress to apical periodontitis, including an acute apical abscess, without treatment.
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.
Other symptoms may include hypoesthesia, paresthesia, and discomfort. [3] In rare instances, patients may experience associated facial swelling with the presence or absence of pain due to concurrent infection. [4] Patients experiencing symptoms also tend to be older and have the periapical form of cemento-osseous dysplasia. [3]