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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]
Odontogenic infections can be severe if not treated and are associated with mortality rate of 10 to 40%. [4] Furthermore, about 70% of odontogenic infections occur as periapical inflammation, i.e. acute periapical periodontitis or a periapical abscess. [3] The next most common form of odontogenic infection is the periodontal abscess. [3]
"Adult periodontitis" was reclassified "chronic periodontitis" and "early-onset periodontitis" to "aggressive periodontitis". [1] This article follows the 1999 classification, although the ICD-10 (10th revision of the International Statistical Classification of Diseases and Related Health Problems) differs significantly.
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.
ICD-9 chapters; Chapter Block Title I 001–139: Infectious and Parasitic Diseases II 140–239: Neoplasms III 240–279: Endocrine, Nutritional and Metabolic Diseases, and Immunity Disorders IV 280–289: Diseases of the Blood and Blood-forming Organs V 290–319: Mental Disorders VI 320–389: Diseases of the Nervous System and Sense Organs ...
If the tooth has pre-existing periodontal disease, with pockets and loss of alveolar bone height, it is more likely to be a periodontal abscess; whereas if the tooth has relatively healthy periodontal condition, it is more likely to be a periapical abscess. In periodontal abscesses, the swelling usually precedes the pain, and in periapical ...
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 ...
Diagnosis is important so that the treating doctor does not confuse it for another periapical disease such as rarefying osteitis or condensing osteitis. Incorrect diagnosis could lead to unnecessary root canal treatments , or biopsy or surgical intervention which can be invasive and increase the risk of infection. [ 5 ]