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During this time, the signs and symptoms of periodontal diseases were firmly established. [15] Rather than a single disease entity, periodontal disease is a combination of multiple disease processes that share a common clinical manifestation. The cause includes both local and systemic factors.
The inflammation pathway of periodontitis is such that as the infection grows, bacteria, including P. gingivalis are targeted by neutrophils and natural killer immune cells. These cells phagocytize the bacteria, while simultaneously cytokine molecules in the area lead to a proinflammatory
Periodontitis is very common, and is widely regarded as the second most common dental disease worldwide, after dental decay, and in the United States has a prevalence of 30–50% of the population, but only about 10% have severe forms. Chronic periodontitis affects about 750 million people or about 10.8% of the world population as of 2010. [86]
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.
Gingivitis is a non-destructive disease that causes inflammation of the gums; [1] ulitis is an alternative term. [2] The most common form of gingivitis, and the most common form of periodontal disease overall, is in response to bacterial biofilms (also called plaque) that are attached to tooth surfaces, termed plaque-induced gingivitis.
S. mutans is naturally present in the human oral microbiota, along with at least 25 other species of oral streptococci. The taxonomy of these bacteria remains tentative. [ 6 ] Different areas of the oral cavity present different ecological niches, and each species has specific properties for colonizing different oral sites.
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 ...
Periodontal pathogens are bacteria that have been shown to significantly contribute to periodontitis. Dental plaque, the precursor of periodontal disease, is a complex biofilm consisting mainly of bacteria, but also archaea, protozoa, fungi and viruses. Viruses that specifically infect bacteria—bacteriophages—are most common in the oral ...
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