Infections caused by anaerobic bacteria are common, and may be serious and life-threatening. Anaerobes predominant in the bacterial flora of normal human skin and mucous membranes, and are a common cause of bacterial infections of endogenous origin. Infections due to anaerobes can evolve all body systems and sites. The predominate ones include: abdominal, pelvic, respiratory, and skin and soft tissues infections. Because of their fastidious nature, they are difficult to isolate and are often overlooked. Failure to direct therapy against these organisms often leads to clinical failures. Their isolation requires appropriate methods of collection, transportation and cultivation of specimens. Treatment of anaerobic bacterial infection is complicated by the slow growth of these organisms, which makes diagnosis in the laboratory only possible after several days, by their often polymicrobial nature and by the growing resistance of anaerobic bacteria to antimicrobial agents.

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Wednesday, September 16, 2015

Alzheimer's disease and periodontists. Is there a connection?

Alzheimer's disease (AD) is a neurodegenerative disease which increases with age and is characterized by the salient inflammatory features, microglial activation, and increased levels of pro nflammatory cytokines which contribute to the inflammatory status of the central nervous system (CNS).Elevated blood inflammatory markers predict risk for dementia and incidence of cognitive impairment. Periodontitis is also considered to be one of the probable risk factors for AD.

Twomechanisms have been postulated to explain the association of periodontitis and AD. The first mechanism is due to the generation of a state of systemic/peripheral inflammation due to an increase in the levels of pro inflammatory cytokines, periodontopathic microorganisms and the host response cause. These pro inflammatory molecules are capable of compromising the blood brain barrier and enter the cerebral regions. This leads to priming/activation of microglial cells and the adverse repercussions leading to neuronal damage.

The second mechanism is thought to be due to direct invasion of brain by microorganisms present in the dental plaque biofilm. The brain is accessed either through the blood stream or via peripheral nerves. These microorganisms and their products elicit an inflammatory mechanism within the CNS resulting in cognitive impairment, such as that seen in AD. This inflammatory impairment is attributed to cytokine arbitrated interactions between neurons and glial cells.

The role of anti-inflammatory agents has been studied in the AD  Anti-inflammatory Prevention Trial  and hypothesized that the beneficial effect of anti-inflammatory drugs is evident only in the early, asymptomatic, phases of the disease.

Since periodontitis has a tendency to infiltrate the systemic circulation with inflammatory mediators and result in systemic disease outcome; thus, it would always be advisable and better option to prevent periodontal disease progression to prevent further systemic outcomes.

Inflammation could serve as a connecting link between periodontitis and AD. Further research including animal studies are warranted to explore the relationship between AD and periodontitis.

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