Effects Of Periodontal Disease On Arthrosclerosis

Each and every human mouth contains microorganisms, good and bad. It has been concluded that there are up to 1,000 variety of microorganisms residing in the oral cavity. Many of these bacteria are harmless to humans and are natural to the body. However, there are several that can cause decay and chronic infection in the oral cavity, which are also known as gram negative bacteria (Gehrig & Willmann, 2016). Biofilm, also known as plaque that forms on teeth, contains an organized matrix of microorganisms, which consists of these gram negative bacteria that can cause periodontitis. There are several types of biofilm in nature, but plaque in the oral cavity can be very destructive to a human’s periodontium and can place other organ systems at risk for harm. Bacteria reproduce very quickly and form huge colonies quickly as well (Gehrig & Willmann, 2016). It is important for women, who are pregnant or whom are trying to become pregnant, to have a thorough periodontal exam,

As individual’s age, one becomes more susceptible to several different types of ailments as the immune system becomes less able to fight infections. One of these ailments also includes periodontitis, which is inflammation of the gingival tissue caused by bacterial infection.

The pathogenesis of arthrosclerosis is a progressive disease of the vascular system, it starts while we are young and progresses throughout our lives. The progression of arthrosclerosis, starts with an injury to the endothelial lining of the arteries, from such diseases as, hypertension, high cholesterol, diabetes and smoking. The damage to the endothelial cells causes dysfunction and the area with endothelial cell inflammation draws leukocytes, cholesterol, vascular smooth muscle cells and other debris, the buildup creates atherosclerotic plaque deposits in areas on an artery wall causing an inflammatory process (Hoffman, 2007).

Apical periodontitis occurring after Root Canal Treatment presents a more complex etiologic & therapeutic situation than Primary Apical Periodontitis. There is a universal consensus that intra-radicular infection is an essential cause of primary as well as a major contributor of post treatment apical periodontitis. Enterococcus faecalis is the most commonly implicated microorganism in asymptomatic persistent infections1,2.

Nair in 1987 using light and electron microscopy examined 31 lesions, obtained by extraction of teeth with gross coronal caries and infected root canal system. He observed microstructure of inflammatory tissues and noticed the formation of layers

RESULTS: Out of the 10 cases, only 2 cases could be supported with a microbial evaluation. The remaining 8 cases were clinically and radiologically suggestive of Aggressive Periodontitis.

The purpose of this review is to assess the links between rheumatoid arthritis and periodontal disease. Past narrative reviews have identified relationships such as cytokine profiles and inflammatory mediators, supporting the association that inflammation may be central to rheumatoid arthritis and periodontal disease. Studies to date provided evidence that the pathological process in rheumatoid arthritis and periodontal disease are similar. However the relationship between the extent and severity is to be defined.

infection.(1–3) Students and clinicians need to understand that long-term clinical success of these teeth requires

(178) published a paper in the form of a clinical trial in order to examine the effect of periodontal treatment on the biological and clinical parameters of RA. Their proposed study was randomized controlled trial including participants with both RA and periodontitis. The investigators plan to involve a total of 40 individuals into two groups (intervention group including full-mouth SRP, followed by systemic antibiotics, amoxicillin or clindamycin, if allergic to penicillin, for seven days, oral hygiene instructions, and rinsing with 0.12 % chlorhexidine gluconate for 10 days after periodontal treatment). Patients will be followed for three months, and the same intervention will then be applied to the control group. The primary outcome of this study was a change in DAS28 score by decreasing RA activity. A major drawback of this study is the use of amoxicillin or clindamycin adjunctive to SRP. This antimicrobial approach should not be used as periodontal pathogens have been shown to be resistant to these

faecalis is the most dominant post-treatment microbe isolated in apical periodontitis and has often been isolated from the root canal in pure cultures. Prevalence of this bacterial infection ranges from 24% to 77% in asymptomatic persistent endodontic infections. E. faecalis are frequently isolated from obturated root canals of teeth that exhibit chronic periapical pathology. E.faecalis, intrinsically or via acquisition, may be resistant to a wide range of antibiotics which, if used may shift the micro biota in favor of E.faecalis.4 Over the past decade oral microbiota have shown resistance to some the commonly used antibiotics which in turn increases the need for monitoring susceptibility patterns periodically by using susceptibility tests and various efficacy

Based on our clinical findings and the patient’s complaint, I believe the patient has symptomatic apical periodontitis. The likely anatomical structures affected are the pulp of #31 (needing root canal therapy), the periodontium surrounding #31, possible involvement of the gingiva surrounding #30 (tooth directly anterior to #31). Depending on the path the infection has taken, it could have caused bone resorption and the infection could be cause nerve pain if allowed to progress. Infectious material courses through the path of least resistance, so it likely would have traveled from the apex of #31 into the surrounding gingiva, and up through the sulcus. The infection could also spread into the vestibule or floor of the mouth causing swelling

The periodontal diseases are highly prevalent and can affect up to 90% of the worldwide population. Gingivitis ,the mildest form of periodontal disease, is caused by the bacterial biofilm (dental plaque) that accumulates on teeth adjacent to the gingiva (gums). However, gingivitis does not affect the underlying supporting structures of the teeth and is reversible. Gingivitis, the mildest form of periodontal disease ,is highly prevalent and readily reversible by simple, effective oral hygiene. Gingivitis affects 50–90% of adults worldwide, depending on its precise definition3.

Periodontal disease is the infection and inflammation of tissues that support your teeth. Many adults have some sort of form of the disease. Periodontal disease can ange from gum inflammation to a serious disease that’s causes damage to the tissues and even bone that support the teeth and can cause teeth to be lost. Like cavities whatever is in our mouth turns into acid, and causes build up knowns as plaque. Plaque

Periodontitis is an inflammatory disease of the gums and supporting tissues of the teeth, resulting in attachment loss and bone resorption. The ethiopathogenesis of periodontitis is still somewhat unclear, but several different factors such

Periodontitis is recognised as chronic, low-grade, inflammatory and pathogenic infection, which continuously changes at a systemic level (Reddy, Phulambriker, Wanjari, Srivastava, 2012). Persistent inflammatory infection as a result of Gram-negative anaerobic bacteria lead to the destruction of bone and other tooth-supporting structures; an outcome of periodontitis is periodontal pockets (Usin et al., 2014). This fact enables bacteria and their by-products to spread to areas indirectly through the body’s immune-inflammatory response (Usin et al., 2014), thus creating potential damages to other systems and organs.