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Periodontal disease and systemic conditions: a bidirectional relationship

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Federal government websites often end in. The site is secure. For decades, physicians and dentists have paid close attention to their own respective fields, specializing in medicine pertaining to the body and the oral cavity, respectively. However, recent findings have strongly suggested that oral health may be indicative of systemic health. Currently, this gap between allopathic medicine and dental medicine is quickly closing, due to significant findings supporting the association between periodontal disease and systemic conditions such as cardiovascular disease, type 2 diabetes mellitus, adverse pregnancy outcomes, and osteoporosis.

Significant effort has brought numerous advances in revealing the etiological and pathological links between this chronic inflammatory dental disease and these other conditions.

Therefore, there is reason to hope that the strong evidence from these studies may guide researchers towards greatly improved treatment of periodontal infection that would also ameliorate these systemic illnesses.

Hence, researchers must continue not only to uncover more information about the correlations between periodontal and systemic diseases but also to focus on positive associations that may result from treating periodontal disease as a means of ameliorating systemic diseases. Periodontal disease refers to the inflammatory processes that occur in the tissues surrounding the teeth in response to bacterial accumulations, or dental plaque, on the teeth.

The bacterial accumulations cause an inflammatory response from the body. The chronic and progressive bacterial infection of the gums leads to alveolar bone destruction and loss of tissue attachment to the teeth.

Periodontal disease has many states or stages, ranging from easily treatable gingivitis to irreversible severe periodontitis. Periodontal disease is increased by several risk factors: cigarette smoking; systemic diseases; medications such as steroids, anti-epilepsy drugs and cancer therapy drugs; ill-fitting bridges; crooked teeth and loose fillings; pregnancy; and oral contraceptive use.

In addition to these variables, any medical condition that triggers host antibacterial defense mechanisms, such as human immunodeficiency virus HIV infection, diabetes, and neutrophil disorders, will likely promote periodontal disease. The most prevalent form of periodontal disease is a mild form called gingivitis.

In diagnosing the extent of periodontal disease, the probing depth is a good indicator of the advance of the disease. In a healthy periodontium, there is no loss of epithelial attachment or pocket formation, and the periodontal pocket is less than 2 mm deep. Clinically, patients with periodontal pockets of 4 mm or more are diagnosed with periodontitis.

Patients with periodontal pockets of 6 mm or more are diagnosed with advanced or severe periodontitis. Left untreated, gingivitis may progress to irreversible periodontitis, resulting in tooth loss. Once diagnosed, most periodontal diseases can be treated successfully. The therapeutic goals in periodontal disease are: first, to alter or eliminate the origin of the microbes as well as contributing risk factors, thereby preventing the progression of the disease and preserving the healthy state of the periodontium.

Second, the recurrence of periodontitis must be prevented. Finally, in severe cases, regeneration of the periodontal attachments must be attempted. Supplemental treatment may include an antiseptic mouth rinse and medication, either to aid the healing process or to further control the bacterial infection.

Often, antibiotics may be administered, which may offer an effective alternative to scaling and root planing. Tetracycline or a combination of amoxicillin and metronidazole may be used in order to kill a broad range of bacteria.

Another drawback to antibiotic therapy lies in the difficulty of identifying and targetting a specific pathogen, due to the numerous species residing in the plaque. Surgical treatment along with antibiotic therapy may therefore be beneficial to periodontal disease patients.

If the periodontal pockets are not reduced, or if further loss of alveolar bone is observed, then surgical intervention is clearly needed to try to prevent tooth loss. Surgical treatment of periodontal disease by a periodontist consists of removing inflamed tissues to reduce the damage to the alveolar bone around the area of infection.

Furthermore, surgery allows dentists to access areas where scaling and root planing cannot remove tartar and plaque. The elimination of bacterial accumulations helps regenerate bone and tissue, to help reduce pockets.

Additional procedures, such as bone grafts, target bone regeneration and growth. If the periodontal disease has caused excessive loss of gum tissue, then soft-tissue grafts may be performed to reduce further gum recession and bone loss. The oral cavity is an open system exposed to the environment. Furthermore, the possibilities of foreign material entering the system from the oral cavity are heightened due to the constant intake of food and liquids through the mouth.

The presence of the large numbers of bacteria can induce tissue destruction indirectly by activating host defense cells, which in turn, produce and release mediators that stimulate the effectors of connective tissue breakdown. Components of microbial plaque have the capacity to induce an initial infiltrate of inflammatory cells, including lymphocytes, macrophages, and polymorphonuclear leukocytes PMNs.

Microbial components, especially lipopolysaccharide LPS , activate macrophages to synthesize and secrete a variety of proinflammatory molecules, including the cytokines interleukin-1 IL-1 and tumor necrosis factor-alpha TNF-alpha ; prostaglandins, especially prostaglandin E 2 PGE 2 ; and hydrolytic enzymes.

These cytokines manifest potent proinflammatory and catabolic activities, and play key roles in periodontal tissue breakdown through collagenolytic enzymes such as metalloproteinases MMPs.

This provides a microbial niche, such that periodontal pockets with depths of 4 to 12 mm can harbor on the order of 10 7 to 10 9 bacterial cells. Several amplification and suppression mechanisms are also involved in the process. The progression and extent of tissue degradation is determined in large part by the relative concentrations and halflives of IL-1, TNF-alpha, and related cytokines, of competing molecules such as the IL-1 receptor antagonist, and of suppressive molecules such as transforming growth factor TGF -beta and PGE 2.

Another effective host defense mechanism is the highly vascularized nature of the gingival tissue, presenting an oxidative barrier to the penetration of anaerobic bacteria from dental plaque. This provides the anaerobes ample time to survive in the tissues and to activate latent collagenases.

The selection for anaerobes rather than for more harmful facultative species may actually be beneficial to the host, because facultative species, if dominant, have even worse effects, causing tissue invasion and necrosis. In the past three decades, marked advances have occurred in our understanding of the infectious agents of periodontal disease. Approximately different bacterial entities and various human viruses are associated with dental microbial plaque. Socransky et al.

This complex is strongly related to pocket depth and bleeding on probing. Within the past 10 years, many studies have been published indicating a positive or negative relationship between periodontal disease and various systemic disorders and diseases.

Depending on the outcome of the studies, a positive correlation reflects a strong case for the relationship as opposed to a negative or no correlation.

Significant associations between periodontal disease and cardiovascular disease, diabetes mellitus, preterm low birth weight, and osteoporosis have been discovered, bridging the once-wide gap between medicine and dentistry.

Researchers have hypothesized the etiologic role of periodontitis in the pathogenesis of these systemic illnesses. Therefore, patients diagnosed with periodontal disease may be at higher risk due to a compromised immune system. Infectious and opportunistic microbes responsible for periodontal infection may thus bring a burden onto the rest of the body.

Furthermore, these microbes can release products that elicit an inflammatory response. Periodontal lesions are recognized as continually renewing reservoirs for the systemic spread of bacterial antigens, Gram-negative bacteria, cytokines, and other proinflammatory mediators.

The same study showed a statistically significant correlation between coronary artery disease and periodontitis. Periodontal disease may be associated with CVD due to mutual risk factors for atherogenesis and periodontal disease.

In order to consider periodontal disease as a risk factor for atherosclerosis and other CVDs, the presence of pathogens associated with periodontal infection should be localized in serum or atheromatous plaques. In addition to carotid, coronary, and aortic atherosclerotic plaques, these various oral bacteria were also detected in occluded arteries from patients with Buerger Disease.

Etiologically, gentle mastication releases bacterial endotoxins from the oral cavity into the bloodstream, inducing cytokine production TNF, IL-1, and PGE 2. Etiologically, the chronic presence of periodontal microbes can lead to atherogenesis via two pathways: 1 direct invasion of the arterial wall 23 and 2 the release, in response to infection, of systemic inflammatory mediators with atherogenic effects.

Recent studies have shown that CRP may directly interfere with endothelial nitric oxide NO availability, by both decreasing the expression of NO synthase and simultaneously increasing the production of reactive oxygen, which inactivates NO. Further investigation of this hypothesis i. Another mechanism through which the bioavailability of NO is decreased is oxidative inactivation by reactive oxygen species.

Triggered by bacterial components such as LPS from P. These macrophages can then transform into foam cells, inducing the production of proinflammatory cytokines, leading to endothelial dysfunction. These results led to the conclusion that periodontitis was directly associated with the ability of isolated LDL to activate macrophages through its main mediators.

These findings may prove valuable clinically, because impaired endothelium-dependent vasodilation induced by increased CRP serum levels may be used as a precursor in diagnosing CVD in the future. Another predictor of CVD, in particular coronary heart disease CHD , may be serum levels of antibodies directed against periodontal pathogens. Pussinen et al.

In a linear regression model, they concluded that the combined antibody response to P. The study was the first of its kind and was quite insightful in expanding beyond P.

An alternative approach for studying the link between periodontal disease and CVD may be through the evaluation of peripheral arterial disease PAD. PAD of the legs is a state of insufficient tissue perfusion to meet metabolic demand. PAD shares similar pathological features to both stroke and CHD, in that atherosclerotic plaques are present. Recognizing the relationship between periodontal disease and PAD is valuable in trying to understand the clinical effect of periodontal diseases and how the treatment of these diseases may reduce the risk of developing CVD.

New findings have suggested that tooth loss, rather than periodontal disease, may be the important link between CVD and oral health. Elter et al. However, the investigation of this claim has many limitations, which explains the weaker association between periodontal disease and CHD in older subjects. These important studies shed new light on the association between periodontal disease and atherosclerotic events. Given that endothelial dysfunction appears to be an early event in the development of atherosclerosis, also predicting for plaque instability, these findings strengthen the link between periodontal disease and atherosclerosis.

Thus, it is now critical to test the hypothesis that reversal of periodontal disease prevents atherosclerotic events, and to explore different therapeutic approaches to achieve this aim. More studies that elucidate mechanisms for possible anti-atheroscelorosis therapies are needed.

Diabetes mellitus is a metabolic disorder characterized by hyperglycemia due to the defective secretion or activity of insulin. The condition affects more than 16 million people in the United States. Type 1 diabetes mellitus results from the destruction of beta-cells within the islets of Langerhans of the pancreas, which leads to complete insulin deficiency. Type 2 diabetes mellitus ranges from insulin resistance progressively leading to pancreatic beta-cell failure.

Lastly, gestational diabetes mellitus is a glucose intolerance that begins during pregnancy. The number of adults diagnosed with type 2 diabetes worldwide is expected to grow from million in to approximately million in A recent hypothesis links chronic subclinical inflammation with insulin resistance, initiating the development of type 2 diabetes.

The triggers of inflammation are many and potentially include oral infection, which may lead to a cascade of events, including increased cytokine production, activation of acute-phase protein synthesis, and consequent insulin resistance that produces pathogenic changes resulting in type 2 diabetes. However, no statistically significant correlations were revealed. Furthermore, the results suggested that E. Periodontal disease, more specifically periodontitis, is one of the many complications resulting from type 1 and type 2 diabetes.

Numerous studies have found a higher prevalence of periodontal disease among diabetic patients than among healthy controls; 4 thus, an established relationship exists between periodontal disease and diabetes.

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Sim. Microsoft Corp co-founder Bill Gates will retire from the company on Friday and move to a full-time role at his charitable organization.