thanks...
Kabin
Konteyner

send green star

(part VI)
Furthermore, tricyclic antidepressants, antihyper-tensives, antihistamines, and anticholinergics may cause dry mouth (xerostomia) and reduce salivary flow. These side effects may diminish natural cleansing of the oral cavity and thus increase frequency of periodontal disease and caries of both supragingival and subgingival roots.
Finally, the importance of dentists' involvement in the diagnosis, treatment recommendations, and monitoring of periodontal disease cannot be overemphasized. Variables affecting the resolution of periodontal disease are numerous and formidable, and may eventually require all health care professionals to participate in patient care. Moreover, health insurance may recognize the importance of periodontal medicine and provide better coverage to dental practitioners.


Reference/original article:

www.medscape.com/content/2000/00/40/95/409578/409578_ref.html

send green star

(part V)
Physicians may require education on infective agents and associated ACVD. They may change their clinical practice pattern whereby they may screen for a history of periodontal disease as a potential risk factor for CHD. If necessary, they may refer patients for oral examination. These actions should increase the diagnosis of periodontal disease; however, they also may add one more task to already overburdened physicians. A referral system may assist in identifying patients who require immediate dental intervention.
Since pharmacists work closely with most health professionals, it is important that they too educate themselves about periodontal disease and other infective agents associated with ACVD. Their main role would be to educate patients on treatment alternatives as part of interdisciplinary management. With proper training, they can help screen patients for periodontal disease in the hospital and community settings, particularly those with poor oral hygiene and who are at high risk for CHD. For example, with each Peridex prescription, the pharmacist could provide drug education and urge compliance with dental appointments. Pharmacists should be aware of drugs that cause gingival hyperplasia and may predispose to periodontal disease, such as phenytoin, nifedipine, and cyclosporine. These drugs can stimulate proliferation of gingival fibroblasts, causing overgrowth of gingivae. Furthermore, tricyclic antidepressants, antihyper-tensives, antihistamines, and antic

send green star

(part IV)
It is always a risk to predict trends. Several years ago, few would have predicted the potential impact of infective agents on ACVD and even fewer of periodontal disease on ACVD. However, if future evidence provides a strong link between the diseases, it may have significant implications for clinical practice, as witnessed by emerging therapies.
Increased awareness of systemic consequences of periodontal disease will alert the public, physicians, and other health professionals. Heightened awareness by the public may eliminate misconceptions about periodontal disease; for example, that it is caused by food or dietary deficiency, or results from osteoporosis, and that mouth rinse or oral antibiotics can cure it. People will learn that tobacco smoking and diabetes are the principal exacerbating factors in periodontal disease and be more inclined to modify these risk factors. In addition, they will be more compliant with dental check-ups and scheduled appointments, as well as treatment regimens prescribed by dentists.
Diagnosing periodontal disease involves several decision levels that allows dental professionals to differentiate, identify, formulate, and monitor treatments

send green star

(cont-partIII)
Both periodontal disease and atherosclerosis have numerous characteristics in common. They are most likely to occur in individuals who are elderly, male, of low economic and education status; who smoke; have diabetes, elevated cholesterol, and systemic hypertension; and are stressed. These commonalties indicate that the diseases may share similar etiologic pathways.
As about pathogenesis, under normal conditions a thin film of glycoprotein (pellicle), derived from saliva, coats the teeth. Gram-positive bacteria (aerobic and facultative) from saliva adhere to pellicle and colonize on supragingivae. Within days, gram-negative anaerobic or facultative bacteria including Porphyromonas gingivalis, Bacteroides forsythus, and Actinobacillus actinomycete-mocomitans colonize in proximity to, or overlap on, supragingivae by binding to a specific unknown receptor on gram-positive bacteria. Bacterial plaque develops at gingival margins, extending into subgingivae, resulting in epithelial cell disruption and acute inflammation. This chronic inflammatory burden from bacteria and host develops into periodontitis. Periodontal tissue destruction results from endotoxins including, but not limited to, LPS released by gram-negative anaerobic bacteria in subgingival plaque and host immunoinflammatory responses induced against the bacteria and LPS. Thus, subgingival biofilms constitute an enormous and continuing bacterial load. This may result in gingival ulceration causing edema,

send green star

(continue)
Atherosclerotic cardiovascular diseases (ACVD) such as myocardial infarction and stroke are a major health problem, causing nearly 50% of deaths in the American population and other developed countries. Reducing conventional modifiable risk factors (e.g., smoking, systemic hypertension, diabetes mellitus, hyperlipidemia) is effective in preventing ACVD. However, these strategies, together with interventions to reduce nonmodifiable risk factors (e.g., age, gender, family history), do not explain why the frequency of ACVD has not decreased as much as would be expected on epidemiologic grounds. Thus, it is likely that other, unrecognized factors contribute to the pathogenesis of atherosclerosis. This led many to speculate that ACVD may have an infectious etiology.
Local dental infections, specifically periodontal disease, may increase the risk for ACVD. Periodontal disease is an inflammatory response to predominately gram-negative anaerobic bacterial infections of tissues surrounding the tooth, including periodontal ligament, cementum, and alveolar bone. A chronic inflammatory burden ensues in the absence of treatment. Periodontitis refers to actual loss of periodontal ligament around the tooth resulting from gram-negative, anaerobic bacteria and the host response to these pathogens. Moderate to severe forms of disease affect approximately 15% of Americans over age 18 years and perhaps more in other countries.

send green star

Recent evidence suggests that periodontal disease may predispose to atherosclerotic cardiovascular disease. Data support mechanisms of host-derived local and systemic proinflammatory responses similar to atherosclerosis, consisting of monocytic-derived cytokines and other inflammatory mediators, which are induced by periodontal pathogens and its endotoxin, lipopolysaccharide. These mechanisms may contribute to the start of vascular endothelial dysfunction and further sequelae leading to atherosclerosis. Experimental evidence and biologic plausibility appear to support this proposal. However, clinical evidence from a MEDLINE search from January 1966-December 1999 proposed a weak or no correlation primarily due to confounding factors. The aim of care is to reduce vulnerable pathogens from the infected periodontium by standard treatment; however, new approaches appear promising. Increased awareness of a potential link among infective agents, immunoinflammatory processes, and atherosclerosis may clarify clinical implications.
Atherosclerotic cardiovascular diseases (ACVD) such as myocardial infarction and stroke are a major health problem, causing nearly 50% of deaths in the American population and other developed countries. Reducing conventional modifiable risk factors (e.g., smoking, systemic hypertension, diabetes mellitus, hyperlipidemia) is effective in preventing ACVD. However, these strategies, together with interventions to reduce nonmodifiable risk factors (e.g., age, g

send green star

Excellent health blip!!!

send green star

While I was a microbiology student several years ago, we learned that the bacteria that causes tooth plaque is the same as, or at least closely related to, the bacteria that causes plaque in the blood vessels leading to clots. The bloody gums are not the only issue...and I strongly agree with the post about diet. Why does it take sooo long before the rest of the world hears about these discoveries?

send green star

This is something very interesting that I just found out about last week. It's a kind of chocolate that's actually good for your teeth since it contains Xylitol which kills bacteria (kinda like the gum but more benefits). Also aids weight loss, over 3000 ORAC points per piece and my friend lost 20 pound in a month with it. I'm slim already so I plan to use it just for health reasons and maintain my weight.

If you'd like some more info on Xylitol, I'm in the middle of putting together an article about it so email me and I'll send you a copy when I'm done: detoxexpert@gmail.com.

I'm glad to see this kind of information being presented here. I used to work in a holistic dentist's office and it's amazing how people's health issues can reverse themselves with some good dental work.

send green star