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Conscious sedation Periodontal treatment of medically compromised patients Periodontal therapy in the female patient Periodontal treatment for older adults Treatment of aggressive and atypical forms of periodontitis Section 3 — Diagnosis and Treatment of Periodontal Emergencies Acute gingival disease Treatment of periodontal abscess Diagnosis and management of endodontic-periodontic lesions Section 4 — Non-surgical Treatment Phase I: Periodontal therapy Plaque biofilm control for the periodontal patient Scaling and root planing Sonic and ultrasonic instrumentation and irrigation Anti-infective therapy Occlusal evaluation and therapy Pathologic tooth migration: A case report online-only Breathe malodor Phase II: Periodontal therapy Surgical anatomy of periodontal and implant areas General principles of periodontal surgery Gingival surgical techniques Treatment of gingival enlargement The flap technique for pocket therapy Resective osseous surgery Periodontal regeneration and reconstructive surgery Furcation involvement and treatment Periodontal plastic and esthetic surgery Periodontal microsurgery After the inflammatory stimulus there is increased production of prostaglandin E2 PGE2 and of matrix metalloproteinases MMP , which lead to extracellular destruction of the gingiva and the periodontal ligament, stimulating resorption of alveolar bone.
All of the MMPs are important in the immunoresponse, but MMP-8 is the only proteinase that is able to fragment types I and III collagen, which are important for maintaining the structure of teeth. Bone resorption takes place as a result of fragmentation of the elements of the extracellular matrix by osteoclasts. Controllable risk factors include smoking, stress, poor oral hygiene and infrequent visits to the Dentist. Non-controllable risk factors include heredity, systemic diseases and age.
The genetic component does not cause the disease; however it does make patients more susceptible to emergence of periodontal pathologies or to more serious disease course. One hypothetical model with a biological basis is the suggestion that individuals with cardiac and periodontal diseases have an exacerbated immunoresponse to bacterial infections.
People who have the hyperinflammatory monocyte phenotype secrete from three to ten times more mediators in response to bacterial lipopolysaccharides, when compared with people who are phenotypically normal. Thus, the interaction between bacterial lipopolysaccharides and the monocytes that release a range of different cytokines is fundamental to initiation and progression of PD and also to its systemic effects, such as atherogenesis and thrombogenesis. Elevated CRP concentrations increase the risk of cardiovascular events by 1.
Results for plasma fibrinogen tests, white blood cell counts and von Willebrand factor assays are all elevated in patients with periodontal problems. Plasma fibrinogen concentrations are increased during chronic inflammations and infections, creating a hypercoagulable state. Thrombogenesis is related to atherogenesis and to growth of atherosclerotic plaques. There were differences between groups with good dental hygiene CRP: 3.
While treating PD results in a transitory increase in proinflammatory cytokine levels, which is probably related to manipulation of the inflamed tissues and transitory bacteremia, inflammatory activity normalizes in 24 to 48 hours and, over the long term, if PD responds to treatment then concentrations of these cytokines will reduce.
Relative risks for angina and for fatal coronary events were 1. There is then recruitment of monocytes, and increase in expression of endothelial adhesion molecules and increased uptake of lipids by macrophages. Administration of systemic antibiotics to patients with periodontitis resulted in reductions in the levels of systemic markers of inflammation. However, according to some authors the relationship between periodontitis and CVDs is still unproven.
One example of this is smoking, which increases the incidence both of PD and of AD and could give a false impression that atherosclerosis increases the incidence of periodontitis or vice-versa. Health professionals will therefore have to illustrate to the population the importance of preserving natural teeth even if this demands greater care and expenditure on each individual person's health.
In order to achieve this, health services must implement strategies designed to facilitate access to dental care, in particular for less privileged populations, among which the prevalence of periodontal diseases is higher. It is sometimes difficult to deal with this paradigm and it is even possible to find authors publishing in the medical literature who argue against preservation of natural teeth on the basis that someone who has no teeth also has no PD and is therefore at lower risk of the systemic repercussions of periodontitis.
Working from the same principal, perhaps they will also begin to recommend removing kidneys to avoid kidney stones or removing the heart to avoid myocardial infarction. Dumitrescu AL. Influence of periodontal disease on cardiovascular diseases. Rom J Intern Med. Eur J Cardiovasc Prev Rehabil. Balan H. Do cardio-vascular and periodontal diseases have a close, causal relationship?
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