Periodontal Studies

Clinical studies support the theory that tobacco use is an important variable affecting the prevalence and progression of periodontal diseases. In studies in which plaque levels were adjusted between smokers and non-smokers, greater bone loss, probing depths, and clinical attachment loss and have been reported in smokers. Several studies confirmed that duration of tobacco use, smoking status, and amount of daily tobacco intake is directly related to the severity of periodontal disease.

Smoking has been recognized as one of the major predictive variables for response to periodontal therapy.

In maintenance patients followed at least 5 years, patients who smoked were twice as likely to lose teeth. The majority of studies involving nonsurgical

Heavy cigarette smoking also reduces root coverage after free gingival graft procedures, and there are conflicting reports on smoking’s effect on the success of sub-epithelial connective tissue grafts.

Although smokers benefit from periodontal therapy, clinical improvements are less than those for non-smoking patients. Studies comparing therapy response in former smokers, current smokers, and never smokers demonstrate that former smokers respond in a similar manner to never smokers to periodontal therapy. Based on this evidence, dental health professionals should advise patients of tobacco’s negative health effects as well as the benefits of quitting tobacco use, and tobacco cessation counseling should be part of the armamentarium of the dental office.

* Differences between type 1 and type 2 diabetes:

Type 1 diabetes is usually present in children and adolescents, although some studies showed than 15% to 30% of cases were diagnosed after 30 years of age. It results from cellular mediated autoimmune destruction of pancreatic b -cells, leading to total loss of insulin secretion. Markers of autoimmune destruction have been identified and can be used for diagnosis or risk

Type 2 patients have transformed insulin production; however, autoimmune destruction of b -cells does not occur as it does in type 1, and patients keep the capability to produce some insulin. Type 2 diabetes once called non–insulin dependent diabetes, results from insulin resistance, which alters the use of endogenously produced insulin at the target cells. Because the type 2 diabetic still produces insulin, the incidence of ketoacidosis is very low compared to type 1; however, ketoacidosis can occur in association with the stress of another illness such as infection.

Type 2 patients can be undiagnosed for many years because the hyperglycemia appears slowly and usually without symptoms. In some patients, the production of pancreatic insulin is increased to compensate for insulin resistance. As the disease progresses, pancreatic insulin production may lessen over time due to the prolonged increase in secretory demand caused by the insulin resistance. Insulin secretion becomes insufficient to counteract for insulin resistance. Although type 2 patients do not need insulin treatment to survive, insulin is often taken as part of the medical