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

therapy have shown less probing depth reduction and less attachment gain in smokers as compared to non-smokers. Among patients who have been surgically treated for periodontitis and then longitudinally followed, smokers exhibited less reduction in probing depths, less gain in clinical attachment levels, and less gain in bone height than non-smokers.

Clinical attachment gains are less in smokers as compared to non-smokers following regenerative procedures.

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

assessment.

The decreased production of insulin in patients with type 1 diabetes makes the use of exogenous insulin necessary to sustain life, hence the previous name ‘‘insulin-dependent diabetes.’’ In the absence of insulin, these patients develop ketoacidosis, a life-threatening condition.

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

management.

* Is level of glycemia relevant to management of periodontal disease?
Strong evidence proposes that diabetes is a risk factor for gingivitis, and the level of glycemic control seems to be an important determinant in this relationship.

In adults with type 1 diabetes, the overall degree of gingival inflammation was similar between diabetic subjects as a whole and non-diabetic control subjects with similar plaque accumulation. However, when diabetic patients were stratified according to their level of glycemic control, significantly greater gingival bleeding was seen in poorly controlled diabetic patients than in either well-controlled diabetic subjects or non-diabetic controls. The number of bleeding sites decreased as glycemic control improved. Greater gingival inflammation was also seen in adults with type 2 diabetes than in non-diabetic controls, with the highest level of inflammation in subjects with poor glycemic control.

An experimental study on gingivitis showed speedy and noticeable development of gingival inflammation in well-controlled adult type 1 diabetics patients than in non-diabetic controls, regardless similar levels of plaque accumulation and similar bacterial composition of plaque, suggesting a hyper-inflammatory gingival response in diabetes. This study concluded that the presence of diabetes is often, but not always, related to the increased gingival inflammation. In addition, level of control of glycaemia may play a role in the gingival response to bacterial plaque in people with diabetes.

The majority of evidence indicates that diabetes also increases the risk of periodontitis. A thorough meta-analysis concluded that the majority of studies exhibit a more severe periodontal condition in diabetic adults than in adults without diabetes. These studies included over 3,500 diabetic adults and clearly demonstrated a significant relationship between diabetes and periodontitis.

In well-controlled patients, the response to scaling and root planing appears similar to that in non-diabetic subjects. Although many diabetic individuals show improvement in clinical parameters of disease immediately after therapy, patients with poorer glycemic control may have a faster recurrence of deep pockets and less favorable long-term results. In a recent study, 20 diabetic and 20 non-diabetic individuals received scaling and root planing, modified Widman flap surgery at sites with residual deep probing >5 mm, and routine maintenance therapy. Within five years following the baseline examination, both groups had a similar percentage of sites showing gain, loss, or no change in clinical attachment.