Diabetes Mellitus induced periodontal breakdown
Severe gingival inflammation, deep periodontal pockets, rapid bone loss, and frequent periodontal abscesses are often occurring in diabetic patients with poor oral hygiene. Children with type-I diabetes tends to have more destruction around the first molars and incisors than elsewhere, but this destruction becomes more generalized at older ages. The majority of well controlled diabetes mellitus related studies show a higher prevalence and severity of periodontal disease in individuals with diabetes than in non-diabetic persons with similar local factors where findings include a greater loss of attachment, increased bleeding on probing and increased tooth mobility. Uncontrolled or poorly controlled diabetes is associated with an increased susceptibility and severity of infections including periodontitis.
Certain mechanisms those are responsible for initiating periodontal diseases. These are mentioning one by one =>
1. Bacterial pathogens :
The glucose content of gingival fluid and blood is higher in individuals with diabetes than in those without diabetes with similar plaque and gingival index scores. The patient with diabetes whose have higher glucose level in gingival fluid could change the environment of the microflora includes qualitative changes in bacteria that can contribute to the severity of periodontal diseases.
2. Polymorphonuclear leukocyte function:
The increased susceptibility of diabetic patients to get infected has been hypothesized as being caused by polymorphonuclear leukocyte deficiencies resulting in an impaired chemotaxis, defective phagocytosis or impaired adherence. The function of polymorhponuclear leukocytes and monocytes or macrophages is impaired. As a result, the primary defense against periodontal pathogen is diminished and bacterial proliferation is unchecked. No alteration of Immunoglobulin A (Ig A), G (Ig G), M (Ig M) has been found in diabetic patient.
3. Altered collagen metabolism:
Increase collagenase activity and decrease collagen synthesis is found with poorly controlled diabetes , who also has chronic hyperglycaemia. Decreased collagen synthesis, osteoporosis, and reduction in height of alveolar bone occur in diabetic patient.
Chronic hyperglycaemia adversely affects the synthesis, maturation, and maintenance of collagen and extra-cellular matrix. In hyperglycaemic state, numerous proteins, and matrix molecules undergo a non-enzymatic glycosylation resulting in Accumulated Glycation End Products (AGEs). AGEs forms at normal glucose level as well in hyperglycaemic state. In hyperglycaemic state, AGEs forms in an excessive amount. Many types of molecules are affected including proteins, lipids, and carbohydrates. Collagen is cross linked by AGE formation, making it less soluble and less likely to be normally repaired or replaced. Cellular migration through cross linked collagen is impeded and tissue integrity is impaired as a result of damaged collagen remaining in the tissues for longer periods. As a result, collagen in the tissues gets aged and more susceptible to breakdown (less resilient to destruction by the periodontal infections).
AGE plays central role for the complications of diabetes. It may also play a significant role in the progression of periodontal disease as well. Poor glycaemic control with associated increased level of AGEs renders the periodontal tissues more susceptible to destruction. The cumulative effects of altered cellular response to local factors, impaired tissue integrity, and altered collagen metabolism play a significant role in the susceptibility of diabetic patients to infections and destructive periodontal diseases.
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