Diabetes and Periodontal Disease PDF

Systemic Predisposing Factors (HORMONAL DISORDERS) By Dr. Heba Shawky  INTRODUCTION Periodontal disease is considered as a state of bacterial injury. Bacteria appear to play a significant role in initiating and maintaining inflammation with subsequen...

Systemic Predisposing Factors (HORMONAL DISORDERS) By Dr. Heba Shawky  INTRODUCTION Periodontal disease is considered as a state of bacterial injury. Bacteria appear to play a significant role in initiating and maintaining inflammation with subsequent connective tissue destruction. The bacterial accumulations cause an inflammatory response from the body.  A state of dynamic equilibrium exists between bacteria and the host. Recent discoveries about periodontitis showed that the host response varies between individuals and that either and inadequate host immune response or an exaggerated host immune response to bacterial pathogens leads to more severe forms of the disease.  Thus the host response to bacterial pathogens is very important and likely explains the differences in disease severity from one individual to another. Remember: Systemic disorders do not initiate chronic destructive periodontitis, but they may predispose, accelerate, or otherwise increase its progression toward periodontal tissue destruction.  Systemic modifying factors 1- Hormonal disorders 2- Hematological disorders 3- Genetic disorder 4- Smoking 6- Psychological disturbance (stress)  I- Hormonal Disorders 1. Metabolic disorder: e.g. Diabetes mellitus 2. Sex-hormone disorders: e.g. Pregnancy  It is a complex metabolic disease characterized by chronic hyperglycemia due to an absolute or relative deficiency of insulin. Lipid and protein metabolism is also altered. Uncontrolled diabetes mellitus is characterized by metabolic abnormalities and long-term complications involving the eyes, kidneys, nervous system, vasculature, and periodontium.  The gingival and periodontal signs in poorly controlled diabetic patients include: 1. Severe gingival inflammatory response to bacterial plaque.  The gingival and periodontal signs in poorly controlled diabetic patients include: 2. Tendency towards enlarged gingiva, sessile or pedunculated gingival polyps and polypoid gingival proliferations. 3. Simultaneous formation of multiple periodontal abscesses 4. Development of periodontitis with periodontal pocketing 5. Persistence of gingival inflammation after standard periodontal treatment (thorough supra- and subgingival scaling and cleaning, oral hygiene instruction) 6. Continuing alveolar bone loss despite periodontal treatment. 7. Increased tooth mobility and tooth migration  How does diabetes influence the periodontium? 1. Bacterial Pathogens 2. Changes in periodontal vasculature 3. Altered immune response 4. Impaired bone formation 5. Altered collagen metabolism 1- Bacterial Pathogens Some early studies reported higher proportions of certain bacteria in the periodontal pockets of patients with diabetes. Patients with type I diabetes with periodontitis have been reported to have a subgingival flaora composed mainly of Actinomyces species. P. gingivalis, P. intermedia, and C. ractus which are prominent in severe periodontal lesions of patients with type II diabetes.  Other studies denoted that Porphyromonas gingivalis, Prevotella intermedia which are Actinobacillus actinomycetemcomitans common in periodontal lesion of non-diabetic individual are present in low numbers in those with the disease. Later studies involving cultures generally revealed few differences in periodontally diseased sites of subjects with diabetes and those of subjects who did not have diabetes.  Thus, the pathogens associated with periodontitis do not appear to differ greatly in people with and without diabetes, Researchers have focused attention on potential differences in the immuno-inflammatory response to bacteria between people with diabetes and those without diabetes.  2- Changes in periodontal vasculature AGEs formation: An advanced glycation end-product (AGE) is formed through normal metabolism and aging. Excess glucose in the blood settles into the cells and will bind to protein or lipid molecule, a process known as Glycation.  A chain of chemical reactions after an initial glycation reaction takes place resulting in the formation of an advanced glycation end-product (AGE).  Accumulation of AGEs in periodontal vasculature will results in: Induction of abnormal endothelial cell function, capillary growth and vessel proliferation. Increased thickness of small vessel walls results in narrowing of the lumen, altering normal periodontal tissue homeostasis  Enhanced cross-linking of AGE-containing collagen in the basement membrane inhibits the normal degradation of these proteins, increasing the thickness of the membrane. This in turn will alter normal homeostatic transport across the membrane. i.e. this thickening will impair oxygen diffusion and nutrient provision across basement membrane.  3- Altered immune response Diabetic patients show alteration in function of cells involved in this response including: Neutrophils Monocytes Macrophages  The increased susceptibility of diabetics to infection has been hypothesized as being due to polymophonuclear leukocyte deficiencies resulting in: * Impaired adherence * Impaired chemotaxis * Defective phagocytosis  Inhibition of normal function of these cells will prevent destruction of bacteria in the periodontal pocket, thereby increasing periodontal destruction.  The accumulation of AGEs in patients with diabetes also increases the intensity of the immuno-inflammatory response to periodontal pathogens, because inflammatory cells such as monocytes and macrophages have receptors for AGEs.  Macrophages and monocytes often exhibit elevated production of proinflammatory cytokines and mediators such as tumor necrosis factor (TNF) and interleukin 1 ß (IL- 1 ß) in response to periodontal pathogens, which may increase host tissue destruction. The hyper-responsiveness of these immune cells is due to AGE-RAGE interaction.  4 – Impaired bone formation The fundamental feature of bone in IDDM patients seems to be the retardation of remodeling, primarily due to a reduced bone formation. This outcome is due to a decrease in the number and functions of osteoblasts (bone formation cells).  4 – Impaired bone formation (Cont.) Insulin exerts direct anabolic actions in osteoblasts by activation of its receptor Diabetes significantly enhances apoptosis of osteoblastic cells. Ostoeblastic apoptosis is stimulated by advanced glycation endproducts (AGEs).  5- Altered collagen metabolism: Altered wound healing is a common problem in people with diabetes. The primary reparative cell in the periodontium, the fibroblast, does not function properly in high-glucose environments.  Increased production of matrix metalloproteinases such as collagense, gelatinases and elastases in diabetes allows rapid degradation of the collagen through stimulation of collagenase. Collagenases degrade more newly formed collagen molecules (more soluble).  On the other hand, the formation of AGEs on collagen will result in increased collagen cross-linking which makes the collagen macromolecules less soluble and more resistant to normal enzymatic degradation  Thus, the end-result of the previous alterations (predominance of older, highly cross-linked collagen and increased destruction of recently synthesized collagen by collagenase) is an alteration of wound healing in response to both microbial and physical periodontal injury.