Systemic Predisposing Factors PDF

Systemic Predisposing Factors Systemic modifying factors:  II. Associated with genetic disorder I.Haematologic 1. Familial & cyclic disorders: neutropenia IV. Drug 1. Leukemia 2. Down syndrome...

Systemic Predisposing Factors Systemic modifying factors:  II. Associated with genetic disorder I.Haematologic 1. Familial & cyclic disorders: neutropenia IV. Drug 1. Leukemia 2. Down syndrome III.Hormonal: induced 3. Lazy leukocyte 1. Diabetes disorders: 2. Anaemia 3. syndrome 2. Sex hormones 1. Phenytoin 4. Papillon-Lefevre imbalance (Dilantin) Thrombocytopen syndrome 2. Nephedipine ia * Puberty 5. Chediak-Higashi * Pregnancy (calcium 4. Disorders of channel syndrome * Oral leukocytes blocker) 3. 6. Aggressive contraceptives Steroids Agranulocytosis periodontitis V. Nutritional Leukocyte 7. Ehler Danlos VI. disorders related syndrome (type IV& Psychosomatic to genetic VIII) VII. Aging conditions. 8.Hypophosphatasia VIII.Viral Others. 9. Hereditary gingival fibromatosis 10. Others. ⯁ All blood cells play a role in the maintenance of a healthy periodontium. ⯁ White blood cells (WBCs) are involved in peripheral and inflammatory reactions. ⯁ Disorders of blood elements can have a profound effect on the periodontium.  ⯁ Disorders of leukocytes: ⯁ Neutrophils play a key role in the host defense against extracellular bacteria, especially pyogenic bacteria. ⯁ Patients with neutrophil defects often suffer from oral mucosal ulceration, gingivitis and/or periodontitis. ⯁ -Primary leukocytes’ disorders characterized by severe periodontal disease include leukemia, neutropenia (agranulocytosis and cyclic neutropenia), Chediak Higashi syndrome and early onset periodontitis. ⯁ -Leukocytes’ abnormalities that occur secondary to underlying systemic disease and that are also associated with severe periodontal disease include diabetes mellitus and AIDS “acquired immunodeficiency syndrome”. ⯁ Leukemias are malignant neoplasias of white blood cell precursors. ⯁ The most prevalent types of leukemia are acute monocytic leukemia and acute myelocytic leukemia and are characterized by: ⯁ 1- Diffuse replacement of bone marrow with proliferating immature leukemic cells. 2 Abnormal numbers and forms of immature white cells in the circulating blood. 3 Widespread infiltrates in the liver, spleen, lymphnodes and other sites throughout the body. ⯁ In acute leukemia the gingiva appears bluish red and cyanotic. ⯁ The interdental papillae is enlarged, spongy, friable and bleeds upon slightest provocation or even spontaneously. ⯁ Superimposed bacterial infection leads to ulceration and necrosis of the marginal gingiva with pseudomembrane formation. ⯁ In case of infiltration of the alveolar bone by leukemic cells there is alveolar bone resorption and looseness of the teeth. ⯁ Leukemic gingival enlargement is not found in edentulous patients or in patients with chronic leukemia. ⯁ Causes of gingival bleeding in leukemia: ⯁ The replacement of bone marrow elements by the increased number of immature leukemic cells reduces the production of red blood cells and platelets, leading to anaemia and thrombocytopenia (with increased bleeding tendency) respectively. ⯁ Causes of gingival enlargement in leukemia: ⯁ Leukemic cells can infiltrate the gingiva that creates gingival pockets, where bacterial plaque accumulates initiating a secondary inflammatory lesion, which contributes also to the enlargement of the gingiva, and less frequently affect the alveolar bone.  Agranulocytosis ⯁ Itis characterized by disappearance of circulating granulocytes which is generally due to severe infections or due to the ingestion of certain drugs as barbiturates, sulfonamides and gold salts. ⯁ -There are painful, large ulcerations without inflammatory reaction. ⯁ -Necrosis and severe infection of the oral mucosa and gingival margin. ⯁ -Foul odor and bleeding and occasional involvement of the attached gingiva. ⯁ It occurs in cyclic episodes and is characterized by periodic, monthly (3-5 days) decrease in the number of neutrophils during infancy and childhood. ⯁ -The gingiva may be edematous, friable and hyperplastic with fetid odor. ⯁ -Deep periodontal pockets and generalized periodic alveolar bone loss involving the permanent dentition (rapidly destructive periodontitis). ⯁ -The gingiva assumes its normal appearance when the neutrophil count returns to normal. ⦿ It is an autosomal dominant trait which does not manifest until the eruption of the teeth and is mostly associated with permanent teeth. -The enlarged gingival tissues appear firm and pink with exaggerated stippling. -The tissue may cover the crowns of the teeth and interfere with speech and mastication. -The hyperplasia is due to excessive production of collagen in the gingival corium as fibroblasts are permanently activated. They have increased proliferative rates and so increased production of collagen and fibronectin. ⦿ It is a congenital disease caused by chromosomal abnormality (Trisomy of chromosome 21) and characterized by mental deficiency and growth retardation. Generalized periodontal disease which tends to be more severe in the lower anterior region can be explained by two factors: 1) Reduced resistance to infections because of poor circulation especially in areas with poor terminal vascularization such as the gingival tissue. 2) Defect in T cell maturation and polymorphonuclear leukocyte chemotaxis. ⦿ There is a defect in neutrophil chemotaxis which fail to migrate from the peripheral circulation to the site of tissue injury. ⦿ However, phagocytosis and intracellular killing are not affected. There is gingivitis and periodontitis. ⦿ Papillon-Lefevre syndrome is an autosomal recessive trait, characterized by hyperkeratotic skin lesions in palms and soles of feet (hyperkeratosis palmoplantaris) and severe destruction of the periodontium with early loss of deciduous and permanent teeth. Etiology: The presence of virulent pathogens as P.intermedia and Aa. Impairment of neutrophils’ chemotaxis. Deficient monocyte function, reduced lymphocyte response and increased circulating NK cells. It may be an inherited ectodermal defect. ⦿ It is a rare genetically transmitted autosomal recessive disease that affects cell organelles found in almost every cell in the body. It affects mostly the melanocytes, the platelets, and the phagocytes. ⦿ This produces partial oculo-cutaneous albinism, photophobia, mild bleeding disorders and multiple recurrent pyogenic infections. ⦿ -There is defective chemotaxis, degranulation and intracellular killing of PMNs with normal phagocytosis. In addition, there is granulocytopenia. -The gingiva is edematous, with areas of desquamation. -Periodontitis with rapid destruction of alveolar bone leading to marked mobility and early loss of all teeth. ⦿ -This is a familial autosomal recessive trait characterized by rickets, poor cranial bone formation ⦿ and premature loss of primary teeth particularly the incisors due to severe loss of alveolar bone. -Patients have low serum alkaline phosphatase. -The cementum is absent or hypoplastic.. Endocrine disturbances and hormonal fluctuations: ⦿ affect the periodontal tissue directly, ⦿ modify the tissue response to local factors and ⦿ produce anatomic changes in the gingiva that may favor the plaque accumulation and disease progression.  III.Hormonal DIABETES MELLITUS ⦿ Diabetes mellitus is an extremely important disease from a periodontal aspect ⦿ It is complex metabolic disorder characterized by chronic hyperglycemia. ⦿ Uncontrolled diabetes (chronic hyperglycemia) is associated with several long term complications, including: ⦿ Microvascular diseases (retinopathy, nephropathy, neuropathy). ⦿ Macrovascular diseases (cardiovascular, cerebrovascular). ⦿ Increased susceptibility to infection. ⦿ Poor wound healing. ⦿ In uncontrolled or poorly controlled diabetes the following findings have been described: ⦿ Diminished salivary flow leading to: - Burning mouth or tongue. - The xerostomia may be conductive to candidiasis. - Increase incidence of dental caries and periodontal disease. - Diabetes does not cause gingivitis or periodontal pockets, but it alters the response of the periodontal tissues to local irritants, hastening bone loss and retarding post therapy healing of the periodontal tissues. - There is severe gingival inflammation, deep periodontal pockets, rapid bone loss, and frequent periodontal abscess formation especially in diabetics with poor oral hygiene. - In type I diabetes, there is often more extensive periodontal destruction especially around the first molar and incisors resembling juvenile periodontitis, but this destruction becomes more generalized at older ages. - In well controlled diabetes there are normal tissue responses with no increase in incidence of caries or periodontal disease. ⦿ Factors contributing to the development of periodontal disease in diabetes mellitus: - The increased glucose content in the gingival fluid may lead to an increase as well as alteration in the microorganisms. - There is thickening of the blood vessel walls caused by deposition of AGEs leading to narrowing of capillaries (microangiopathies). This leads to decreased blood supply to the gingiva with decreased oxygen consumption besides the reduced oxidation of glucose. - Consequently, there is an overgrowth of certain anaerobic microorganisms that are more virulant and pathogenic. - There is also impaired chemotaxis, phagcytosis and intracellular killing by neutrophils which lower the host response. - Chronic hyperglycemia affects the synthesis, maturation and maintenance of collagen and extracellular matrix, with an increased collagenase activity - AGEs formation cross-links collagen making it less soluble and less likely to be normally repaired or replaced. - Therefore AGEs render periodontal tissues more susceptible to destruction. ⦿ Increase the susceptibility to infection (candidiasis & periodontitis) due to: ⦿ Hyperglycemia: ⦿ Decrease phagocytic ability of neutrophils. ⦿ Good media for growth of microorganisms. ⦿ Ketoacidosis: ⦿ Decrease phagocytic ability. ⦿ Decrease chemotaxis. ⦿ Vascular wall disease: ⦿ Decrease blood flow. ⦿ Decrease mobilization of neutrophils. ⦿ Decrease oxygen tension. ⦿ V) Hyperlipidemia: ⦿ Interferes with macrophages function & dysregulation of cytokine release from macrophages. ⦿ These cytokines aid in wound healing. ⦿ That is why the diabetic patient has a poor wound healing. ⦿ Bacterial pathogens: ✓ Patients with diabetes mellitus and periodontitis have been reported to have a subgingival flora composed mainly of Capnocytophaga, anaerobic vibrios and actinomyces species, Porphyromonas gingivalis, Prevotella intermedia, and Aggregatibacter actinomycetemcomitans AGEs: ⦿ Chronic elevation of systemic glucose level in diabetes results in accelerated formation of advanced glycolysated end products (AGEs) {non enzymatic glycation of body proteins}. ⦿ AGEs interact with their receptors on the fibroblasts leading to decrease collagen production. ⦿ AGEs interact with their receptors on the cell surface of monocytes leading to monocytic hypersecretory trait & increase in IL-1, TNF-α & IL-6 production. ⦿ These cytokines lead to gingival inflammation, destruction of C.T. & bone resorption and resulting in periodontal disease. ⦿ Gingival inflammation and hyperplasia with bleeding tendency is sometimes noticed during puberty, pregnancy, menstrual cycle and menopause due to physiologic changes in the sex hormones. ⦿ a. The gingiva in puberty: ⦿ Pubertal gingivitis is caused by the hormonal imbalance that modifies the gingival tissue response to local irritants. There is frequently an exaggerated response to any local irritant with pronounced inflammation, bluish red discoloration, edema and gingival enlargement. ⦿ It occurs during the time of mixed dentition and is possibly related to: -Changes in plaque microbiota. -Exfoliation of primary dentition. ⦿ b. Gingival changes associated with the menstrual cycle: ⦿ As a rule, the menstrual cycle is not accompanied by notable changes, but occasionally there is: -Increased prevalence of gingivitis. -Bleeding or a tense feeling in the gums in the days preceding menstruation. However, it is important to maintain oral health during these hormonal fluctuations, including proper oral hygiene measures and regular professional dental care. ⦿ Pregnancy affects the severity of previously inflamed areas, but it does not alter healthy gingiva. ⦿ If there are no local irritating factors, then there will be no inflammation. ⦿ The increased gingival inflammation in pregnancy is usually noticed in the second month of gestation, and reaches its peak in the eighth month, and there is also a marked reduction in gingival inflammation following labor correlating with the abrupt decrease in the secretion of hormones. ⦿ The increased levels of progesterone produce dilatation of gingival microvasculature, circulatory stasis and increased vascular exudation. ⦿ The integrity of the capillary endothelial cells is also affected. Progesterone influences the biosynthesis of prostaglandins. ⦿ There is a depression of the cell mediated immunity during pregnancy leading to an altered response to plaque. ⦿ Sex hormones mediate alteration of the subgingival flora. ⦿ The number of gram -ve anaerobic microorganisms increases fourfold the base line level during the fourth month of pregnancy. ⦿ Prevotella intermedia also increase greatly, and this appeared to be associated with the increased levels of estrogen and progesterone which substitute menadione which is an essential growth factor for P.intermedia. ⦿ 1) Localized or generalized gingival inflammation; gingiva varies in color from bright red to dark red. ⦿ 2) Bleeding on brushing or during eating is the most striking clinical feature. ⦿ 3) The marginal and interdental gingivae are hyperplastic, edematous, smooth, shiny soft, ⦿ friable and sometimes presents bright red, isolated, mulberry surface, tumor like, hyperplastic masses interproximally, referred to as pregnancy tumor. ⦿ Histologically, the pregnancy tumor is identical to pyogenic granuloma, and consists of a circumscribed mass of connective tissue which contains numerous newly formed capillaries. ⦿ Meticulous plaque control, scaling and root planning should be the only periodontal procedure performed during pregnancy. ⦿ The second trimester is the safest period to perform any treatment. Long stressful appointments and periodontal surgery should be delayed until the post partum period, during which the lesions will regress. ⦿ Pregnancy tumor requires postgestation surgical excision. ⦿ -Hormonal contraceptives aggravate the gingival response to local irritants in a manner like that seen in pregnancy. ⦿ -Proper oral hygiene measures and professional care are essential to ensure gingival and periodontal health. ⦿ -Metronidazole, an adjunctive antibiotic used in periodontal therapy, should not be prescribed to females taking oral contraceptives to avoid the risk of drug interaction that can lessen the contraceptive effect. -Mild signs and symptoms sometimes appear with the earliest menopausal changes. Oral disturbances are not a common feature of menopause. ⦿ -The gingiva and remaining oral mucosa are dry and shiny and vary in color from abnormal paleness to redness and bleed easily. ⦿ There are no drugs that have been proved to initiate periodontal disease, but the following drugs influence the periodontal tissues and their response to local irritants. ⦿ a) Phenytoin (Dilantin) ⦿ This is antiepileptic drug that causes some degree of gingival enlargement in about 60% of patients receiving the drug. It occurs more frequently in younger patients and is rarely seen over 40 years of age. The degree of hyperplasia is not related to the dosage of the drug Clinical features: The lesion starts as a painless, soft, red, oedemetous, bead like enlargement of the labial gingival margins of the interdental papillae of the anterior upper and lower teeth and then spreads to involve the entire gingival unit. When uncomplicated with inflammation the lesions become firm, fibrotic, pale pink and have no tendency to bleed. As the condition progresses the marginal and papillary enlargements unite and develop into a massive tissue fold covering a considerable portion of the crown and sometimes interfering with occlusion. The presence of the enlargement makes plaque control difficult, resulting in secondary inflammatory process that complicates the gingival enlargement more and leads to wedging of the teeth apart especially in the anterior region. ⦿ -Severe and diffuse inflammation especially close to the gingival crevice. ⦿ -There is acanthosis of epithelium. ⦿ -Connective tissue exhibits densely arranged collagen bundles with an equivalent increase in the number of fibroblasts. ⦿ -This picture resembles hereditary gingival fibromatosis and fibroid epulides.  - Conservative periodontal therapy including, frequent subgingival scaling and vigorous home care regime, can prevent gingival enlargement. - Surgical elimination of the hyperplastic tissues by a gingivectomy procedure. However, recurrence of gingival enlargement occurs within 1-2 year if proper oral hygiene is not maintained. - Replacing phenytoin with an alternate drug after consulting the patient’s neurologist. ⦿ Nifedipine is a calcium channel blocker (calcium antagonist). It is used in the treatment of angina pectoris and hypertension. Gingival overgrowth occurs in 20 % of cases and there is no age or sex predilection. ⦿ Clinical features: All segments of the dentition are susceptible to overgrowth (similar to phenytion), but the anterior facial aspects are most frequently and severely affected. Secondary inflammatory manifestations are common because proper oral hygiene performance is hindered by the excess tissue. ⦿ Etiology: It has been proposed that nifedipine may affect the rate of cell death (turn over rate), rather than the rate of cell division leading to tissue overgrowth. ⦿ Treatment: Establishment of excellent plaque control and regular scaling and root planning and surgical excision of excess tissue. ⦿ Cyclosporine is an immunosuppressant. A positive correlation has been found between the dose and duration of cyclosporine administered and the severity of gingival enlargement in humans which occurs in 25% of cases. ⦿ Clinical features: The gingival overgrowth is often undistinguishable from that elicited by phenytoin. The lesion ⦿ originates in the interdental area and all segments of the dental arch may be affected. ⦿ Histopathologic picture: -The overgrowth is due to increase in the collagenous element of the C.T matrix without an ⦿ absolute increase in the fibroblast number. -There is epithelial thickening fibroplasia and secondary manifestation of inflammation. ⦿ Etiology: ⦿ 1. Cyclosporine increased protein and collagen synthesis by fibroblasts. 2. It decreases the collagenase activity of fibroblast in a dose dependent manner, thus inhibiting matrix breakdown, which eventually leads to their accumulation (lack of turnover). ⦿ The relationship of steroids and periodontal disease or alveolar bone loss is conflicting. Long term corticosteroid therapy may predispose the patient to osteoporosis, but no loss of alveolar bone has been observed. ⦿ Some studies proved that hydrocortisone impaired collagen and mucopolysaccharide synthesis in bone. ⦿ The relationship between nutrition and chronic periodontal disease remains a controversial issue. ⦿ The effect of malnutrition on periodontal disease is indirect, i.e. modification of existing disease rather than initiation of periodontal disease. ⦿ Deficiency states do not influence the inflammatory response if no local factor, such as plaque, is present to initiate the inflammation. ⦿ Vitamin C : It is important for the maintenance of collagen, cell respiration and capillary integrity. In individuals with ascorbic acid deficient diet, gingival changes found in the presence of existing gingivitis. Gingivitis and tooth mobility do not improve with ascorbic acid supplements if the existing local of inflammation, plaque and calculus are not removed.  Gingivitis and -The lack of periodontitis plaque control in appear to be more psychologically prevalent in disturbed psychologically patients. disturbed individuals. -Direct effect of the autonomic This is either nervous system on caused by: the physiologic tissue balance. -The development of habits (grinding, clenching etc.) that are injurious to the periodontium.  Stress leads to increase secretion of adrenal hormones such as corticosteroids and catecholamines affect periodontal tissue and make it more susceptible to periodontal destruction , also immunosuppresive effects of corticosteroids and catecholamines may also be important NUG Stress often includes other variables such as poor diet, smoking, lack of sleep 55 ⦿ In periodontal disease, the age of the patient and the duration of the initial manifestations of the disease process may be vital factors. ⦿ Clinicians observe that both incidence and severity of periodontal disease increase with age probably due to the cumulative effect of plaque over time. ⦿ Acquired Immunodeficiency syndrome (AIDS): ⦿ The human immunodeficiency virus (HIV) has strong affinity for cells of immune system especially the T-helper lymphocytes, but monocytes, macrophages and Langerhans cells may also be involved. The overall effect of the virus is to gradually impair the immune system rendering the patient susceptible to opportunistic infections and malignancies. ⦿ Periodontal infection and destruction increase as the immune system becomes more compromised. ⦿ HIV gingivitis: ⦿ Linear erythematous gingivitis: A persistent linear easily bleeding erythematous gingivitis. Linear lesions may be localized or generalized. It is limited to the marginal tissue or extending into attached gingiva as diffuse erythema. ⦿ HIV periodontitis: Painful rapidly progressive necrotizing, ulcerative periodontitis (NUP) with marked interproximal ⦿ bone loss. The alveolar bone often becomes exposed and undergoes necrosis and sequestration. THANK YOU