Systemic Predisposing Factors in Periodontology

Systemic Predisposing Factors

• Systemic factors can affect the periodontium, including hematological disorders, genetic disorders associated with other conditions, hormonal imbalances, drug-induced disorders, nutritional deficiencies, psychosomatic conditions, aging, and viral infections.

I. Hematologic Disorders

• All blood cells play a role in maintaining a healthy periodontium.
• White blood cells (WBCs) are involved in peripheral and inflammatory reactions.
• Disorders of blood elements profoundly affect the periodontium.
• Neutrophils are crucial in host defense against extracellular bacteria.
• Patients with neutrophil defects frequently experience oral mucosal ulceration, gingivitis, and/or periodontitis.
• Primary leukocyte disorders causing severe periodontal disease include leukemia, neutropenia, Chediak-Higashi syndrome, and early-onset periodontitis.
• Secondary leukocyte abnormalities emerge due to underlying systemic disease, including diabetes mellitus and AIDS.
• Leukemia is a malignant neoplasia of white blood cell precursors.
• Acute monocytic and myelocytic leukemias are the most prevalent types, marked by diffuse bone marrow replacement with immature leukemic cells, abnormal white blood cells circulating in the blood, and wide-spread infiltrates in organs.
• In acute leukemia, the gingiva appears bluish-red and cyanotic.
• Interdental papillae are enlarged, spongy, friable, and bleed with slight or spontaneous provocation.
• Bacterial infection leads to marginal gingiva ulceration and necrosis, pseudomembrane formation.
• Alveolar bone resorption and teeth looseness result from leukemic cell infiltration.
• Leukemic gingival enlargement isn't observed in edentulous or chronic leukemia patients.
• Gingival bleeding in leukemia stems from reduced red blood cell and platelet production (anemia and thrombocytopenia), respectively.
• Leukemic cell infiltration into the gingiva creates pockets, attracting plaque accumulation, and contributing to gingiva enlargement.

II. Associated with Genetic Disorders

• Familial and cyclic neutropenia involves periodic, monthly (3–5 days) decline in neutrophils during infancy and childhood.
• The gingiva may manifest as edematous, friable, and hyperplastic with foul odor.
• Deep periodontal pockets and generalized periodic alveolar bone loss (rapidly destructive periodontitis) characterize the disease.
• Gingiva regains normal appearance when neutrophil counts normalize.
• Down syndrome, a congenital disease caused by chromosomal abnormality (Trisomy 21), is marked by mental deficiency and growth retardation.
• Generalized periodontal disease is more prevalent in the lower anterior region, due partially to reduced resistance to infections and a defect in cell maturation and chemotaxis.
• Lazy Leukocyte Syndrome: defect in neutrophil chemotaxis, so neutrophils fail to migrate to tissue injury sites.
• Phagocytosis and intracellular killing aren't affected.
• Papillon-Lefèvre syndrome: autosomal recessive trait with hyperkeratotic skin lesions (palms and soles) and severe periodontium destruction, leading to early loss of deciduous and permanent teeth.

III. Hormonal Imbalances

• Diabetes Mellitus: A complex metabolic disorder characterized by chronic hyperglycemia, is crucial regarding periodontitis.
• Uncontrolled diabetes is associated with microvascular (retinopathy, nephropathy, neuropathy) and macrovascular (cardiovascular, cerebrovascular) diseases, increased susceptibility to infections, and poor wound healing.
• Oral manifestations of uncontrolled diabetes include diminished salivary flow (xerostomia, burning mouth/tongue), increased dental caries and periodontal disease.
• Increased glucose content in gingival fluid may elevate microorganisms.
• Advanced glycation end products (AGEs) thickens blood vessels, reducing gingival blood supply.
• Infections, impaired chemotaxis, phagocytosis, intracellular killing, and altered collagen synthesis occur due to hyperglycemia.
• AGEs render periodontium more vulnerable to degradation.
• Increased susceptibility to infection (candidiasis and periodontitis) due to hyperglycemia.
• Ketoacidosis, reduced phagocytic ability and chemotaxis; vascular wall disease, reduced blood flow and neutrophil mobilization, decreased oxygen tension.
• Hyperlipidemia affects macrophage function and cytokine release, contributing to poor wound healing.
• Bacterial pathogens include Capnocytophaga, anaerobic vibrios, actinomyces, Porphyromonas gingivalis, Prevotella intermedia, and Aggregatibacter actinomycetemcomitans.
• Diabetes may not cause gingivitis/periodontal pockets but worsens the response to local irritants, hastening bone loss and slowing post-therapy healing.
• Advanced periodontal disease (severe gingival inflammation, deep pockets, rapid bone loss, frequent abscess formation) often occurs, especially in diabetics with inferior oral hygiene.
• In type I diabetes, extensive periodontal destruction occurs initially around the first molars and incisors.
• Normal tissue responses, no caries or periodontal disease increase with proper diabetes control.

IV. Drug-Induced Disorders

• No drug has proven to initiate periodontal disease, but some medications impact periodontal tissues and responses to irritants.
• Phenytoin (Dilantin) often results in mild to moderate gingival enlargement, more common in younger patients and less observed over 40.
• Dihydropyridine (Nifedipine), a calcium channel blocker used to treat angina pectoris and hypertension, can cause gingiva overgrowth in 20% of cases, commonly affecting anterior teeth. No age/sex specific preference is noted.
• Cyclosporine, immunossupressant, displays increased correlation between administered dose/duration and severity of gingiva enlargement in 25% of cases.

V. Nutritional Disorders

• Nutrition's role in chronic periodontitis is debatable.
• Malnutrition indirectly influences by changing the existing disease rather than initiating it.
• Deficiency states don't affect inflammatory response in the absence of local triggers like plaque.
• Vitamin C is essential for collagen maintenance, cell respiration, and capillary integrity.
• Ascorbic acid deficiency may exhibit gingivitis changes and tooth mobility that usually don't improve with supplements unless existing condition triggers are removed.

VI. Psychosomatic Disorders

• Psychological disturbances affect periodontium.
• Lack of plaque control in psychologically disturbed patients frequently associates with gingivitis and periodontitis.
• Physiologic tissue balance can be directly affected by the autonomic nervous system.
• Habits that damage the periodontium (grinding, clenching) emerge due to psychological reasons.
• Stress increases adrenal hormone secretion (corticosteroids, catecholamines), impacting periodontal tissue and making it more susceptible to destruction, and having immunosuppressive effects.
• Additional variables can include eating habits, smoking, lack of sleep, etc.

VII. Aging

• Age and initial disease duration are essential factors in periodontal disease.
• Incidence and severity of periodontal disease increase with cumulative plaque effects over time, causing both incidence and severity to increase.

VIII. Viral Infections

• Acquired Immunodeficiency Syndrome (AIDS): HIV has a strong affinity for immune cells (T-helper lymphocytes, monocytes, macrophages, Langerhans cells), hindering the immune system, leaving patients prone to opportunistic infections and malignancies.
• HIV gingivitis: Characterised by a persistent linear easily bleeding erythematous gingivitis, localized or generalized, involving the marginal and attached gingiva.
• HIV periodontitis: Painful, rapidly progressive, necrotizing, ulcerative periodontitis (NUP) with notable interproximal bone loss. Exposed and necrotic alveolar bone occurs with subsequent sequestration.

Other Systemic Factors

• Hormonal fluctuations (puberty, pregnancy, menstruation, menopause) can cause hormonal imbalances leading to exaggerated gingival responses to irritant with inflammation, bluish-red discoloration, edema, and gingival enlargement frequently during mixed dentition. -Pregnancy affects previously inflamed areas without affecting healthy areas; increased gingival inflammation peaks during the second to eighth months of gestation then decreases after labor alongside hormonal decrease.

IX. Steroids

• Steroids are not found to be a direct initiator to periodontal disease or alveolar process.

Explore the impact of systemic factors on periodontal health, focusing on hematological disorders and their effects on the periodontium. This quiz examines the roles of blood cells, particularly white blood cells, in maintaining oral health and the implications of various disorders. Test your understanding of how these systemic conditions influence periodontal disease.