Influence of Systemic diseases on the Peridontium

Endocrine disorders

Endocrine disorders such as diabetes and hormonal change s associated with puberty and pregnancy are systemic conditions which adversely affect the periodontium.
Diabetes mellitus
Diabetes mellitus: is complex metabolic disorder characterized by chronic hyperglycemia due to diminished insulin production or impaired insulin action. Lipid and protein metabolism is altered as well. There are 2 type of diabetes: type1-IDDM, is caused by autoimmune destruction of beta cells in the pancreas. Type 2-NIDDM, cause by resistant to the insulin action
Oral Manifestations: dry and cracked mucosa, burning mouth and tongue, decrease salivary flow, alteration in microbial flora with predominance of Candida Albicans, increase rate of dental caries. Periodontal diseases in diabetic patients follow no distinct pattern. Severe gingival inflammation, deep perio pockets, severe bone loss, and frequent perio abscesses are often occur in diabetic patients.
The increase glucose content in gingival fluid and blood promote qualitative changes of bacteria that contribute to the severity of periodontal diseases. Subgingival flora is composed of: Capnocytophaga, anaerobic vibrios, and Actinomyces spicies. A.A, P. Gingivalis, and P. Intermidia are common in periodontal lesions of patients with diabetes. In patients with uncontrolled diabetes the functions of PMN’s and macrophages are impaired as a result the primary defense is diminished and plaque proliferation continues.
Collagen synthesis, maturation, and maintenance are decreased in patient with chronic hyperglycemia. The cumulative effect of altered cellular response, impaired tissue integrity and collagen metabolism play role in susceptibility of diabetic patients to infections and perio disease.
Female sex hormones:
The gingiva in puberty: hormonal changes in puberty cause exaggerated response of the gingiva to plaque; the symptoms include inflammation, bluish red color, edema, and gingival enlargement. In the adulthood the severity of gingival reaction decreases.
Gingival changes associated with menstrual cycle: hormonal imbalance during menstruation can cause gingival changes. The symptoms may include bleeding f the gums, tenderness, exudate for the inflamed gingiva, the salivary bacteria count is increased during menstruation and up to 14days earlier.
Gingival Disease in pregnancy: pregnancy itself does not cause gingivitis; it is caused by bacterial plaque. Hormonal changes during pregnancy exaggerate the response of the gingival tissue to the plaque. Increased level of progesterone cause dilation of gingival microvasculature and cause an increase in susceptibility to mechanical irritation. The severity of gingivitis during pregnancy is increased during second and third trimester. Clinical characteristics” ease of bleeding, bright red and bluish red color, edematous of marginal and interdental gingiva, formation of “tumor like masses” pregnancy tumor.
Hormonal contraceptives and the gingiva:
Hormonal contraceptives exaggerate the gingival response to the presence of the plaque.
Menopausal gingivostomatitis:
During menopause the level of estrogen decreases, as the result the gingivostomatitis can develop. The gingiva and oral mucosa are dry and shiny, bleed easily, burning sensation, abnormal taste (salty, peppery, or sour), and areas of ulceration.
Corticosteroid hormones:
Exogenous cortisone may have adverse effect on quality of the bone. The systemic administration of cortisone may result in development of osteoporosis of alveolar bone, capillary dilation, hemorrhage in periodontal ligament, and decrease number of collagen fiber.
Hyper secretion of parathyroid hormones can cause demineralization of skeleton, increase osteoclsis with proliferation of connective tissue in enlarged marrow spaces and formation of the bone cists. Oral changes may include malocclusion, tooth mobility, osteoporosis, whitening of PDL, absence of lamina dura, and radiolucent cist-like spaces filled with fibrous tissue, macrophages, and giant cells. Radiographically is ground like appearance of trabecular pattern

Hematological disorders:

All blood cells play important role in maintenance of healthy periodontium. White blood cells play role in inflammatory reactions and responsible for cellar defense against microorganisms. Red blood cells are responsible for gas exchange, normal homeostasis and nutrient supply. Disorder of any blood cells or blood-forming organs can have effect on periodontium.
Malignant neoplasias of WBC are characterized by replacement of bone marrow with leukemic cells, abnormal number of circulating immature WBC and widespread of infiltrates in liver spleen and lymph nodes.
Classification of leukemia: lymphocytic and myelocytic; acute with rapid progression, subaccute, and chronic.
In all leukemias the production of RBC, WBC, and platelets lead to anemia, leukopenia and thrombocytopenia.
Oral and periodontal manifestations of leukemia include: gingival enlargement, bluish, red, and cyanotic color of the gingiva, spontaneous bleedings, oral ulcerations and infections. Microscopically there is a diffuse infiltration of immature leukocytes in attached, marginal gingiva and connective tissue. The most common clinical finding in leukemic patients is gingival hemorrhage caused by thrombocytopenia.
Anemia is a deficiency of quantity and quality of the blood due to decreased number of erythrocytes and amount of hemoglobin. Anemia can result from blood loss, defective blood formation, or increased RBC destruction.
Pernicious anemia:
Tongue appears red smooth and shiny because of atrophy of papilla, pallor of the gingiva.
Iron deficiency anemia:
Glossitis, ulcerations of oral mucosa, and inducing dysphagia.
Sickle cell anemia:
Hereditary chronic hemolytic anemia occurs frequently in African-Americans. It is characterized by pallor, jaundice, weakness, rheumatoid manifestations, and generalized osteoporosis of the jaw with specific step-ladder alignment of the trabeculae.
Aplastic anemia:
Failure of bone marrow to produce erythrocytes caused by toxic drugs or leukemia. Oral changes include pallor of oral mucosa and susceptibility to infections.
Reduced platelet count due to lack of platelet production of increased loss of platelets. Thrombocytopenia purpura refers to purplish appearance of skin or oral mucosa and caused by decreased platelets, which can cause prolong clotting and bleeding tongue. Spontaneous bleeding, petechiae, and hemorrhage into the skin and oral mucosa are common. The gingiva is swollen, soft, friable, and bleeds spontaneously.
Leukocyte disorders:
Characterized by decreased level of neutrophils. If absolute neutrophil count is less than 1500 cells per microliter it is considered to be neutropenia. Causes: can be drug induced, genetic, and viral infections. It may be chronic or cyclic. Neutropenia can be life threatening if absolute neutrophil count decreases as low as 500.
Characterized by reduction in number of circulating granulocytes. The most common cause is drug idiosyncrasy. The onset of the disease can be accompanied by fever, general weakness and sore throat. The oral mucosa has isolated necrotic patches those are black and grey and demarcated form adjusted area. The gingival hemorrhage, increased salivation, and fetid odor are accompanied clinical features.
Lazy Leukocyte syndrome:
Characterized by severe microbial infections, neutropenia, and abnormal inflammatory response.
Leukocyte adhesion deficiency:
Rare genetic disorder diagnosed at birth. LAD result from inability to produce cell surface integrin, which is needed for leukocytes to adhere to the vessel walls at the site of the infection. As the result, bacterial infections are able to continue to destroy host tissue. Clinically: extremely acute inflammation and proliferation of gingival tissue with rapid distraction of bone, often result in early tooth loss.

Nutritional Disorders

*There are no nutritional deficiencies that cause gingivitis or periodontitis, but the presence of these deficiencies can exaggerate the symptoms of plaque-induced inflammation. There are however, nutritional deficiencies that produce changes to the oral cavity.

Vitamin A Deficiency:
The main function of vitamin A is to maintain the integrity of epithelial cells of the skin and mucous membranes. Vitamin A may play a role in protecting against microbial invasion due to the fact that the main function of epithelial cells is to provide a barrier against microorganisms. The absence of vitamin A can result in degenerative changes to the epithelial tissues, which results in keratinizing metaplasia.

Vitamin D Deficiency:
The main function of vitamin D is to provide adequate absorption of calcium from the GI tract and to maintain the calcium-phosphorus balance in the body. A vitamin D deficiency can cause rickets in children and osteomalasia in adults. There is no information that links vitamin D deficiency with periodontal disease. There are studies conducted on dogs that have shown vitamin D deficiency to be linked with osteoporosis of alveolar bone, uncalcified osteoid, failure of osteoid to resorb, reduction in width of PDL space, and distortion of growth pattern of alveolar bone.

Vitamin E Deficiency:
The main function of vitamin E is its antioxidant properties, which limits the amount of free radical reactions and protects cells from lipid peroxidation. Cell membranes are most damaged in vitamin E deficiencies. There are no links between vitamin E deficiency and oral disease in humans. Studies on rats have shown that systemic vitamin E accelerates wound healing.

B-Complex Deficiency:
The vitamin B complex includes thiamin, riboflavin, niacin, pyridoxine (B6), biotin, folic acid, and cobalamin (B12). Oral disease associated with vitamin B-complex is generally seen with a deficiency in multiple vitamins. Oral changes commonly seen with vitamin B complex deficiency are gingivitis, glossitis, glossodynia, angular cheilitis, and inflammation of the entire oral mucosa.

Thiamin Deficiency:
Also known as beriberi. Oral manifestations include hypersensitivity to the oral mucosa, minute vesicles on the buccal mucosa, under the tongue, or on the palate that simulate herpes, and erosion of the oral mucosa.

Riboflavin Deficiency:
Oral manifestations include glossitis, angular cheilitis, seborrheic dermatitis, and superficial vascularizing keratitis. In mild to moderate cases of deficiency, the tongue presents with a patchy atrophy of the lingual papillae and engorged fungiform papillae, which resemble pebble like elevations. In severe forms of the deficiency, the tongue presents with a flat dorsum, which is usually fissured.

Niacin Deficiency:
Early signs of niacin deficiency include glossitis and stomatitis. Other oral manifestations include gingivitis and NUG, usually in areas of local irritation.

Folic Acid Deficiency:
Oral manifestations in humans include generalized stomatitis, ulcerated glossitis, and angular cheilitis.

Vitamin C Deficiency:
Severe vitamin C deficiency, also known as scurvy, is characterized by defective formation and maintenance of collagen, impairment of osteoid formation, impaired osteoblastic function, increases capillary permeability, susceptibility to traumatic hemorrhages, and sluggishness of blood flow. Vitamin C deficiency may result in susceptibility to infections, impaired wound healing, bleeding swollen gingival, and loose teeth, and loss of periodontal bone.

Protein Deficiency:
Protein deficiency, also known as hypoproteinemia, is characterized by muscular atrophy, weakness, weight loss, anemia, leukopenia, edema, impaired healing, lymphoid depletion, and reduced ability to form certain hormones and enzymes systems. Studies on animals have shown a link between protein deficiency and degeneration of the connective tissue of the gingival and PDL, osteoporosis of the alveolar bone, impaired deposition of cementum, delayed wound healing, and atrophy of the epithelium of the tongue.

Immunodeficiency disorders

An immune deficiency resulting from inadequate antibody production, caused by a deficiency in B cells. This immune deficiency can be both congenital or aquired. Congenital agammaglobulinemia is caused by an X-linked recessive gene, which means only males have this disease. This gene is responisible for the developmend of B cells. Without B cells, people lack lymphoid tissue and plasma cells so antibodies cannot be developed. In acquired agammaglobulinemia, is caused by failure of B-lymphocytes differentiation into plasma cells. Aggamaglobulinemia presents with recurrent bacterial infections and patients are more susceptible to periodontal infections, and young children who suffer from this disease often present with aggressive periodontitis.

Acquired Immunodeficiency Syndrome:
Characterized by opportunistic infections, such as oral candidasis, hairy leukoplakia, kaposi’s sarcoma, oral hyperpigmentation, and atypical ulcers. Both NUG and NUP are more prevalent in patients who are immunocompromised, including destructive periodontal lesions and malignancies.

Cardiovascular disorders

Congenital Heart Disease

Congenital Heart disease occurs about 1% in live births. If left untreated it can be fatal. Cardiac defect involves the heart the adjacent vessels or a combination of both. One of the most striking feature is cyanosis which is caused by shunting of deoxygenated blood from the right to left which in return the of poorly oxygenated blood to the systemic circulation. Patient with congenital heart defects are at risk of the development of infective endocarditis. Prophylactic antibiotic should be evaluated before any dental treatment. Clinical features include cyanosis of the lips and oral mucosa, delay eruption of both deciduous and permanent dentition, increase positional abnormalities and enamel hypoplasia. The teeth have a bluish white appearance, severe caries and periodontal disease however the dental disease is associated with poor oral hygiene rather than the disease itself.
Tetralogy of Fallot :
Is a characteristic of four cardiac defects
1. Ventricular septal defect
2. Pulmonary stenosis
3. Malposition of the aorta to the right
4. Compensatory right ventricular enlargement.
Clinical features include cyanosis, audible heart murmurs and breathlessness. Oral changes include purplish red discoloration of the lips and gingiva. Severe marginal gingivitis and periodontal destruction the tongue appears coated fissured and edematous with extreme reddening of the fungiform and filiform papillae.
Eisenmenger’s Syndrome:
Greater blood flow from the strongest left ventricle to the right ventricle( backward flow) through the septal defect causing an increase of pulmonary blood flow which leads to progressive pulmonary fibrosis small vessel occlusion and high pulmonary vascular resistance. Increase in cyanosis over many years can lead to cardiac failure. Clinical features are much less severe cyanosis of the lips, cheeks, and buccal mucous membranes are often seen in patients and severe generalized periodontitis.