Inflammation is the primary pathological feature of periodontal disease Host susceptibility accounts for differences in the severity of periodontal disease from one individual to another Susceptibility to periodontitis influenced by a number of factors, including systemic diseases and conditions. Presence of chronic inflammatory periodontal disease may significantly affect systemic conditions such as coronary heart disease, stroke glycaemic control or pregnancy outcomes.
The relationship between periodontal diseaseand systemic health is thus a two-way road,with systemic host factors acting locally toreduce resistance to periodontal destruction,and the local bacterial challenge generatingwidespread effects with the potential to induceadverse systemic outcomes.
Certain systemic disorders and conditions alter host tissues and physiology, which may impair host barrier integrity and host defence to periodontal infection, resulting in more destructive disease. The interrelationships between periodontal infections and host defence are complex. Environmental, physical, and psychosocial factors have the potential to alter periodontal tissues and the host immune response, resulting in more severe periodontal disease expression. These disorders and conditions do not initiate periodontitis, but they may predispose, accelerate, or
Endocrine disorders and hormonal changes Haematological disorders and immune deficiencies Stress and psychosomatic disorders Nutritional influences Other systemic conditions
Diabetes mellitus Female sex hormones Corticosteroid hormones Osteoporosis Hyperparathyroidism
Reduction in defence mechanisms and increased susceptibility to infections Higher prevalence and severity of periodontal disease in diabetics than in non-diabetic persons with similar local factors. Findings include ↑LOA ↑BOP ↑tooth mobility.
A, Adult with diabetes (blood glucose level 400 mg/dl). Note the gingival inflammation, spontaneous bleeding, and oedema. B, Same patient as in A after 4 days of insulin therapy (blood glucose level <100 mg/dl). The clinical periodontal condition has improved without local therapy. C, Adult patient with uncontrolled diabetes. Note the enlarged, smooth, red gingiva with initial enlargement in the anterior area. D, Lingual view of the right mandibular area in same patient as in C.E, Suppurating abscess on the buccal surface of the maxillarypremolars in a patient with uncontrolled diabetes.
The Diabetic patient.A, Gingival inflammation andperiodontal pockets in 34-year-oldpatient with diabetes of longduration.B, Extensive, generalized bone loss inthe patient shown in A.
Gingivitis in puberty, with oedema, discoloration, and enlargement
A, Marginal B, Localized,gingivitis and easily incipient gingivalbleeding gingiva in a enlargementwoman 5 months between thepregnant. maxillary central and lateral incisors in a woman 4 months pregnant. C, D, Extensive Generalized gingival gingival enlargement enlargement localized on the of the papilla buccal surfaces of and gingival lower molars in a margins on pregnant woman. the facial surface of the maxillary incisors in a pregnant woman.
Immuno-suppressive therapy (exogenous steroids) May affect bone density and physiology Widespread effects on the periodontium Stress- induced (endogenous) cortisol may produce some effects on periodontium by diminishing the immune response.
Generalized demineralization of the skeleton Proliferation of the connective tissue in the enlarged marrow spaces Formation of bone cysts and giant cell tumours Oral changes include malocclusion and tooth mobility, radiographic evidence of alveolar osteoporosis with closely meshed trabeculae widening of the periodontal ligament space absence of the lamina dura radiolucent cyst-like spaces
Secondary hyperparathyroidism in 35-year-old woman with advanced kidneydisease. This periapical radiograph showsground-glass appearance of bone and lossof lamina dura. (Courtesy Dr. L. RoyEversole, San Francisco.)
A, Periapical, and B, occlusal,radiographic views of brown tumoursin patient with hyperparathyroidism.(Courtesy Dr. L. Roy Eversole, SanFrancisco.)
Leukaemias Anaemias Thrombocytopaenia Hypo/agammaglobulinaemia Defects of leucocyte (PMNL and lymphocyte) formation Antibody deficiency disorders
Leukemic infiltration causinglocalized gingival swelling of theinterdental papillae.
Acute myelocytic leukaemia.A, View of patients face.Note the elevated, flatmacules and papules(leukaemia cutis) on the rightcheek. B, Close-up view of skin lesions.C, Intraoral view showingpronounced gingivalenlargements.D, Occlusal view of upperanterior teeth. Note themarked enlargement in boththe facial and the palatalaspects. (Courtesy Dr. Spencer
A, Anterior view of patient with acutemyelocytic leukemia. Interdental papillaeare necrotic with a highly inflamed andswollen base.B, Palatal view demonstrating extensivenecrosis of interdental and palatal tissue.
Diffuse pallor of gingiva in patient withSmooth tongue in anaemia. Thepatient with discoloured, inflamedpernicious anaemia. gingival margin stands out in sharp contrast to the adjacent pale, attached gingiva.
Thrombocytopenic purpura.A, Hemorrhagic gingivitis in patient withthrombocytopenic purpura. Spontaneous bleeding from the gingival sulcus in patientB, Marked reduction in severity of gingival with thrombocytopenia.disease after removal of surface debris and careful Normal coagulation isscaling. evident by the large clot that forms in the mouth. However, platelets are inadequate to establish haemostasis.
Pre-pubertal periodontitisA, Clinical presentation of 10-year-old male withcyclic neutropenia and agammaglobulinemia. Notethe severe erythema and migration of teeth causedby loss of bone support.B, Panoramic radiograph demonstrating severe boneloss around all permanent teeth that have eruptedinto the oral cavity.
Dentition of 17-year-old boy withPapillon-LefèvreSyndrome. The Severe periodontalmissing teeth were destruction in 14-year-oldexfoliated. patient with Down’s Syndrome.
Documented relationship between stress and acute necrotizing ulcerative gingivitis (ANUG) Connection between psychological conditions such as stress and other forms of periodontal disease (e.g., chronic periodontitis) has been difficult to establish. The types of stress that lead to periodontal destruction appear to be more chronic or long term, and less likely to be controllable by the individual.
Psychosocial stress, depression and coping Stress-induced immuno-suppression Influence of stress on periodontal therapy outcomes Self-inflicted injury
Type of stress Ability and manner of coping of the with stress Correlate with destructive periodontal disease. Emotional coping methods appear to render the host more susceptible to the destructive effects of periodontal disease than do practical coping methods.
Depression might have a negative effect on periodontal treatment outcomes Non-responsive patients generally have a more passive, dependent personality. Non-responders often report more stressful life events in their past.
Impact the periodontal health through changes in the individuals behaviour Complex interactions among the nervous, endocrine, and immune systems. Individuals under stress may have poorer oral hygiene, may start or increase clenching and grinding of their teeth may smoke more frequently. Individuals under stress may be less likely to seek professional care.
Neurotic habits, such as grinding or clenching the teeth, nibbling on foreign objects (e.g., pencils, pipes), nail biting, smoking, are all potentially injurious to the teeth and the periodontium. Self-inflicted gingival injuries have been described in both children and adults
Severe gingival recession of all lower incisors, which was discovered under general anaesthesia in an uncooperative, institutionalized adult with mental impairment. The patient was known topace around the home with all four fingers inside his lower lip.
There are no nutritional deficiencies that by themselves can cause gingivitis or periodontitis. Nutritional deficiencies may accentuate the effects of plaque-induced inflammation in susceptible individuals. There are nutritional deficiencies that produce changes in the oral cavity. These changes include alterations of tissues of the lips, oral mucosa, gingiva, and bone. These alterations are considered to be periodontal and oral manifestations of nutritional disease.
Genetic (inherited) conditions e.g.hypophosphatasia Congenital heart disease Metal intoxication
Rare familial skeletal disease characterized by rickets, poor cranial bone formation, craniostenosis, and Premature loss of primary teeth, particularly the incisors and reduced cementum formation. In patients with minimal bone abnormalities, premature loss of deciduous teeth may be the only symptom. In adolescents, this disease resembles localized "juvenile" (aggressive) periodontitis.
Fallot’s tetralogy Eisenmenger’s syndrome
Extensive marginal Characteristic clubbing of theinflammation with ulcero- fingers in adolescent patientnecrotic lesions and with Tetralogy of Fallot,periodontal destruction consistent with untreated congenital cyanotic heart disease.The apparent increase in dental disease may be attributed to poor oral hygieneand a general lack of dental care rather than a disease-related aetiology.
The ingestion of metals such as Mercury, Lead, and Bismuth in medicinal compounds and through industrial contact may result in oral manifestations caused by either intoxication or absorption without evidence of toxicity.
A, Linear discoloration of thegingival in relation to localirritation in a patient receivingbismuth therapy.B, Biopsy specimen showingbismuth particles engulfed bymonocytes/macrophages.