influenceofsystemiccondition on periodon

Influence of systemic condition on periodontium

1. Influence of Systemic disorders on Periodontium (Hematologic Disorders And Immune Deficiencies) Bds 3 rd year lecture Dr. Akanksha Singh {Senior Lecturer} Department of periodontology Date: 13.06.24

2. CONTENT Introduction Hematological disorders Immune deficiencies Suggested reading University questions

3. INDEX Introduction Endocrine Disorders & Hormonal Changes Diabetes Mellitus Female Sex Hormones Hyperparathyroidism Hematologic Disorders & Immune Deficiencies Leukemia Anemia Thrombocytopenia Antibody Deficiency Disorders Leukocyte ( Neutrophil ) Disorders Genetic Disorders Chédiak -Higashi Syndrome Lazy Leukocyte Syndrome Leukocyte Adhesion Deficiency Papillon-Lefèvre Syndrome Down Syndrome

4. INTRODUCTION Systemic diseases, or conditions themselves do not cause periodontitis . Systemic diseases alter host tissues & physiology & predispose, accelerate or increase the progression of periodontal disease. A variety of systemic diseases and conditions can affect the course of periodontitis or have a negative impact on the periodontal attachment apparatus.

5. There are many diseases and conditions that can affect the periodontal tissues either by 1) Influencing the course of periodontitis Affecting the periodontal supporting tissues independently of dental plaque biofilm -induced inflammation. These include: 1a. Mainly rare diseases that affect the course of periodontitis eg ., Papillon Lefevre Syndrome, leucocyte adhesion deficiency, and hypophosphatasia They have major impact resulting in the early presentation of severe periodontitis .

6. 1b. Mainly common diseases and conditions that affect the course of periodontitis e.g., diabetes mellitus The magnitude of the effect of these diseases and conditions on the course of periodontitis varies . They result in increased occurrence and severity of periodontitis . It is as an important modifying factor rather than as a distinct disease. 2. Mainly rare conditions affecting the periodontal supporting tissues independently of dental plaque biofilm induced inflammation e.g., Squamous cell carcinoma, Langerhans cell histiocytosis This is a more heterogeneous group of conditions which result in breakdown of periodontal tissues . Some of the conditions may mimic the clinical presentation of periodontitis .

7. HEMATOLOGIC DISORDERS AND IMMUNE DEFICIENCIES

8. Primary (inherited) Secondary (acquired) -caused by Immunosuppressive drug therapy Pathologic destruction of the lymphoid system. e.g.Leukemia , Hodgkin’s disease, lymphomas, and multiple myeloma

9. Leukemia Malignant neoplasias of WBC precursors characterized by : (1) Diffuse replacement of the bone marrow with proliferating leukemic cells (2) Abnormal numbers and forms of immature WBCs in the circulating blood (3) Widespread infiltrates in the liver, spleen, lymph nodes, & other body sites According to the Cell type- lymphocytic or myelogenous . According to their evolution, acute, (rapidly fatal), subacute , or chronic .

10. Classification

11. Periodontium in Leukemic Patients Leukemic infiltration: Gingival Enlargement Highest incidence in Acute monocytic leukemia (66.7%). Not in edentulous patients or in chronic leukemia. Clinically, the gingiva appears bluish red and cyanotic , with a rounding and tenseness of the gingival margin

12. Carranza , 13 th ed SA

13. Oral Bleeding Common and early finding in leukemic patients, even in the absence of clinically detectable gingivitis . Also manifest in the skin and throughout the oral muco sa , where petechiae are often found, with or without leukemic infiltrates.

14. Oral Ulceration and Infection Discrete, punched-out ulcers penetrating deeply into the submucosa and covered by a firmly attached white slough . Common sites - buccal mucosa & palate . Patients with past history of herpes virus infection may develop recurrent herpetic oral ulcers .

15. Anemia Deficiency in the quantity or quality of the blood manifested by a reduction in the number of erythrocytes and in the amount of hemoglobin. Etiology- Blood loss, defective blood formation, or increased blood destruction. Classified according to cellular morphology and hemoglobin content as Macrocytic hyper-chromic anemia (pernicious anemia) Microcytic hypochromic anemia (iron deficiency anemia) Sickle cell anemia Normocytic-normochromic anemia (hemolytic or aplastic anemia )

16. Pernicious anemia – Tongue changes in 75% of cases M arked pallor of the gingiva Iron deficiency anemia - Induces similar tongue and gingival changes. Plummer-Vinson syndrome- A syndrome consisting of glossitis and ulceration of the oral mucosa and oropharynx, inducing dysphagia in patients with Iron deficiency anemia.

17. Sickle cell anemia Hereditary form of chronic hemolytic anemia. Occurs exclusively in blacks. Periodontal infections may precipitate sickle cell crisis. Oral changes: Generalized osteoporosis of the jaws. Stepladder alignment of the trabeculae of the interdental septa. Pallor & yellowish discoloration of the oral mucosa.

18. Thrombocytopenia Secondary to some known etiologic factor Aplasia of the marrow , as in leukemia Replacement of the marrow by tumor Destruction of the marrow by irradiation or by drugs such as benzene, aminopyrine , and arsenical agents Low platelet count A prolonged clot retraction and bleeding time Normal or slightly prolonged clotting time Condition of reduced platelet count that results from either a lack of platelet production or an increased loss of platelets.

19. Clinical Features of Thrombocytopenia Spontaneous bleeding into the skin or from mucous membranes. Petechiae & hemorrhagic vesicles - palate, tonsillar pillars, & the buccal mucosa. Gingivae are swollen , soft , & friable show abnormal response to local irritation.

20. Antibody Deficiency Disorders Agammaglobulinemia Results from a deficiency in B cells. T-cell function remains normal. Congenital (X-linked or Bruton's agammaglobulinemia ) X –linked recessive gene ( bruton’s tyrosine kinase ). The gene is responsible for B-cell development so production of antibodies is deficient.

21. 2. Acquired or late-onset agammaglobulinemia /common variable immunodeficiency disease (CVID) Onset of recurrent bacterial infections in the 2 nd & 3 rd decades of life. Basic immunological defect is failure of B-lymphocytes differentiation into plasma cells . Enlarged spleen and swollen glands or lymph nodes. Autoantibodies against their blood cells. Cause unknown ., Not genetic, Aggressive periodontitis is a common finding.

22. Oral manifestation : Acute gingival inflammation of both primary and permanent dentitions. Gingival proliferation Extremely acute inflammation Rapid destruction of bone Recession Tooth mobility Pathologic migration Early tooth loss Cases of periodontal disease that are attributed to LAD are rare. They begin during or immediately after the eruption of the primary teeth.

23. Leukocyte (Neutrophil) Disorders Neutropenia Caused by diseases, medications, chemicals, infections, idiopathic conditions, or hereditary disorders. Chronic or cyclic Classification based on the Absolute Neutrophil Count (ANC) measured in cells per micro liter of blood: Mild neutropenia : 1000 to 1500 cells/ μ l Moderate neutropenia : 500 to 1000 cells/ μ l Severe neutropenia : less than 500 cells/ μ l

24. Agranulocytosis More severe neutropenia involving neutrophil , basophils & eosinophils ( ANC <100 cells/ μl ) . Characterized by reduction in number of circulating granulocytes. Leads to severe infection ( eg.ulcerative necrotizing lesions of the oral mucosa, skin). Most common Causes- Drug idiosyncrasy ( unexplained). G enerally acute , may be chronic or periodic with recurring neutropenic cycles ( e.g , cyclic neutropenia).

25. Clinical Features : Onset: fever, malaise, general weakness, & sore throat. Ulceration in the oral cavity( oropharynx ), & the throat is characteristic. Absence of a notable inflammatory reaction is a striking feature. Mucosa : isolated necrotic patches (black & gray) ,sharply demarcated from the adjacent uninvolved areas. Gingival hemorrhage, necrosis, increased salivation, & fetid odor. With cyclic neutropenia , the gingival changes recur with recurrent exacerbation of the disease.

26. Carranza, 11 th ed A : Clinical presentation of periodontal condition B: Panaromic radiograph demonstrating severe bone loss around all the erupted permanent teeth . Fig: Aggressive periodontitis in 10 year old male with cyclic neutropenia & agammaglobulinemia

27. GENETIC DISORDERS

28. Chediak -Higashi Syndrome Mostly affect melanocytes, platelets, & phagocytes. Causes partial albinism, mild bleeding disorders, & recurrent bacterial infections. Neutrophils contain abnormal, giant lysosomes . Oral findings : severe gingivitis, ulcerations of the tongue and buccal mucosa. Early onset periodontitis leading to premature loss of both deciduous & permanent dentitions.

29. Lazy Leukocyte Syndrome Neutropenia Defective chemotactic response by neutrophils and an abnormal inflammatory response. Clinical features : Recurring infections due to both a deficiency in neutrophil chemotaxis and a systemic neutropenia . Oral manifestations: Painful stomatitis, gingivitis, recurrent ulcerations of the buccal mucosa & tongue. Periodontitis progressing to the point of advanced alveolar bone loss & tooth loss has been reported.

30. Leukocyte Adhesion Deficiency (LAD) An inherited disorder ( autosomal recessive pattern : chromosome 21q22.3). Involves a deficiency in cell surface antigen CD18. L eukocytes cannot adhere to the vessel wall at the site of infection , cannot migrate to the site of infection . Extremely acute inflammation and proliferation of the gingival tissues with rapid destruction of the bone . Frequent respiratory tract infections ,sometimes otitis media. An early tooth loss ( primary & the permanent teeth ).

31. Papillon–Lefèvre Syndrome Occur in siblings, male and females are equally affected . Mutations in the cathepsin C gene, on chromosome 11 Primary teeth lost by 5-6 years of age. Permanent dentiotion erupts normally but lost within a few year . By age of 15 years, patients are usually edentulous. Microscopic features: Marked chronic inflammation Predominant plasma cell infiltrate Considerable osteoclastic activity and lack of osteoblastic activity Alterations in cementum

32. Hyperkeratosis of skin Early tooth loss and severe bone loss around the remaining teeth Carranza, 13 th ed SA

33. Down Syndrome Congenital disorder due to Trisomy 0f Chromosome 21 Mental deficiency and growth retardation Prevalence of periodontal disease is high (almost 100% of patients younger than 30 years ). Oral hygiene is poor, the severity of periodontal destruction exceeds that explainable by local factors alone. Deep periodontal pockets with substantial plaque accumulation & moderate gingivitis. Impaired Action of immune regulatory gene ( poor PMN functions)

34. Carranza, 13 th ed SA

35. REFERENCES

36. Carranza FA, Newman MG., Takei HH, Klokkevold PR.Carranza’s Clinical Periodontology : ed 11 th .2011; 206-209. Carranza FA, Newman MG, Takei HH, Klokkevold PR.Carranza’s Clinical Periodontology : ed 13 th south asian . 2018; 721-815. American Diabetes Association. 2. Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes-2020. Diabetes Care. 2020 ; 43 (1): S14 -31.

37. LINK TO VIDEOS https://www.youtube.com/watch?v=lKi-O9DxXZM

38. SUGGESTED READING Clinical periodontology; Carranza 11 th edition, 13 th edition & 14 th edition

39. UNIVERSITY QUESTION Influence of hematological disorders on periodontium

40. Thank You