Clinical Mucosal Immunology

Transcription

1 Clinical Mucosal Immunology

2 Natural caries immunology in human It is sure, there is natural anti-caries immunity in human. Persons with low caries frequency have high anti-s.mutans IgG antibody level in the circulation, while in high caries frequency this level is low. This is not true in other cariogen bacteria such as Lactobacillus casei, L. viscosus and Actinobacillus viscosus.

3 Immunology of the Periodontium

4 Classification of Periodontits can be found in the University book of Prof. I. Gera Periodontlology 700 types of bacteria can be shown out in Periodontal disease. About 50% of these bacteria which closely connect to this disease: Porphyromonas Gingivalis, with Chronic Periodontitis, and Actinobacillus Actinomycetemcomit- tans with Aggressive Periodontitis.

5 Chronic Periodontitis

6 Aggressive Perodontitis

7 Provetella Intermadie and Spirochetes can be found in Acute Necrotizing Ulcerative Gingivitis. Capnocytophages can be found in the Periodontitis of immune compromised patients.

8 Culture of Aggrigatobacter Actinomycetem- comittans

9 Culture of Porphyromonas Gingivalis

10 Culture of Fusobacterium Nucleatum

11 The product of periopathogene bacteria ex.. leuctoxin from A.a. or capsel antigen of other periopathogene bacteria and enzymes destroying the bone and connective tissue such as: hydrolytic enzymes: phospholipase, collagenase, hyaluronidase and reductive materials: ex.. mercaptan. Against of the many destroying factors it is a herd, that not the total population have Periodontitis

12 There is a higher antibody titer against Gramnegative bacteria in the Periodontitis patients sera, than in the healthy population, which increase with the severity of the disease. By this way the antibody titer of a Periodontitis patients reflect the severity of the disease.

13 The antibody titer of the Gingival Crevice Fluid (GCF) in generally higher, than the serum titer, this means local production. It is not clear this increased titer is a part of the pathogenesis, or the result of the continuous antigen presence.

14 Chronic periodontitis

15 In chronic Periodontitis increased titer has been found against P. Gingivalis, while the antibody titer against Provetella Intermedia increased rather in ANUG. Antibodies and opsonising materials have been shown out in the GCF, but only in human. Antibody against P. Gingivalis impend the bacterial colonization at least for a year. This suggest immunological techniques against the oral flora seems to be a good method to prevent Periodontitis.

16 Steps of the development of Chronic Periodontitis Not all Gingivitis become Periodontitis, but all Periodontitis are preceded by Gingivitis. There are four steps in the development of Periodontitis. Initial lesions Early lesions Developed lesions Advanced lesions It depends on the quantity of plaque

17 More information about Periodontal Immunology can be found in the Books of PERIODONTOLOGY

18 Oral Medicine Immunological point of wiev

19 At the last decade there was a big progression in understanding of interaction between basal membrane antigens and adhesion molecules. These interactions have effect on cellular processes such as: proliferation, differentiation, and apoptosis. The importance of adhesion molecules were recognized in blistering and erosive oral diseases.

20 Adhesion molecules in mucosal dermatoses Dermatoses Some pemphigoid forms Target antigen bullous pemphigoid Target antigen benign mucosal pemphigoid Linear IgA dermatoses Pemphigus Skin Mucosa Erythaema exudativum multiforme Adhesion molecule target. Laminin BPAG1 (BP230 50%) BPAG2 (BP180 50%) IV type collagen DSG1 DSG3 Desmoplacine

21 Basalis keratinocyta Plasma membran Hemidesmosomális plakk cytosceleton E p it h e li u m BPAG1 NH2 4 6 integrin Lamina lucida LAD1 NC16A Laninin 5 BPAG2 Basalis Mem-brán Lamina densa COOH Extracelluláris mátrix Horgonyzó plakk VII. Típusú collagén Kötő szövet

22 Pemphigoid The autoantibodies are able to suffer the interaction between laminin 5 and 6, by this way the integrity of basal membrane. PEMPHIGOID is a blistering disease of the skin or oral mucosa. Its two antigens BP230 and BP180 was recovered in Both are the part of hemidesmosomes.

23 The BPAG2/Bp180 comes from the VII. collagen, it is a transmembrane molecule differ from the ά 6 β 4 integrin, which is also a part of hemidesmosomes. The anchoring fibers are built up by VII. collagen too, and they three dimensional form bind to basal membrane to the underlying connecitve tissue.

24 Benign mucosal Pemphigoid

25 Histological picture of a case Mucosal Pemphigoid

26 BPAG1 (IgG1 type) autoantibody in a case of Mucosal Pemphigoid

27 Aphthous Oral Ulcer Immunological Aspects

28 The three forms of RAS Recurrent aphthous ulcer (Mikulicz) Aphthous Oral Ulcers Herpetiform ulcers (Cooke) Periadenitis mucosae necrotica recurrens (Sutton)

29 Aphthous Ulcer I. Recurrent aphthous ulcer (Mikulitz and Kümmer 1898) Autoantibodies against the oral mucosa can be shown in the circulation % of the total aphthous disease cases. It heal spontaneously in days without scar.

30 Aphthous Ulcer II. Periadenitis necrotica recurrent mucosae oris (Sutton.1911) Autoantibodies against the oral mucosa can be shown. 5% of the total disease It heals in 40 days with scar.

31 Aphthous Ulcer III. Herpetiform ulcer (Cooke.1960) It can develop in any place in the oral cavity There is no autoantibody against the oral mucosa 20-25% of the total disease It heal without scar

32 Aetiological factors They could be congenital, natural hypersensitivity bent, social, psychological, endocrine factors, microbial and chemical constituents of the food. Hematological deficiency diseases (iron, folic acid, B 12 ) can help to develop erosions on the mucosal surfaces.

33 In the aphthous oral ulcer anti-mucosal autoantibodies and cytotoxic lymphocytes and HSP can be shown in the patients. This suggest that the aphthous oral ulcers are introduced by a microbial HSP, which stimulate the mucosal Langerhans cells to develop autoreactive T cell clones.

34 According to the literature viruses play a smaller role in the development of the disease. By DNA hybridizing technique herpes simplex virus (HSV1) homologs was shown out in a lot of aphthous oral ulcer patients.

35 Candidasis Immunological aspects of the diseases

36 The Candida genus (yeast) have two forms: capsulated and filamentary. They can be found as saprophytes in 40% of the oral cavity in the total population, about 800/ml saliva. If the infection develop this number increase to /ml saliva. This infection frequently develop in immune compromised, xerostomia, immunosuppressive drug takers, and denture holders.

37 The pathogenic forms of Candida Albicans Crusei Glabarata Tropicalis Parapsilosis Dubliniensis (mainly in immunecompromised patients, in HIV).

38 Candidasis in immune compromised patient

39 Acute atrophic Candidasis Develop as a result of antibiotic therapy. This is a reaction if the normal flora decrease in the oral cavity. The erythematous patches occupy a big area as erythematous stomatitis and depapillation of the tongue.

40 Chronic atrophic Candidasis (Denture Stomatitis) Frequently symptomless, it could be present as a diffuse erythema or inflammation where the denture cover the palatal area. This disease is the colonization of the Candida on the denture surface.

41 Chronic hyperplastic Candidasis (Papillomatosis palati) Develop rather in adolescent or elder patients. It is a chronic nodular form of the disease. And this is the invasive form of the disease caused by the filamentary form of the fungi. If it combined with leukoplakia it has high risk for malignant transformation.

42 Acute pseudomembranous Candidasis (thrush) Frequent disease in mainly newborn or elder persons with decreased immune responsiveness. The white patches easily wipeable (under it easy bleeding). The white patches contain: Candida filaments and sporules, epithelial and PMN cells. The disease in HIV infected patients are chronic.

43 Theoretically siga and serum IgG translocating through the mucosal epithelium and the delayed type immunity also play role in the mucosal response of the Candida infection.

44 Chronic Mucocutan Candidasis In this disease severe T cell functioning deficiency has been described together with other humoral immunological deficiencies. But it is not clear the immunodeficiency is a primary or a secondary reaction.

45 Lichen Oris

46 Lichen Ruber Planus It can develop not only in the oral cavity, but on the skin and genital region. This is a so called MUCOCUTAN disease. This disease can develop in any part of the oral mucosa and has different clinical forms. The efflorescence is PAPULA.

47 Papular form

48 Reticular form

49 Plaque-like form

50 Bullous form

51 Erosive form

52 Atrophic form

53 Very few data can be found about the autoimmune origin of Lichen ruber planus, the degeneration developing in the basal epithelial layer and the lymphocyte infiltration among them suggest the importance of immunological occurrence in the pathogenesis of the disease.

54 The increased number of Langerhans cells in the early stage showing the importance of antigen presenting cells and develop contacts with the intra epithelial lymphocytes. The antigen causing Lichen Oris not clear until now, but lichen specific epidermal antigen were shown in the basal and spongy cell layer.

55 Infiltrating lymphocytes in the connective tissue are mainly CD25+ activated T cells, but CD8+ cytotoxic/suppressor lymphocytes also can be found among them. In lichenoid reactions the intraepithelial antigen could be virus infection or any took drugs.