title: Local cell proliferation in rheumatoid synovial tissue: analysis by cyclin expression.
abstract: The immunohistochemical staining of cyclins was done to evaluate the proliferating cells in synovial tissue of rheumatoid arthritis (RA). Synovial specimens obtained from 18 patients with RA, 12 with osteoarthritis (OA), and 8 with traumatic arthritis (TA) were used for immunostaining of cyclins A and B1 and proliferating cell nuclear antigen (PCNA). The positive cells in lining layer (synoviocytes) and sublining layer (lymphoid and nonlymphoid cells) were counted. Moreover, the relationship between the frequency of their positive cells and clinical data of RA patients was analyzed statistically. In general, cyclin-A-, cyclin-B1-, and PCNA-positive cells in RA were more frequently observed as compared with those in OA and TA. Significant differences were found between RA and OA or TA in cyclin-A-, cyclin-B1-, and PCNA-positive sublining lymphoid cells, between RA and OA or TA in cyclin-B1- and PCNA-positive sublining nonlymphoid cells, and between RA and OA in cyclin-B1-positive synoviocytes. The ratio of cyclin-A- or cyclin-B1-positive cells per PCNA-positive cells was significantly higher in sublining lymphoid cells in RA than TA and in sublining lymphoid and nonlymphoid cells of RA than OA or TA. Moreover, a better relationship was observed between the frequency of cyclin-A-positive synoviocytes and age and between cyclin-A-positive sublining nonlymphoid cells and duration of the disease in RA patients. Our data demonstrated clearly that synoviocytes, as well as sublining lymphoid and nonlymphoid cells, could divide in situ, and more frequent cell division and a higher ratio of cyclin-A- or cyclin-B1-positive/PCNA-positive sublining cells could occur in RA than OA and TA.
authors.affiliation: Department of Orthopedic Surgery, Rheumatic Center, Niigata Prefectural Senami Hospital, 2-4-15, Senami-Onsen, Murakami, 958-8555, Niigata, Japan. xkffg160@yahoo.co.jp
authors.forename: Chikako
authors.initials: C
authors.lastname: Takahashi Tohyama
authors.forename: Mitsunori
authors.initials: M
authors.lastname: Yamakawa
authors.forename: Akira
authors.initials: A
authors.lastname: Murasawa
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Nakazono
authors.forename: Hajime
authors.initials: H
authors.lastname: Ishikawa
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000378:metabolism; D001168:Arthritis / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D001172:Arthritis, Rheumatoid / Q000378:metabolism* / Q000473:pathology*; D049109:Cell Proliferation; D019925:Cyclin A / Q000378:metabolism; D019926:Cyclin B / Q000378:metabolism; D056744:Cyclin B1; D016213:Cyclins / Q000378:metabolism*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D007596:Joints / Q000293:injuries; D008297:Male; D008875:Middle Aged; D010003:Osteoarthritis / Q000378:metabolism / Q000473:pathology; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D013194:Staining and Labeling; D013583:Synovial Membrane / Q000378:metabolism* / Q000473:pathology*; D013997:Time Factors; D014947:Wounds and Injuries / Q000150:complications
chemical_list: C534699:CCNB1 protein, human; D019925:Cyclin A; D019926:Cyclin B; D056744:Cyclin B1; D016213:Cyclins; D018809:Proliferating Cell Nuclear Antigen