title: The mandibular cartilage metabolism is altered by damaged subchondral bone from traumatic impact loading.
abstract: Osteoarthritis (OA) in the temporomandibular joint (TMJ) is a degenerative disease caused by excessive external loading. Recently, it was reported that the damage in the mineralized subchondral bone caused by traumatic impact-loading is responsible for the initiation and progression of cartilage degeneration. Thus far, we have hypothesized that cytokines released from damaged subchondral bone from impact-loading affect the cartilage catabolism under pathological conditions. An impactor of 200 gw was dropped onto the top of a porcine mandibular condyle. After organ culture for 2 days, we investigated the association between the subchondral bone and cartilage using histological and biochemical experiments. The impact-loading induced the expression of IL-1beta immunohistochemically and prominently up-regulated IL-1alpha and IL-1beta mRNA levels in subchondral bone. We confirmed a significant decrease in type II collagen and aggrecan mRNA expressions in chondrocytes by co-culture with osteoblasts after impact-loading, and significant increase in mRNA and protein expressions of IL-1beta in subchondral osteoblasts from impact-loaded subchondral bone. The mRNA expressions of type II collagen, aggrecan, and type X collagen in chondrocytes were decreased significantly by the co-culture with osteoblasts pre-treated by IL-1beta, -6, and TNF-alpha. Among them, osteoblasts pre-treated by IL-1beta affected chondrocytes most strongly. It was also shown that IL-1beta-treated osteoblasts enhanced the MMP-1 mRNA level most markedly in chondrocytes among the four cytokines. These results suggest that the TMJ subjected to impact-loading can increase directly IL-1beta synthesis in the subchondral region, subsequently altering the metabolism of adjacent cartilage and may eventually resulting in the onset and progression of TMJ-OA.
authors.affiliation: Department of Orthodontics and Craniofacial Developmental Biology, Hiroshima University Graduate School of Biomedical Sciences, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8553, Japan.
authors.forename: Yu-Yu
authors.initials: YY
authors.lastname: Lin
authors.forename: Nobuaki
authors.initials: N
authors.lastname: Tanaka
authors.forename: Satoru
authors.initials: S
authors.lastname: Ohkuma
authors.forename: Takashi
authors.initials: T
authors.lastname: Kamiya
authors.forename: Ryo
authors.initials: R
authors.lastname: Kunimatsu
authors.forename: Yu-Ching
authors.initials: YC
authors.lastname: Huang
authors.forename: Motoko
authors.initials: M
authors.lastname: Yoshioka
authors.forename: Tomomi
authors.initials: T
authors.lastname: Mitsuyoshi
authors.forename: Yuki
authors.initials: Y
authors.lastname: Tanne
authors.forename: Kotaro
authors.initials: K
authors.lastname: Tanimoto
authors.forename: Eiji
authors.initials: E
authors.lastname: Tanaka
authors.forename: Kazuo
authors.initials: K
authors.lastname: Tanne
mesh_terms: D000818:Animals; D002356:Cartilage / Q000378:metabolism* / Q000503:physiopathology*; D016207:Cytokines / Q000378:metabolism*; D053583:Interleukin-1beta / Q000378:metabolism*; D008334:Mandible / Q000503:physiopathology*; D009924:Organ Culture Techniques / Q000379:methods; D013552:Swine; D016474:Weight-Bearing; D014949:Wounds, Nonpenetrating / Q000503:physiopathology*
chemical_list: D016207:Cytokines; D053583:Interleukin-1beta