title: Osteoblasts and osteocytes express MMP2 and -8 and TIMP1, -2, and -3 along with extracellular matrix molecules during appositional bone formation.
abstract: Our previous studies suggested that a part of bone extracellular matrix (ECM) molecules are degraded and remodeled during embryonic bone formation. In contrast, little is known about ECM remodeling in postnatal appositional bone formation. The present study was designed to investigate expression of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) during experimentally initiated appositional bone formation in rats. Expressions of ECM molecules, MMPs, and TIMPs were examined using in situ hybridization. Osteoblasts and osteocytes expressed MMP2 and -8, TIMP1, -2, and -3, as well as type I collagen, osteopontin, and osteocalcin in the course of the appositional bone formation, while they showed few transcripts of MMP13. The results indicated that while osteoblasts and osteocytes in the apposed bone produce ECM molecules, they degrade ECM molecules with MMPs and regulate the degradation by inhibiting the activity of MMPs using TIMPs. Osteoblasts and osteocytes may reorganize the ECM composition to mature the bone matrix in appositional bone formation.
authors.affiliation: Division of Advanced Prosthetic Dentistry, Tohoku University Graduate School of Dentistry, Sendai, Japan. hatori@moon.co.jp
authors.forename: Kouki
authors.initials: K
authors.lastname: Hatori
authors.forename: Yasuyuki
authors.initials: Y
authors.lastname: Sasano
authors.forename: Ichiro
authors.initials: I
authors.lastname: Takahashi
authors.forename: Shinji
authors.initials: S
authors.lastname: Kamakura
authors.forename: Manabu
authors.initials: M
authors.lastname: Kagayama
authors.forename: Keiichi
authors.initials: K
authors.lastname: Sasaki
mesh_terms: D000818:Animals; D016723:Bone Remodeling / Q000502:physiology; D024042:Collagen Type I / Q000378:metabolism; D017364:Collagenases / Q000378:metabolism*; D005109:Extracellular Matrix / Q000378:metabolism*; D017403:In Situ Hybridization; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism; D020784:Matrix Metalloproteinase 8 / Q000378:metabolism; D010006:Osteoblasts / Q000201:enzymology*; D015675:Osteocalcin / Q000378:metabolism; D010011:Osteocytes / Q000201:enzymology*; D010012:Osteogenesis / Q000502:physiology*; D053495:Osteopontin; D010294:Parietal Bone / Q000201:enzymology / Q000254:growth & development; D051381:Rats; D017208:Rats, Wistar; D012795:Sialoglycoproteins / Q000378:metabolism; D013997:Time Factors; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000378:metabolism; D019716:Tissue Inhibitor of Metalloproteinase-2 / Q000378:metabolism; D019717:Tissue Inhibitor of Metalloproteinase-3 / Q000378:metabolism; D019714:Tissue Inhibitor of Metalloproteinases / Q000378:metabolism*
chemical_list: D024042:Collagen Type I; D012795:Sialoglycoproteins; C506897:Spp1 protein, rat; D019715:Tissue Inhibitor of Metalloproteinase-1; D019717:Tissue Inhibitor of Metalloproteinase-3; D019714:Tissue Inhibitor of Metalloproteinases; D015675:Osteocalcin; D053495:Osteopontin; D019716:Tissue Inhibitor of Metalloproteinase-2; D017364:Collagenases; D020778:Matrix Metalloproteinase 2; D020784:Matrix Metalloproteinase 8