Abstract
The contraction of connective tissue cells may facilitate their production and maintenance of extracellular matrix architecture and can benefit healing through wound closure. However, aberrant cell contraction can result in pathological contracture. Implants may stimulate this process leading to contracture of the surrounding fibrous capsule. In the case of compliant porous matrices used for tissue engineering the cell contraction may cause the constriction of pores and the distortion of the implant. The objective of this study was to determine if osteoblasts expressed a specific muscle actin, α-smooth muscle actin (SMA), that could provide for their contraction. Immunohistochemistry revealed the presence of SMA in some cells in all of three human and three canine trabecular bone specimens. The majority of the cells of an osteoblastic cell line, MC3T3-E1, also expressed this actin isoform in two-dimensional culture and when seeded into a collagen-glycosaminoglycan (GAG) matrix. These SMA-containing cells were found to cause contraction of the collagen-GAG analog of extracellular matrix. These findings demonstrate that osteoblasts can display contractile behavior that might help to explain the mechanism by which they impart architecture to bone matrix, including that at implant interfaces. An understanding of this process could also guide the development of matrices for bone tissue engineering.
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