Dura mater maintains rat cranial sutures in vitro by regulating suture cell proliferation and collagen production.

Craniosynostosis, the premature osseous obliteration of cranial vault sutures, can result from mutations in genes encoding components of growth factor signaling systems or the extracellular matrix (ECM). Little is known of the capacity of osteoprogenitor cells of the cranial sutures to divide or to synthesize ECM in situ. Osteoblasts derived from patients with prematurely fused sutures were reported to express alkaline phosphatase and osteocalcin at elevated levels, while proliferating at a rate comparable to control cells [DePollack et al., JBMR, 1996]; however, the suture osteoprogenitors, the population most likely to show proliferative abnormalities, were not present in the fused sutures used for this study. A model in which rat coronal sutures and associated bones develop normally in vitro, but in which sutures can be induced to fuse in the absence of dura mater, was used to examine cell proliferation and total protein synthesis in unfused sutures cultured in the presence of dura mater or in sutures induced to fuse in the absence of dura mater. Significantly increased cell proliferation was seen in suture cells prior to sutural obliteration, which returned to control levels as sutural fusion proceeded. Collagen synthesis in fusing sutures was elevated compared to non-fusing sutures and comparable to that seen in bone. Results indicated that in the absence of intercellular signals provided by the dura mater, suture cell proliferation increased initially, followed by increased synthesis of collagenous ECM within the suture and subsequent osseous obliteration of the suture. Thus factors originating in the dura mater affected suture cell proliferation and ECM production and were required for the maintenance of suture patency.