The Bone Lining Cell: Its Role in Cleaning Howship's Lacunae and Initiating Bone Formation

Abstract

In this study we investigated the role of bone lining cells in the coordination of bone resorption and formation. Ultrastructural analysis of mouse long bones and calvariae revealed that bone lining cells enwrap and subsequently digest collagen fibrils protruding from Howship's lacunae that are left by osteoclasts. By using selective proteinase inhibitors we show that this digestion depends on matrix metalloproteinases and, to some extent, on serine proteinases. Autoradiography revealed that after the bone lining cells have finished cleaning, they deposit a thin layer of a collagenous matrix along the Howship's lacuna, in close association with an osteopontin-rich cement line. Collagenous matrix deposition was detected only in completely cleaned pits. In bone from pycnodysostotic patients and cathepsin K-deficient mice, conditions in which osteoclastic bone matrix digestion is greatly inhibited, bone matrix leftovers proved to be degraded by bone lining cells, thus indicating that the bone lining cell "rescues" bone remodeling in these anomalies. We conclude that removal

Cementum‐like tissue deposition on the resorbed enamel surface of human deciduous teeth prior to shedding

“…Based on studies on bone remodeling, several authors reported that a variety of mononuclear cell types, e.g., mononuclear phagocytes or macrophage-like cells (Tran Van et al, 1982), preosteoblasts (McKee andNanci, 1996a), bone-lining cells (Everts et al, 2002), and partially released osteocytes (Tran Van et al, 1982;Oguro and Ozawa, 1989) were observed along the resorbed bone surface during the reversal period. Thus, some authors considered that these mononuclear cells might scavenge the bone surface at the end of osteoclastic resorption (Heersche, 1978; Tran Van et al, 1982;Everts et al, 2002) and that the cement line/reversal line seen on the resorbed surface might be formed by these mononuclear cells (Heersche, 1978; Tran Van et al, 1982;McKee and Nanci, 1996a;Everts et al, 2002).…”

“…Thus, some authors considered that these mononuclear cells might scavenge the bone surface at the end of osteoclastic resorption (Heersche, 1978; Tran Van et al, 1982;Everts et al, 2002) and that the cement line/reversal line seen on the resorbed surface might be formed by these mononuclear cells (Heersche, 1978; Tran Van et al, 1982;McKee and Nanci, 1996a;Everts et al, 2002). In the case of tooth resorption, it was also reported that similar kinds of mononuclear cell types, e.g., cementoblast-like cells (Sasaki et al, 1990), machrophage-like cells or fibroblast-like cells (Tanaka et al, 1990;Okamura et al, 1993), and a special class of mononuclear cells (Bosshardt and Schroeder, 1998) were seen lining the resorption surface.…”

Histogenetic Characterization of Giant Cell Tumor of Bone

“…These data indicate that although SC express early osteogenic markers, their differentiation to a classic fully osteoblastic phenotype cannot be achieved even after appropriate induction. To verify if SC might be considered similar to another cell type, the socalled ''bone lining cell'' [12], expressing very low levels of Type I collagen and osteocalcin and known to contribute to bone collagen degradation, we analyzed the mRNA for ICAM-1, the expression of which is increased in this osteoblast subtype [12,43]. Interestingly, ICAM-1 plays a pivotal role in osteoclastogenesis, because osteoblasts expressing ICAM-1 support bone resorption activity [44,45].…”

The role of proteases in pathologies of the synovial joint

“…Further studies have implied that MMP-mediated collagen proteolysis may be physiologically important in removing any remaining matrix from areas vacated by osteclasts at the end of the resorption cycle (Everts et al, 2002). This enzyme appears to be MMP-13 derived from cells other than osteoclasts (Delaissé et al, 2003;Fuller & Chambers, 1995).…”

“…A number of degenerative changes have been reported including, hypoxia, loss Drake et al (1996), Everts et al (1992), Garnero et al (1998), Hou et al (1999), Kamiya et al (1998) MMP-13 Metallo Cleavage of matrix from demineralised zones Delaissé et al (2003), Everts et al (2002), Fuller and Chambers (1995) Osteoclast activation and migration MMP-13 Metallo Cleavage of type I collagen generating an activation factor for osteoclasts Millar et al (1998), Riley et al (2002) of fibrillar collagen structure, glycosaminoglycan accumulation between the collagen fibres and cell rounding together with an absence of inflammatory cells (Kannus & Józsa, 1991). Similar changes have been reported in chronic tendinopathy, including an abnormal fibre structure and arrangement, focal changes in cellularity, rounded cells and an increase in proteoglycan content (Movin, Gad, Reinholt, & Rolf, 1997).…”