Loss of Proteinpolysaccharides at Sites Where Bone Mineralization Is Initiated

Abstract

In both ground sections and demineralized frozen sections of the rat tibial cortex, osteoid but not mature bone matrix stained for proteinpolysaccharides with the Alcian Blue and toluidine blue techniques. The loss of proteinpolysaccharide staining occurred precisely at the mineralizing front, which was identified by in vivo lead or procion markers, not only in normal animals but also in animals in which osteoid width was either increasing or decreasing. In vitro, both proteases and saccharidases abolished proteinpolysaccharide staining of osteoid. Critical electrolyte concentration and other procedures indicated that the major acid polysaccharide component in osteoid is chondroitin sulfate. Consistent with these findings, electron microprobe analyses revealed that sulfur concentration was high in osteoid but dropped abruptly as calcium concentration increased at the mineralizing front. The precise synchronization between loss of proteinpolysaccharides and onset of mineralization under various experimental conditions provides strong indirect evidence that the loss of these macromolecules is somehow involved in initiation of mineralization in bone.

The distribution of 3H‐proline in alveolar bone of the mouse as seen by radioautography

“…It is likely that grain removal reflects the loss of protein cores of proteoglycans coincident to mineralization (Baylink et al, 1972) or the loss of labeled short-lived matrix proteins including terminal peptides of procollagen (Fessler and Fessler, 1978;Josephsen and Warshawsky, 1982).…”

Inhibition of Bone Matrix Formation, Mineralization, and Resorption in Thyroparathyroidectomized Rats

“…Total serum calcium and phosphorus determinations were made as previously described (1) (7). Osteoid maturation rate is probably a better measurement of the onset of mineralization than is osteoid width since an increase in osteoid width may be related to either an increase in matrix apposition or a delay in the onset of mineralization, whereas the osteoid maturation rate is independent of apposition (1).…”

“…The onset of mineralization appears to be dependent upon osteoid maturation. Accordingly, matrix changes in lipid concentration, acid phosphatase activity, and particularly proteinpolysaccharide concentration are coordinated both spatially and temporally with the onset of mineralization (7,15,16). Because osteoid maturation implies that the onset of mineralization is at least partially under cellular control, it seems likely that hypocalcemia inhibits the onset of mineralization by adversely affecting cell-mediated processes.…”

Differential Effects of Fibromodulin Deficiency on Mouse Mandibular Bones and Teeth: A Micro-CT Time Course Study

“…For years there has been a debate about the functions of GAGs or PGs with regard to whether they are mineralization inhibitors or promoters; because GAGs are more abundant in osteoid and predentin, but are decreased in bone or in dentin, PGs were considered to be inhibitors that had to be enzymatically degraded before the onset of mineralization [Baylink et al, 1972;Hall et al, 1999;Embery et al 2001]. Other reports established that CS/DS and KS PGs are present in mineralized tissues [Embery et al, 2001].…”