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Evidence for an inhibitor of osteoclast attachment in dentinal matrix

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Abstract The ability of osteoclasts to colonize in vitro different preparations of dentin extracted with guanidinium hydrochloride (GuHCl) was studied in order to establish morphological evidence for an extractable inhibitor of osteoclast spreading within dentin. Osteoclasts were isolated from neonatal rats and seeded onto pieces of fully mineralized dentin, demineralized dentin and predentin extracted with GuHCl. Osteoclasts were also seeded onto unextracted tissues. The results were evaluated with scanning electron microscopy. Osteoclasts colonized and resorbed fully mineralized dentin, whereas clastic cells were not observed on unextracted demineralized dentin and predentin. In contrast to this, osteoclasts attached and spread on demineralized dentin and predentin extracted with GuHCl. It was concluded that the non‐collagenous organic component of dentin contains an extractable inhibitor of osteoclastic attachment and spreading. It is tempting to speculate that the inhibitor may be responsible for the naturally occuring resistance of dentin to resorption.
Title: Evidence for an inhibitor of osteoclast attachment in dentinal matrix
Description:
Abstract The ability of osteoclasts to colonize in vitro different preparations of dentin extracted with guanidinium hydrochloride (GuHCl) was studied in order to establish morphological evidence for an extractable inhibitor of osteoclast spreading within dentin.
Osteoclasts were isolated from neonatal rats and seeded onto pieces of fully mineralized dentin, demineralized dentin and predentin extracted with GuHCl.
Osteoclasts were also seeded onto unextracted tissues.
The results were evaluated with scanning electron microscopy.
Osteoclasts colonized and resorbed fully mineralized dentin, whereas clastic cells were not observed on unextracted demineralized dentin and predentin.
In contrast to this, osteoclasts attached and spread on demineralized dentin and predentin extracted with GuHCl.
It was concluded that the non‐collagenous organic component of dentin contains an extractable inhibitor of osteoclastic attachment and spreading.
It is tempting to speculate that the inhibitor may be responsible for the naturally occuring resistance of dentin to resorption.

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