Microcracks and Osteoclast Resorption Activity In Vitro

Abstract

During bone remodeling osteoclasts resorb bone, thus removing material, e.g., damaged by microcracks, which arises as a result of physiological loading and could reduce bone strength. Such a process needs targeted bone resorption exactly at damaged sites. Osteocytic signaling plays a key role in this process, but it is not excluded that osteoclasts per se may possess toposensitivity to recognize and resorb damaged bone since it has been shown that resorption spaces are associated with microcracks. To address this question, we used an in vitro setup of a pure osteoclast culture and mineralized substrates with artificially introduced microcracks and microscratches. Histomorphometric analyses and statistical evaluation clearly showed that these defects had no effect on osteoclast resorption behavior. Osteoclasts did not resorb along microcracks, even when resorption started right beside these damages. Furthermore, quantification of resorption on three different mineralized substrates, cortical bone, bleached bone (bone after partial removal of the organic matrix), and dentin, revealed lowest resorption on bone, significantly higher resorption on bleached bone, and highest resorption on dentin. The difference between native and bleached bone may be interpreted as an inhibitory impact of the organic matrix. However, the collagen-based matrix could not be the responsible part as resorption was highest on dentin, which contains collagen. It seems that osteocytic proteins, stored in bone but not present in dentin, affect osteoclastic action. This demonstrates that osteoclasts per se do not possess a toposensitivity to remove microcracks but may be influenced by components of the organic bone matrix.

Study of Osteoclast Adhesion to Cortical Bone Surfaces: A Correlative Microscopy Approach for Concomitant Imaging of Cellular Dynamics and Surface Modifications

“…In contrast to the bulges, SZ rings did not preferentially associate with physiologically relevant structures displaying negative topography, such as osteocyte lacunas and microcracks. A similar phenomenon was also observed on dentin slices . It is, however, possible that during cell interactions, structures with negative topography were filled with organic material, masking their interaction with the SZ rings.…”

Osteoclasts on Bone and Dentin In Vitro: Mechanism of Trail Formation and Comparison of Resorption Behavior

“…In addition, osteocytic proteins, which are present in bone but are missing in dentin, may act on osteoclasts in the bone remodeling processes [ 20 – 23 ]. Removal of organic components and osteocytic proteins from bone matrix was followed by an increased osteoclastic resorption in vitro [ 14 ]. Different osteoclastic resorption activity has also been described for numerous artificial substrates, e.g., hydroxyapatite, β-tricalcium phosphate, calcium phosphate, calcite, and carbonated apatite, including variation of cell adhesion rate on those materials, which we observed as well between bone and dentin [ 24 – 27 ].…”

“…Osteoclasts were generated from human peripheral blood mononuclear cells obtained from 16 healthy donors (aged 19–55 years) as previously described [ 14 ]. Experiments were approved by the Austrian Ethics Committee, and informed consent was obtained from all volunteers.…”

In vivo effects of different orthodontic loading on root resorption and correlation with mechanobiological stimulus in periodontal ligament

“…Osteoclasts were reported to be sensitive to topographical discontinuities that were in the tens of microns in culture matrices [21][22][23][24], but there has not yet been any clear evidence concerning the determinant factors for migration direction of such cells [24]. Possibly, odontoclast progression could be guided by micro/macro-morphological patterns on root surfaces, such as macroscopic surface curvature or surface asperities such as the micro-features resulting from PDL collagen fibre insertion and mineral crystal orientation [48], or the gradients of local mechanobiological stimulation.…”