PMID- 12151080 OWN - NLM STAT- MEDLINE DCOM- 20030204 LR - 20190906 IS - 8756-3282 (Print) IS - 1873-2763 (Linking) VI - 31 IP - 2 DP - 2002 Aug TI - Developmentally regulated monocyte recruitment and bone resorption are modulated by functional deletion of the monocytic chemoattractant protein-1 gene. PG - 282-7 AB - Tooth eruption involves the movement of a tooth from its site of development within the alveolar bone to its functional position in the oral cavity. Because this process is dependent upon monocytes and formation of osteoclasts, it represents an excellent model for examination of these processes under developmental regulation. We investigated the functional role of monocyte chemoattractant protein-1 (MCP-1) in monocyte recruitment and its impact on bone resorption by examining each parameter in MCP-1(-/-) mice as compared with wild-type controls during tooth eruption. The peak number of monocytes occurred on day 5 in the MCP-1(-/-) mice and on day 9 in the wild-type mice. The peak number of osteoclasts followed the same pattern, occurring sooner in the MCP-1(-/-) (day 5) than in wild-type mice (day 9). Consistent with this, MCP-1(-/-) mice had an accelerated rate of tooth eruption in the early phase when the teeth first entered the oral cavity as compared with the wild-type mice. However, there was accelerated eruption in the wild-type group in the later phase of tooth eruption. When examined at the molecular level, inducible nitric oxide synthase (iNOS) and interleukin-11 and -6 were expressed at considerably higher levels in the experimental group with accelerated tooth eruption. This is the first report identifying these factors as potential modulators of bone resorption that can accelerate the rate of tooth eruption. We conclude that, at early timepoints, monocyte recruitment occurs by MCP-1-independent mechanisms. However, at a later timepoint, MCP-1 may play a contributory role in the recruitment of monocytic cells, allowing the wild-type animals to catch up. FAU - Graves, D T AU - Graves DT AD - Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA 02118, USA. dgraves@bsu.edu FAU - Alsulaimani, F AU - Alsulaimani F FAU - Ding, Y AU - Ding Y FAU - Marks, S C Jr AU - Marks SC Jr LA - eng GR - DE07444/DE/NIDCR NIH HHS/United States GR - DE07559/DE/NIDCR NIH HHS/United States PT - Comparative Study PT - Journal Article PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - Bone JT - Bone JID - 8504048 RN - 0 (Chemokine CCL2) SB - IM MH - Animals MH - Animals, Newborn MH - Bone Resorption/*genetics/*metabolism MH - Chemokine CCL2/*deficiency/*genetics MH - *Gene Deletion MH - Gene Expression Regulation, Developmental/*physiology MH - Mice MH - Mice, Inbred C57BL MH - Mice, Knockout MH - Monocytes/*metabolism MH - Tooth Eruption/genetics/physiology EDAT- 2002/08/02 10:00 MHDA- 2003/02/05 04:00 CRDT- 2002/08/02 10:00 PHST- 2002/08/02 10:00 [pubmed] PHST- 2003/02/05 04:00 [medline] PHST- 2002/08/02 10:00 [entrez] AID - S8756328202008293 [pii] AID - 10.1016/s8756-3282(02)00829-3 [doi] PST - ppublish SO - Bone. 2002 Aug;31(2):282-7. doi: 10.1016/s8756-3282(02)00829-3.