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Delayed osteoblast differentiation and altered inflammatory response around implants placed in incisor sockets of type 2 diabetic rats
Author(s) -
Colombo John S.,
Balani Deepak,
Sloan Alastair J.,
Crean St John,
Okazaki Joji,
Waddington Rachel J.
Publication year - 2011
Publication title -
clinical oral implants research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.407
H-Index - 161
eISSN - 1600-0501
pISSN - 0905-7161
DOI - 10.1111/j.1600-0501.2010.01992.x
Subject(s) - osteoblast , osteocalcin , osteopontin , mesenchymal stem cell , progenitor cell , medicine , osseointegration , proinflammatory cytokine , bone healing , bone sialoprotein , pathology , inflammation , endocrinology , chemistry , stem cell , alkaline phosphatase , microbiology and biotechnology , biology , implant , anatomy , surgery , enzyme , biochemistry , in vitro
Objective: Central to the process of osseointegration is the recruitment of mesenchymal progenitor cells to the healing site, their proliferation and differentiation to bone synthesising osteoblasts. The process is under the control of pro‐inflammatory cytokines and growth factors. The aim of this study was to monitor these key stages of osseointegration and the signalling milieu during bone healing around implants placed in healthy and diabetic bone. Methods: Implants were placed into the sockets of incisors extracted from the mandibles of normal Wistar and diabetic Goto‐Kakizaki rats. Mandibles 1–12 weeks post‐insertion of the implant were examined by histochemistry and immunocytochemistry to localise the presence of Stro‐1‐ positive mesenchymal progenitor cells, proliferating cellular nuclear antigen proliferative cells, osteopontin and osteocalcin, macrophages, pro‐inflammatory cytokines interleukin (IL)‐1β, IL‐6, tumour necrosis factor (TNF)‐α and tumour growth factor (TGF)‐β1. Image analysis provided a semi‐quantification of positively expressing cells. Results: Histological staining identified a delay in the formation of mineralised bone around implants placed in diabetic animals. Within the diabetic bone, the migration of Stro‐1 mesenchymal cells in the healing tissue appeared to be unaffected. However, in the diabetic healing bone, the onset of cell proliferation and osteoblast differentiation were delayed and subsequently prolonged compared with normal bone. Similar patterns of change were observed in diabetic bone for the presence of IL‐1β, TNF‐α, macrophages and TGF‐β1. Conclusion: The observed alterations in the extracellular presence of pro‐inflammatory cytokines, macrophages and growth factors within diabetic tissues that correlate to changes in the signalling milieu, may affect the proliferation and differentiation of mesenchymal progenitor cells in the osseointegration process. To cite this article:
Colombo JS, Balani D, Sloan AJ, St Crean J, Okazaki J, Waddington RJ. Delayed osteoblast differentiation and altered inflammatory response around implants placed in incisor sockets of type 2 diabetic rats
Clin. Oral Impl. Res 22 , 2011; 578–586
doi: 10.1111/j.1600‐0501.2010.01992.x