Biological basis of distraction osteogenesis – A review☆

2016 
Abstract Objective Slow but sure bone lengthening using distraction osteogenesis principles is the gold standard for the treatment of hypoplastic facial bones, though the time required for the treatment is a major drawback of this procedure. The objective of this study is to review the contemporary literature and recapitulate the cellular and molecular events occurring during membranous craniofacial distraction osteogenesis. Results Mechanical encouragement by distraction provokes a biological comeback of skeletal renaissance that is accomplished by a cascade of biological processes which include delineation of pluripotent tissue, angiogenesis, osteogenesis, mineralization, and remodeling. Immediately after the osteotomy, hematoma formation and accumulation of inflammatory infiltrates take place which closely resemble as in any standard osteotomy or in fracture. Most authors observed that the levels of proinflammatory cytokines IL-1 and IL-6 are increased which further induce osteoclastic activity and may verify the ‘Coupling Phenomena’ between bone development and resorption and also there is marked increase in the level of transforming growth factor-beta 1 (TGF- β 1) mRNA. These findings suggest that there is a regulatory mechanism for TGF- β 1 in induction of collagen deposition and non-collagenous extracellular matrix proteins involved in mineralization and remodeling of bones. Furthermore, physical factors along with chemical factors also influence the outcome of distraction osteogenesis. Conclusion Knowing the molecular mechanism helps in the development of targeted strategies intended to improve distraction osteogenesis and speed up bone renaissance that may lead to shorten the treatment time and helps craniofacial surgeons in understanding about various factors affecting the distraction process at different stages.
    • Correction
    • Source
    • Cite
    • Save
    • Machine Reading By IdeaReader
    78
    References
    6
    Citations
    NaN
    KQI
    []