Injury
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Bone defects associated with non-unions occur as a result of the initial insult or as a consequence of bone excision following non-union development. Historically management of this clinical scenario consisted mainly of amputation, which provided a short recovery period but a significant loss of limb function. Today treatment has evolved and multiple options are available for reconstruction of the bone defect. Broadly these are: bone shortening with lengthening later or bone transport and 'docking' (distraction osteogenesis based techniques); the use of vascularised and non-vascularised bone grafts; bone substitutes; stem cells; growth factors; scaffolds and gene therapy.
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The current available evidence for the use of bone graft substitutes in the management of subchondral bone defects associated with tibial plateau fractures as to their efficiency and safety has been collected following a literature review of the Ovid MEDLINE (1948-Present) and EMBASE (1980-Present). Nineteen studies were analysed reporting on 672 patients (674 fractures), with a mean age of 50.35 years (range 15-89), and a gender ratio of 3/2 males/females. The graft substitutes evaluated in the included studies were calcium phosphate cement, hydroxyapatite granules, calcium sulphate, bioactive glass, tricalcium phosphate, demineralised bone matrix, allografts, and xenograft. ⋯ The recorded incidence of primary surgical site and donor site infection (3.6%) was not statistically significant different, however donor site-related pain was reported up to 12 months following autologous iliac bone graft (AIBG) harvest. Shorter total operative time, greater tolerance of early weight bearing, improved early functional outcomes within the first year post-surgery was also recorded in the studies reporting on the use of injectable calcium phosphate cement (Norian SRS). Despite a lack of good quality randomised control trials, there is arguably sufficient evidence supporting the use of bone graft substitutes at the clinical setting of depressed plateau fractures.
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Atrophic non-union represents a complex clinical condition and research is ongoing in an effort to elucidate its pathophysiology and to offer new and more efficient treatment modalities. Differences seen in fracture healing responses and final outcome may be attributed among other factors to biological variations between patients resulting in a "disturbed" signalling pathway and an "inert or deficient local biology with reduced potentials for bone regeneration". ⋯ However, preliminary animal and human studies demonstrate the molecular basis of fracture non-unions and correlate genetic variants of the molecules regulating fracture healing and their expression patterns with impaired bone healing and fracture non-union. Further research is needed to clarify the genetic component and its role and interaction with other risk factors that may result in increased susceptibility of a patient to develop this complication.