Genetic predisposition to non-union: Evidence today

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”. The genetic contribution with or without the interaction of other exogenous factors in cases of impaired fracture healing, is yet to be elucidated. 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.