Bone healing is a multifarious process involving mesenchymal stem cells, osteoprogenitor
cells, macrophages, osteoblasts and -clasts, and chondrocytes to restore the osseous tissue. Particularly
in long bones including the tibia, clavicle, humerus and femur, this process fails in 2–10% of all
fractures, with devastating effects for the patient and the healthcare system. Underlying reasons for
this failure are manifold, from lack of biomechanical stability to impaired biological host conditions
and wound-immanent intricacies. In this review, we describe the cellular components involved in
impaired bone healing and how they interfere with the delicately orchestrated processes of bone
repair and formation. We subsequently outline and weigh the risk factors for the development of
non-unions that have been established in the literature. Therapeutic prospects are illustrated and put
into clinical perspective, before the applicability of biomarkers is finally discussed