Mechanisms of bone response to injury

Abstract

Bone, despite its relatively inert appearance, is a tissue that is capable of adapting to its environment. Wolff’s law, first described in the 19th century, describes the ability of bone to change structure depending on the mechanical forces applied to it. The mechanostat model extended this principle and suggested that the amount of strain a bone detects depends on bone strength and the amount of muscle force applied to the bone. Experimental studies have found that low-magnitude, high-frequency mechanical loading is considered to be the most effective at increasing bone formation. The osteocyte is considered to be the master regulator of the bone response to mechanical loading. Deformation of bone matrix by mechanical loading is thought to result in interstitial fluid flow within the lacunar–canalicular system, which may activate osteocyte mechanosensors, leading to changes in osteocyte gene expression and ultimately increased bone formation and decreased bone resorption. However, repetitive strain applied to bone can result in microcracks, which may propagate and coalesce, and if not repaired predispose to catastrophic fracture. Osteocytes are a key component in this process, whereby apoptotic osteocytes in an area of microdamage promote targeted remodeling of the damaged bone. If fractures do occur, fracture repair can be divided into 2 types: primary and secondary healing. Secondary fracture repair is the most common and is a multistage process consisting of hematoma formation and acute inflammation, callus formation, and finally remodeling, whereby bone may return to its original form.