Bone is a hierarchical composite material that sustains microdamage at different structural levels as a result of wear and tear loading in vivo. Unlike engineered composites, bone can repair matrix damage at the microscopic level. Bone`s ability to repair the typical linear microcracks (30-100 µm in length) that result from fatigue loading is a function of the normal bone remodeling system, wherein osteoclasts remove damaged microscopic areas of bone and osteoblasts replace this tissue with new healthy bone. Small-crack damage, sub-micron-sized cracks which occurs in clusters known as diffuse damage, also commonly occurs in bone with normal wear and tear. It is not repaired through the drill and fill process of bone remodeling, and its long-term history and consequences in living bone are not known. We examined the possibility that another hitherto undiscovered mechanisms exist in bone that can directly repair small crack damage in living bone. To test this idea, we first developed a novel in vivo mechanical loading system that creates exclusively diffuse damage in the ulnar cortex of adult rats. We then examined how diffuse damage content introduced into living bone changed over time, using a combination of tissue microarchitectural studies and whole bone and micromechanical testing approaches. We found that diffuse damage caused a significant acute reduction in mechanical properties of bone, evident both at the whole bone level and locally within the diffuse damage regions. By several weeks after damage induction, we discovered that the damage area was markedly reduced and the deterioration in mechanical properties caused by diffuse damage was completely restored to baseline levels. In the restored bones, we did not observe any bone remodeling. We further investigated the matrix location for diffuse damage to gain insight into mechanisms associated with diffuse damage formation in bone, using a novel combination of scanning electron microscopy, image analysis and super-resolution microscopy. We found that small crack damage in bone occurs at discrete levels in bone matrix, and does not represent a single continuum of damage processes from the mineral crystal to the microscopic levels in bone. Our findings indicate that small crack damage in living bone can be repaired directly, without bone remodeling, and demonstrate that alternative repair mechanisms exist to deal with sub-micron-sized matrix cracks in living bone. These findings provided the first confirmed structural and functional evidence of a long and often speculated upon direct repair process for matrix microdamage in living bone.