title: A brief review for orthopedic surgeons: fatigue damage (microdamage) in bone (its determinants and clinical implications).
abstract: Bone modeling can slowly strengthen bones to keep their strains below bone's microdamage (MDx) threshold. When that condition is satisfied the slow basic multicellular unit (BMU)-based remodeling can usually repair the little MDx that occurs anyway, and some always does. While this arrangement minimizes fatigue fractures of whole bones or trabeculae, they can still happen if: (A) drugs, disease, or dead bone impair MDx repair; (B) if bone loads increase faster than the sluggish modeling can strengthen bone to meet the new loads, and/or faster than remodeling can repair the increased MDx; (C) if a cyst, tumor, or surgery removes enough bone to let strains in the remaining bone reach or exceed the MDx threshold; (D) if abnormal properties of bone as a material cause too much MDx to repair; (E) if altered modeling and remodeling thresholds cause an osteopenia that lets normal activities cause bone strains in or above the MDx threshold range; (F) or if strains in the bone supporting a load-bearing implant reach or exceed bone's MDx threshold.
authors.affiliation: Department of Orthopaedic Surgery, Southern Colorado Clinic, 41 Montebello, Pueblo, CO 81001, USA.
authors.forename: H M
authors.initials: HM
authors.lastname: Frost
mesh_terms: D001696:Biomechanical Phenomena; D001846:Bone Development / Q000502:physiology; D001851:Bone Diseases, Metabolic / Q000209:etiology / Q000503:physiopathology; D016723:Bone Remodeling / Q000502:physiology*; D001862:Bone Resorption / Q000503:physiopathology; D015775:Fractures, Stress / Q000209:etiology / Q000503:physiopathology*; D006801:Humans