Microdamage in Bone: Implications for Fracture, Repair, Remodeling, and Adaptation

Abstract

Fatigue microdamage accumulates in bone as a result of physiological loading. The damage is often manifested as microcracks, which are typically 50-100 mum long. These types of cracks develop in the interstitial bone and frequently abut osteon cement lines. In vitro experimentation has shown that an accumulation of fatigue damage reduces the material properties of bone (e.g., elastic modulus). An accumulation of fatigue damage has been implicated in the etiology of stress fractures and fragility fractures. However, bone has a remarkable ability to detect and repair fatigue microdamage. This article reviews the experimental techniques for identifying and quantifying different types of microdamage in bone, the density of in vivo microcracks at different skeletal locations, the effect of microdamage on bone material properties, the role of microdamage in bone fracture, and the biological mechanisms for the detection and repair of fatigue microdamage.

Effects of preexisting microdamage, collagen cross‐links, degree of mineralization, age, and architecture on compressive mechanical properties of elderly human vertebral trabecular bone

“…8,47 Several factors may explain, in part, the disagreement between Wenzel et al and the current study, including the age range of subjects (greater in Wenzel et al than in current study), and the vertebral body examined (T12 vs. L2), and the location of the trabecular core within the vertebral body. 6 Regarding our finding that microdamage was not associated with trabecular bone mechanical properties, Fazzalari et al 8 also found no relationship between the amount of microdamage and the ultimate failure stress in trabecular bone specimens from human femurs.…”

Skeletal Microdamage: Less About Biomechanics and More About Remodeling

“…This has been demonstrated several times by different laboratories using different animal models and is now considered an integral component of bone remodeling physiology [20][21][22][23][24] (Fig. 4).…”

“…But why do the osteocytes die with fatigue loading? The most prominent hypothesis is that osteocyte processes are physically broken by microdamage, disrupting cell-to-cell communication and fluid flow [20,23]. This is supported by the abundance of evidence showing fluid flow plays a key role in osteocyte physiology [21,46,47] and that both fluid flow [35,48] and cell process connections [49] are disrupted following fatigue loading.…”

Is bone quality associated with collagen age?

“…In this review, we use the term "bone quality" as the quality of the bone matrix thus comprising mineralization, posttranslational changes in the collagen molecule that occur with age, and microscopic tissue damage which all are parameters affected by bone remodeling. Recent developments in the field of biochemical marker research have indicated that age-related changes in bone matrix molecules are associated with bone fracture resistance independent of BMD and may thus allow for the monitoring of some aspects of bone matrix quality in a manner that is noninvasive [17,18,[22][23][24][25][26][27][28][29]. In this review, we emphasize the likely connection between bone matrix quality and bone remodeling, highlighting the importance of bone matrix age.…”