Is bone quality associated with collagen age?

Abstract

The World Health Organization defines osteoporosis as a systemic disease characterized by decreased bone tissue mass and microarchitectural deterioration, resulting in increased fracture risk. Since this statement, a significant amount of data has been generated showing that these two factors do not cover all risks for fracture. Other independent clinical factors, such as age, as well as aspects related to qualitative changes in bone tissue, are believed to play an important role. The term "bone quality" encompasses a variety of parameters, including the extent of mineralization, the number and distribution of microfractures, the extent of osteocyte apoptosis, and changes in collagen properties. The major mechanism controlling these qualitative factors is bone remodeling, which is tightly regulated by the osteoclast/osteoblast activity. We focus on the relationship between bone remodeling and changes in collagen properties, especially the extent of one posttranslational modification. In vivo, measurements of the ratio between native and isomerized C-telopeptides of type I collagen provides an index of bone matrix age. Current preclinical and clinical studies suggests that this urinary ratio provides information about bone strength and fracture risk independent of bone mineral density and that it responds differently according to the type of therapy regulating bone turnover.

Dissociation of Bone Resorption and Bone Formation in Adult Mice with a Non-Functional V-ATPase in Osteoclasts Leads to Increased Bone Strength

“…In both human and murine osteopetrosis forms caused by defective acid secretion by the osteoclasts, bone quality is low and fractures are frequent [48][49][50]; however the explanation for this has never been clear, and the possibilities include over-suppression of bone turnover, accelerated osteoblast function, the presence of woven, and therefore immature, bone, and finally failure to resorb calcified cartilage [9,[21][22][23].…”

“…These forms of osteopetrosis are characterized by normal or even increased indices of bone formation despite the presence of high numbers of non-resorbing osteoclasts [17][18][19][20], indicating that bone resorption and bone formation are no longer coupled. Despite the high bone mass, a feature of osteopetrosis is poor bone quality, which has been speculated to be due to the extreme suppression of bone resorption [21,22], the failure to resorb calcified cartilage [9], and to hyper-activity of the osteoblasts [23].…”

Extracellular Matrix Remodeling: The Common Denominator in Connective Tissue DiseasesPossibilities for Evaluation and Current Understanding of the Matrix as More Than a Passive Architecture, but a Key Player in Tissue Failure

“…In other words, EKAHD(a)GGR epitopes are released during degradation of newly synthesized type I collagen, whereas EKAHD(b)GGR epitopes are released from matured type I collagen. It has been established that the a/b ratio is a useful measure of the age of bone tissue; [287][288][289] the lower the ratio, the older the bone tissue. 290 Further, the lysine residue of the CTX residue is cross-linked.…”

Multi-scale characterization of swine femoral cortical bone

“…Aging, for instance, increases bone's susceptibility to fracture Currey et al, 1996;Nalla et al, 2004;Ritchie et al, 2006;Wang and Puram, 2004). Various studies have been conducted on the changes in bone's structure, chemical composition, and mechanical properties due to development or aging (Ager et al, 2005;Boyde et al, 1993;Burstein et al, 1976;Dalzell et al, 2009;Devulder et al, 2008;GourionArsiquaud et al, 2009;Grynpas, 1993;Halloran et al, 2002;Hoffler et al, 2000;Hui et al, 1988;Kavukcuoglu et al, 2007;Leeming et al, 2009;McCalden et al, 1993;Mueller et al, 1966;Parfitt, 1984;Reid and Boyde, 1987;Seeman, 2008;Vashishth et al, 2002;Wall et al, 1979;Wang et al, 2003;Willinghamm et al, 2010;Zioupos and Currey, 1998;Zioupos et al, 2006). However, these studies in general focused on one or two techniques or scales.…”