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Alterations in Bone Homeostasis and Microstructure Related to Depression and Allostatic Load

From early childhood to late adulthood, bones are continuously remodeling and adapting to environmental changes. Various conditions can disturb this remodeling process such as medical interventions, aging and metabolic bone diseases [1]. Remodeling processes require both bone resorption and formation, which are driven by osteoclasts and osteoblasts, respectively. Both cell types are affected by physiological (e.g. age, gender, physical activity and mobility states, hormones) and pathological conditions (e.g. prematurity, growth hormone deficiency, malnutrition, malabsorption, metastatic bone disease) [1], which can negatively impact a bone’s capacity to adapt to present needs. Bone remodeling can be measured through markers of bone formation (e.g. osteocalcin [OC], procollagen type 1 N-terminal propeptide [P1NP]) or bone resorption (e.g. beta-CrossLaps [betaCTX]), both used as clinical markers of bone health. OC is an extracellular, non-collagenous protein secreted by osteoblasts during bone formation that has several hormone-like features such as an influence on energy homeostasis [2] . P1NP is a direct quantitative measure of osteoblast activity synthesizing collagen type 1, a component predominantly located in the bone matrix. It is also used in diagnosis and management of osteoporosis [2].In contrary to OC and P1NP, beta-CTX is released during bone resorption and is a specific marker for degradation fragments of mature type I collagen from bone, which is the main component (approximately 90%) of the protein matrix of bone. Bone turnover markers provide information about rates of bone loss and gain, and therefore reflect the metabolic activity of bones that is complementary to bone health measurements like bone mineral density (BMD) [3].