Biological basis of bone strength: anatomy, physiology and measurement

Abstract

Understanding how bones are innately designed, robustly developed and delicately maintained through intricate anatomical features and physiological processes across the lifespan is vital to inform our assessment of normal bone health, and essential to aid our interpretation of adverse clinical outcomes affecting bone through primary or secondary causes. Accordingly this review serves to introduce new researchers and clinicians engaging with bone and mineral metabolism, and provide a contemporary update for established researchers or clinicians. Specifically, we describe the mechanical and non-mechanical functions of the skeleton; its multidimensional and hierarchical anatomy (macroscopic, microscopic, organic, inorganic, woven and lamellar features); its cellular and hormonal physiology (deterministic and homeostatic processes that govern and regulate bone); and processes of mechanotransduction, modelling, remodelling and degradation that underpin bone adaptation or maladaptation. In addition, we also explore commonly used methods for measuring bone metabolic activity or material features (imaging or biochemical markers) together with their limitations.

Keywords: Cortical; Imaging; Modelling; Remodelling; Trabecular.

Figure 1

Mechanotransduction (adapted from [14,15]): illustrating the hierarchical structure of bone and the organizational structure of osteocytes within (left); and the mechanically induced fluid flow from hydrostatic pressure and osteoprogenitors through which biochemical signals proliferate (right).

Figure 2

Bone mineral density accrual, maintenance and loss through-out the life-span as indication of bone mass alterations; with approximately 50–60% of total adult bone mass gained during adolescent years preceding peak bone mass and skeletal maturity at ~30 years of age. Bone mass deteriorates gradually following peak bone mass into older age to within normal (green), osteopaenic (yellow) or osteoporotic (red) bone density ranges.

Figure 3

A graphical representation of the remodelling cycle (adapted from [24]). Bone resorption (left) is stimulated by a micro-crack which severs canaliculi channels between osteocytes leading to osteocytic apoptosis. Lining cells and osteocytes release signals attracting cells from blood and marrow reservoirs into the damaged area leading to osteoclastogenesis. Bone formation (right) commences with successive streams of osteoblastic activity depositing new lamellar bone. Osteoblasts then transform into new lining cells (extra-cellular layer) or osteocytes (embedded in osteoid and bone matrix).

Figure 4

Material and structural determinants of bone strength or fragility (left) with associated technologies required to examine bone properties (right); along the macroscopic, microscopic and nanoscopic continuum [top to bottom], (adapted from [1]).