This is a transverse (cross-sectional) slice through a shaft of cortical bone — the same view a histology slide or micro-CT scan shows. The bright ring is the cortical shell between the outer periosteal surface and the inner endosteal surface (medullary cavity, the dark hole in the middle); dozens of independent Basic Multicellular Units (BMUs) tunnel through it end-on, so each appears here as a small circle: a cutting cone of osteoclasts widens the circle (a Haversian canal in cross-section), then a closing cone of osteoblasts narrows it back down.
Osteoclast recruitment is gated by the RANK–RANKL–OPG axis: osteoblasts/osteocytes display RANKL, which binds RANK on osteoclast precursors and drives their differentiation; osteoprotegerin (OPG) is a decoy receptor that mops up RANKL and blocks this signal. The RANKL/OPG ratio is the net "go" signal for resorption:
Resorption rate ∝ RANKL / OPG
Canal radius r(t) (in cross-section):
resorbing: r → r_max (cutting cone advances)
forming: r → r_final (closing cone refills)
Remodeling balance per BMU = r_max − r_final
Cortical porosity = Σ(π·r_i²) / annulus area
In healthy adult bone the closing cone almost fully refills the tunnel each cycle (small, controlled deficit). When RANKL/OPG rises — postmenopausal estrogen loss, glucocorticoids, immobilization, CKD-MBD — cutting cones drill wider circles and osteoblast refill lags further behind, so each BMU leaves a bit more open cross-sectional area than before. Multiplied over the many BMUs active in a cortical ring at any time, this per-cycle deficit is the actual mechanism of age-related and osteoporotic bone loss: rising cortical porosity and thinning of the ring, not a single event.
- RANKL/OPG ratio — sets how large each cutting-cone circle grows and how large the formation deficit becomes.
- Activation frequency — how many new BMUs initiate per unit time (higher = more simultaneous remodeling sites, e.g. high bone-turnover states).
- Antiresorptive dose — models a denosumab/bisphosphonate-like effect: suppresses new osteoclast activation and slows existing cutting cones, letting formation catch up.
Real-world relevance: this per-BMU imbalance is exactly what DEXA T-scores and bisphosphonate/denosumab therapy are trying to measure and correct — porosity rising above ~10–15% of cortical cross-sectional area is a strong independent predictor of fracture risk, separate from trabecular bone density.