Cortical bone is not remodeled as a solid block — it is tunneled by thousands of independent Basic Multicellular Units (BMUs). Each BMU is a self-contained team: a cutting cone of osteoclasts drills a cylindrical tunnel (a new Haversian canal) through old bone, followed by a closing cone of osteoblasts that lays down new lamellar bone on the tunnel wall, narrowing 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):
resorbing: r → r_max (cutting cone advances)
forming: r → r_final (closing cone refills)
Remodeling balance per BMU = r_max − r_final
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 and osteoblast refill lags further behind, so each BMU leaves the canal a little wider than before. Multiplied over the ~4-million BMUs active in the adult skeleton at any time, this per-cycle deficit is the actual mechanism of age-related and osteoporotic bone loss: rising cortical porosity and thinning trabeculae, not a single event.
- RANKL/OPG ratio — sets how deep each cutting cone resorbs 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 volume is a strong independent predictor of fracture risk, separate from trabecular bone density.