trabecular bone

**Structure:** Trabecular bone is a network of interconnecting plates and rods (trabeculae) with marrow-filled spaces between them. It is usually lamellar bone. Trabeculae are oriented along lines of mechanical stress (Wolff's law). Unlike cortical bone, it lacks haversian systems (osteons). Nutrients reach osteocytes by diffusion from the marrow space.

**Distribution:** Vertebral bodies, pelvis, ribs, sternum, and the epiphyses and metaphyses of long bones (e.g., femoral neck, distal radius, calcaneus). Cortical (compact) bone is ~80% of skeletal mass and forms the diaphysis and outer shell.

**Physiology:** - ~20% of skeletal mass but ~80% of bone surface area. This gives it a much higher remodeling rate (about 5-10x cortical bone), so it responds fastest to hormonal and metabolic changes. - It is the site of hematopoiesis in the red marrow of adults (axial skeleton). - It is good at absorbing compressive load and shock, and it is less stiff than cortical bone. - Remodeling: osteoclasts resorb (RANKL from osteoblasts binds RANK on osteoclast precursors; OPG is the decoy receptor). Osteoblasts form new bone.

**Clinical significance:** - **Postmenopausal (type I) osteoporosis:** Estrogen loss increases RANKL and osteoclast activity, so trabecular bone is lost preferentially. Typical fractures are vertebral compression fractures (kyphosis, height loss) and distal radius (Colles) fractures. Senile (type II) osteoporosis affects both cortical and trabecular bone, with hip fractures. - **Other causes of preferential trabecular loss:** Glucocorticoid excess, hypogonadism, and hyperthyroidism. In primary hyperparathyroidism, cortical bone is classically affected more (e.g., distal 1/3 radius), while trabecular bone is relatively preserved. - **DEXA:** Measures areal BMD at the lumbar spine (trabecular-rich) and femoral neck/total hip. T-score ≤ -2.5 defines osteoporosis. Early or rapid loss shows up first in the spine. - **Osteopetrosis:** Defective osteoclasts (carbonic anhydrase II or CLCN7 mutations) cause dense but brittle bone, marrow crowding with pancytopenia and extramedullary hematopoiesis, cranial nerve compression, and an "Erlenmeyer flask" deformity. - **Paget disease:** Disordered remodeling causes a mosaic pattern of trabecular and cortical bone, with elevated ALP and normal Ca/PO4. - **Osteonecrosis (avascular necrosis):** Commonly involves subchondral trabecular bone of the femoral head. - **Hematologic disease:** Marrow expansion in thalassemia thins the cortex and causes "hair-on-end" skull on x-ray. - **Treatment:** Bisphosphonates (inhibit osteoclasts; risks include osteonecrosis of the jaw and atypical femoral fractures), denosumab (anti-RANKL), teriparatide (intermittent PTH, anabolic, especially trabecular), and raloxifene (SERM).

**High-yield memory aid:** Trabecular = "spongy, spine, and sooner." It has a high surface area, high turnover, it is lost first, and it is the site of vertebral fractures.