11.4 Skeletal System: Bone, Cartilage & Joints
Key Takeaways
- Bone matrix is type I collagen for tensile strength mineralized by hydroxyapatite crystals for compressive strength, and the skeleton stores about 99% of body calcium.
- Osteoblasts deposit osteoid, osteocytes maintain matrix from within lacunae, and multinucleate osteoclasts derived from the monocyte lineage resorb bone by acidifying a sealed compartment.
- Flat bones form by intramembranous ossification directly from mesenchyme, whereas long bones form by endochondral ossification on a hyaline cartilage model and lengthen at the epiphyseal plate.
- Hyaline cartilage covers articular surfaces, elastic cartilage forms the external ear and epiglottis, and fibrocartilage forms intervertebral discs and menisci.
- Parathyroid hormone raises serum calcium by stimulating osteoclastic resorption indirectly through osteoblast RANKL signaling, while calcitonin directly inhibits osteoclasts.
Functions of the Skeleton
The AAMC outline names four functions, and each has a testable physiological consequence.
- Structural rigidity and support — a rigid framework against which muscles generate movement (see 11.3).
- Calcium and phosphate storage — bone holds about 99% of body calcium, making it the reservoir that buffers serum $\text{Ca}^{2+}$ under hormonal control.
- Physical protection — cranium, vertebral column, rib cage.
- Hematopoiesis — red marrow within spongy bone generates all formed elements of blood (see 10.2).
The skeleton divides into the axial skeleton (skull, vertebral column, rib cage) and the appendicular skeleton (limbs and their girdles). Contrast this endoskeleton — living, internal, mineralized, capable of growth and remodeling — with the arthropod exoskeleton of chitin, which is non-living, external, provides better protection and desiccation resistance, but constrains growth and must be shed periodically in molting (ecdysis).
Bone Microarchitecture
Compact (Cortical) Bone
Dense outer bone organized into repeating cylindrical osteons (Haversian systems):
- A central Haversian canal carries a blood vessel and nerve along the bone's long axis.
- Concentric rings of mineralized matrix called lamellae surround it.
- Osteocytes sit in small cavities called lacunae between lamellae, communicating through tiny channels called canaliculi that carry cytoplasmic extensions joined by gap junctions — the only way nutrients reach cells embedded in solid mineral.
- Volkmann's (perforating) canals run perpendicular, connecting adjacent Haversian canals and the periosteum.
Spongy (Cancellous, Trabecular) Bone
An open lattice of trabeculae oriented along lines of mechanical stress, found at the epiphyses and inside flat bones. It is much lighter than compact bone and its spaces house red marrow. Trabeculae have no osteons; osteocytes are nourished by diffusion from marrow.
Coverings and Cavity
Periosteum (fibrous outer layer, osteogenic inner layer) covers the outside except at articular surfaces; endosteum lines the medullary cavity, which contains yellow (fatty) marrow in adults.
Matrix Composition
- Organic (~35%): type I collagen plus ground substance — provides tensile strength and flexibility. Defects give osteogenesis imperfecta, the brittle-bone disease.
- Inorganic (~65%): hydroxyapatite, $\text{Ca}_{10}(\text{PO}_4)_6(\text{OH})_2$ — provides compressive strength and hardness. Loss gives osteoporosis; defective mineralization from vitamin D deficiency gives rickets in children and osteomalacia in adults.
Bone Cells and Remodeling
| Cell | Origin | Function | Diagnostic marker |
|---|---|---|---|
| Osteoblast | Mesenchymal (osteoprogenitor) | Secretes osteoid (unmineralized type I collagen matrix) and initiates mineralization | Alkaline phosphatase |
| Osteocyte | Osteoblast trapped in its own matrix | Maintains matrix; mechanosensor within lacunae | Resides in lacunae, linked by canaliculi |
| Osteoclast | Monocyte/macrophage lineage; multinucleate | Resorbs bone via a ruffled border sealing a compartment it acidifies with a proton pump, dissolving hydroxyapatite, while cathepsin K digests collagen | Tartrate-resistant acid phosphatase |
Remodeling is continuous — roughly 10% of the adult skeleton is replaced yearly — and it obeys Wolff's law: bone is deposited along lines of mechanical loading and resorbed where load is absent, which is why weight-bearing exercise builds density and why bed rest and microgravity cause rapid loss.
A mechanism worth memorizing. Osteoclasts have no PTH receptor. Parathyroid hormone binds osteoblasts, which then express RANKL; RANKL binds RANK on osteoclast precursors and drives their maturation. Osteoblasts also secrete osteoprotegerin, a decoy receptor that sequesters RANKL and brakes the process. Passages frequently test this indirect route.
Ossification
| Type | Template | Bones formed |
|---|---|---|
| Intramembranous | Mesenchyme directly, with no cartilage intermediate | Flat bones of the skull, clavicle, mandible |
| Endochondral | Hyaline cartilage model that is progressively replaced | Essentially all long bones and the rest of the skeleton |
In endochondral ossification a primary ossification center appears in the diaphysis and secondary centers appear in the epiphyses. Between them, the epiphyseal (growth) plate of proliferating hyaline cartilage continues to lengthen the bone until sex steroids at puberty drive plate closure — which is why estrogen deficiency delays closure and produces tall stature, and why growth hormone excess before closure produces gigantism but after closure produces acromegaly.
Cartilage
Cartilage is an avascular, aneural connective tissue (see 8.3) whose chondrocytes sit in lacunae within a matrix of collagen and highly hydrated proteoglycans; it is nourished by diffusion from the surrounding perichondrium, which is why it heals slowly and poorly.
| Type | Dominant fiber | Location | Property |
|---|---|---|---|
| Hyaline | Type II collagen, fine and dispersed | Articular surfaces, costal cartilage, trachea, epiphyseal plate, fetal skeleton | Smooth, low-friction, resists compression |
| Elastic | Type II collagen plus elastic fibers | External ear (pinna), epiglottis | Maintains shape while flexing repeatedly |
| Fibrocartilage | Thick type I collagen bundles | Intervertebral discs, menisci, pubic symphysis | Greatest tensile strength; shock absorption; no perichondrium |
Joints (Articulations)
| Structural class | Connecting material | Mobility | Examples |
|---|---|---|---|
| Fibrous | Dense fibrous connective tissue | Immobile (synarthrosis) or slightly mobile | Cranial sutures; tibiofibular syndesmosis; tooth gomphoses |
| Cartilaginous | Cartilage | Slightly mobile (amphiarthrosis) | Synchondroses (epiphyseal plate, costal cartilage); symphyses (pubic symphysis, intervertebral discs) |
| Synovial | Fluid-filled cavity enclosed by a capsule | Freely mobile (diarthrosis) | Knee, shoulder, hip, elbow |
A synovial joint has articular (hyaline) cartilage on the bone ends, a two-layer articular capsule whose inner synovial membrane secretes viscous synovial fluid for lubrication and chondrocyte nutrition, and often menisci, bursae and tendon sheaths. Subtypes include hinge, ball-and-socket, pivot, saddle, condyloid and gliding joints. Osteoarthritis is degeneration of this articular cartilage; rheumatoid arthritis is autoimmune inflammation of the synovial membrane (see 10.5).
Tendons and Ligaments
Both are dense regular connective tissue — parallel type I collagen bundles with fibroblasts squeezed between them (see 8.3).
- Tendons attach muscle to bone and transmit contractile force; they are slightly elastic and store energy during locomotion.
- Ligaments attach bone to bone across a joint, limiting the range of motion and providing stability.
Both are poorly vascularized, which is why sprains and tendon ruptures heal slowly.
Endocrine Control of Bone and Calcium
| Hormone | Source | Net effect on serum $\text{Ca}^{2+}$ | Mechanism |
|---|---|---|---|
| Parathyroid hormone (PTH) | Parathyroid chief cells | Increases | Osteoblast RANKL $\rightarrow$ osteoclast resorption; renal $\text{Ca}^{2+}$ reabsorption and phosphate excretion; activates vitamin D |
| Calcitriol (1,25-(OH)$_2$ vitamin D) | Skin $\rightarrow$ liver $\rightarrow$ kidney | Increases | Intestinal $\text{Ca}^{2+}$ and phosphate absorption |
| Calcitonin | Thyroid parafollicular C cells | Decreases | Directly inhibits osteoclasts |
| Growth hormone / IGF-1 | Anterior pituitary / liver | — | Drives epiphyseal plate proliferation and longitudinal growth |
| Sex steroids | Gonads | — | Accelerate growth at puberty, then close the epiphyseal plates; estrogen restrains osteoclast activity, so menopause accelerates bone loss |
This table connects directly to Section 9.4, and it explains the two classic passage scenarios: post-menopausal osteoporosis from estrogen withdrawal, and the elevated serum calcium with low phosphate that signals primary hyperparathyroidism.
A drug is developed that selectively blocks the parathyroid hormone receptor on osteoblasts. What effect on bone resorption is expected?
A child sustains an injury that permanently damages the cartilage of the epiphyseal plate in one femur while the contralateral femur is unaffected. What is the most likely long-term consequence, and what type of cartilage was destroyed?
Which pairing of joint type, connecting tissue and mobility is correct?