hyaline cartilage

**Structure/Histology** - Cells: chondroblasts (produce matrix) → chondrocytes (mature cells sitting in lacunae). Chondrocytes may appear in isogenous groups (clusters from division). - Matrix: type II collagen (fine fibrils, not visible on H&E, giving "glassy" look) + proteoglycans (aggrecan, bound to hyaluronic acid via link protein; chondroitin sulfate and keratan sulfate side chains) + water (~70-80%). Highly hydrated GAGs resist compression. - Perichondrium (dense irregular CT with chondrogenic layer) surrounds most hyaline cartilage EXCEPT articular cartilage (no perichondrium) and fibrocartilage. Matrix is basophilic on H&E (sulfated GAGs). - Avascular, aneural, alymphatic: nutrients reach chondrocytes by diffusion (from perichondrium vessels or synovial fluid in joints). Hence poor regenerative capacity; repair often yields fibrocartilage (type I collagen), which is mechanically inferior.

**Growth** - Appositional growth: new matrix added at the surface by perichondrial chondroblasts. - Interstitial growth: chondrocytes divide within lacunae and secrete matrix from within (only possible because the matrix is still pliable in young cartilage).

**Locations (high-yield)** - Articular surfaces of synovial joints - Epiphyseal (physeal) growth plates - Costal cartilage (ribs to sternum) - Respiratory tract: nasal septum, larynx (thyroid, cricoid, arytenoid—except epiglottis/corniculate which are elastic), tracheal rings, bronchi - Embryonic/fetal skeleton template for endochondral ossification

**Clinical correlations** - Osteoarthritis: degeneration of articular hyaline cartilage ("wear and tear"); ↓ proteoglycans, ↑ water initially, fibrillation, subchondral sclerosis, osteophytes (Heberden nodes at DIP, Bouchard nodes at PIP), joint space narrowing; pain worse with use, relieved by rest. Chondrocytes release MMPs and IL-1/TNF-α in disease. - Rheumatoid arthritis: pannus destroys articular cartilage. - Achondroplasia: FGFR3 gain-of-function mutation → impaired chondrocyte proliferation in the growth plate (endochondral ossification) → short limbs, normal trunk; membranous ossification is spared. - Slipped capital femoral epiphysis: failure through the hypertrophic zone of the physis (adolescent obese males). - Salter-Harris fractures involve the growth plate. - Chondrosarcoma and chondroma: malignant/benign tumors of hyaline cartilage; chondrosarcoma is a malignant tumor of cartilage, commonly in the pelvis/axial skeleton in older adults. - Relapsing polychondritis: autoimmune inflammation of cartilage (ears, nose, tracheobronchial tree) → floppy ears, saddle-nose deformity, airway collapse. - Scurvy (↓ vitamin C → defective collagen hydroxylation) and Ehlers-Danlos affect collagen; costochondral beading ("rachitic rosary") is seen in rickets/scurvy. - Osteochondritis dissecans: segment of subchondral bone and overlying cartilage separates. - Collagen type II mutations (COL2A1): Stickler syndrome, some chondrodysplasias.

**Comparison of cartilage types** - Hyaline: type II collagen; joints, physes, trachea, costal cartilage. - Elastic: type II collagen + elastic fibers; external ear, epiglottis, Eustachian tube; has perichondrium; stains with elastin stains (orcein/Verhoeff). - Fibrocartilage: type I (and II) collagen; intervertebral discs (annulus fibrosus), menisci, pubic symphysis, TMJ disc; no perichondrium; resists tensile/shear forces. - Memory aid: "Type TWO is cartilage" (hyaline, elastic); "bONE" is type I. Fibrocartilage is the exception (type I + II).

**Endochondral ossification (growth plate zones)**: reserve/resting → proliferative (columns) → hypertrophic (chondrocytes enlarge; Ihh/PTHrP feedback; weakest zone) → calcification → ossification. Hyaline cartilage template is replaced by bone.