Physis (Growth Plate): Anatomy & Physiology

Development. The physis develops from cartilage-committed mesenchymal cells expressing the SOX family of genes. It is the site of endochondral ossification, the orderly conversion of a cartilage template into bone that drives longitudinal growth, and its multilayered structure is built by chondrocyte proliferation and hypertrophy. Disturbances of physeal development and physiology produce the skeletal dysplasias.

How much each physis grows. The physes do not contribute equally, which is why some fractures remodel well and why epiphysiodesis timing matters. In the lower limb growth is "around the knee"; in the upper limb it is "away from the elbow":

• Distal femur, the fastest: about 9 to 10 mm per year, roughly 70% of femoral and about 38% of lower-limb growth
• Proximal tibia, next: about 6 mm per year, roughly 55 to 60% of tibial and about 27% of lower-limb growth
• Together the knee physes give about 65% of lower-limb length
• Proximal humerus: roughly 80% of humeral growth
• Distal radius and ulna: about 80% of forearm growth

The elbow. The elbow physes therefore contribute little, which is why elbow fractures remodel poorly and need accurate reduction.

Maturity and remaining growth. Physes close at roughly age 14 in girls and 16 in boys, better judged by bone age (Greulich-Pyle / Sanders). Remaining growth for epiphysiodesis timing is estimated with:

• the Menelaus rule of thumb: about 10 mm a year from the distal femur and 6 mm from the proximal tibia, with girls growing to 14 and boys to 16
• the Green-Anderson growth-remaining charts
• the Moseley straight-line graph
• the Paley multiplier

The physis is read from the epiphyseal side to the metaphyseal side, and the four zones follow in that order.

Where growth happens. Longitudinal growth happens mainly in the proliferative zone, through cell division and column formation. The hypertrophic zone adds height as its cells enlarge.

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Matrix and mineralisation. The matrix is rich in collagens (mainly types II, IX, X and XI) and proteoglycans (aggrecan, decorin). The resting and proliferative zones lay down a type II / IX / XI collagen and aggrecan-rich matrix. In the hypertrophic zone, terminally differentiated chondrocytes switch to type X collagen and release alkaline phosphatase, calcium and matrix vesicles.

Provisional calcification. The matrix then mineralises before the hypertrophic cells undergo apoptosis. Metaphyseal vessels bring in osteoblasts, which form the primary spongiosa.

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Why the hypertrophic zone fails. It has the largest cells, the least extracellular matrix per unit volume and a partially mineralised, transitional structure, which makes it mechanically the weakest layer. Shear and avulsion forces propagate through it, and it is the plane of the Salter-Harris fracture.

Why that usually spares growth. The germinal reserve and proliferative zones lie on the epiphyseal side of that plane and keep their epiphyseal blood supply, so most physeal fractures heal without growth disturbance. Growth arrest follows only when the germinal layers or their blood supply are damaged (crush / SH-V, or a bony bar across the plate).

Epiphyseal vessels supply the reserve and proliferative zones. Their disruption is catastrophic for growth, because it starves the dividing cells and the plate arrests.

Metaphyseal vessels supply the zone of provisional calcification, the ossification front, and remove debris. Their loss impairs ossification, but the germinal cells survive.

The periphery. Two rim structures sit around the plate, and they are easily swapped. The groove of Ranvier is a wedge of cells at the periphery that adds chondrocytes there, driving latitudinal (appositional, width) growth. The perichondral ring of LaCroix is a fibrous collar around the physis that gives mechanical support and limits shear.

Two directions of growth. Examiners like the pairing: proliferative zone = length, groove of Ranvier = width, ring of LaCroix = support.

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The PTHrP-Ihh loop. The pace of chondrocyte maturation is set by a negative-feedback loop. As proliferating chondrocytes begin to mature, they secrete Indian hedgehog (Ihh), which (directly and via the perichondrium) stimulates production of parathyroid hormone-related protein (PTHrP) near the ends of the bone. PTHrP acts on its receptor to keep chondrocytes proliferating and delay their hypertrophic differentiation.

Closing the loop. As cells move away from the PTHrP source they escape its influence, hypertrophy and release more Ihh. The axis therefore tightly controls the proportion of proliferating to hypertrophic cells, and with it the rate of growth.

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Systemic hormones and other local factors act on the same zones:

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Clinical correlations. Because these pathways converge on the physis, their disturbance produces recognisable disease:

• Rickets (defective mineralisation) widens the hypertrophic and provisional calcification zones and frays the metaphysis
• Achondroplasia results from an activating FGFR3 mutation that inhibits proliferation
• Oestrogen, not testosterone, drives physeal closure in both sexes: precocious puberty brings early closure and short stature, and oestrogen deficiency tall stature
• Growth hormone excess or deficiency alters longitudinal growth

Fractures and growth arrest. When a physeal fracture injures the germinal zones, or a physeal bar forms, the result is growth arrest, angular deformity or limb-length discrepancy. Arrest may become evident only after the fracture has united, so comparison of serial radiographs over time is essential.

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Limb-length discrepancy. Serial calibrated standing radiographs document a changing discrepancy during growth. The trend, skeletal maturity and remaining growth determine whether observation, epiphysiodesis, lengthening or deformity correction is appropriate.

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Persistent widening after reduction. Physeal widening that persists after reduction is a warning sign. In the case below, MRI identified periosteum trapped in the anteromedial distal tibial physis, and repeat radiographs remained abnormal until the interposed tissue was addressed: imaging that changed management rather than merely confirming the fracture.

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Infection and surgery. The physis is the route of haematogenous osteomyelitis, through sluggish metaphyseal flow. It is also the target of guided-growth surgery (tension-band plating, for example, or epiphysiodesis) that deliberately modulates the plate to correct deformity or length.

The Hueter-Volkmann law. The physis is mechanosensitive. Increased compression across the plate slows longitudinal growth, while reduced compression (or tension/distraction) accelerates it, and this is the mechanics that makes guided growth work.

Guided growth. A tension-band plate or staple that tethers one side of the physis (a hemiepiphysiodesis) slows that side while the other keeps growing, gradually correcting an angular deformity (e.g. genu valgum/varum). It is reversible: remove the implant and growth resumes. A complete epiphysiodesis is permanent and is used to equalise limb length.

The same law explains deformity. Pathological compression of part of the plate, as at the medial proximal tibia in Blount disease (tibia vara), or an asymmetric physeal bar tethering one region produces progressive angular deformity.