The Widened or Abnormal Physis

Q: Which single radiographic feature best separates a metabolic cause of physeal widening from a traumatic one?

A: Symmetry and multiplicity. Metabolic disease is systemic and therefore affects all fast-growing physes bilaterally and symmetrically. A traumatic, infective or neoplastic cause is focal and unilateral. Always request or examine the contralateral side before committing.

Q: A 4-year-old has rachitic-looking metaphyses. Alkaline phosphatase is LOW. Diagnosis?

A: Hypophosphatasia. Every other cause of rickets raises alkaline phosphatase; hypophosphatasia is defined by deficient tissue non-specific alkaline phosphatase activity from pathogenic ALPL variants. The international working group's three highest-agreement features are a pathogenic ALPL variant, elevation of natural substrates, and early loss of primary teeth — the last costs nothing to ask about. Diagnosis is made on two major, or one major plus two minor, criteria. Enzyme replacement with asfotase alfa is the specific treatment, and bisphosphonates are contraindicated. Caveat: those criteria are proposed by expert consensus and have not been prospectively validated, so no sensitivity or specificity attaches to them.

Q: An MRI in a 12-year-old baseball pitcher shows proximal humeral physeal widening. Does that make the diagnosis?

A: No — calibrate it against the base rate. Bilateral shoulder MRI in 23 ASYMPTOMATIC Little League players aged 10 to 12 found throwing-side abnormalities absent from the other shoulder in 52 per cent, including proximal humeral physeal oedema or widening in five, with the dominant arm 8.5 times more likely to be abnormal. Crucially, 61 per cent had experienced prior shoulder pain and that did not predict an abnormal scan. What did predict it was exposure: none, one or both of year-round play and single-sport specialisation gave a 25, 71 and 100 per cent chance of abnormality. Imaging confirms a clinical diagnosis here; it cannot make one, and it cannot clear a symptom-free child. Twenty-three players, so treat the percentages as small counts.

Q: A 14-year-old elite gymnast has wrist pain and a widened, irregular distal radial physis. Ulnar variance is positive. Mechanism, and how common is it?

A: Chronic repetitive axial loading causes a Salter–Harris I stress injury of the distal radial physis with impaired endochondral ossification. Caine's authors are explicit that this is a stress fracture and not normal adaptive change in gymnasts — the consequence to warn about is premature physeal arrest with relative ulnar overgrowth, positive ulnar variance and ulnar impaction, which is permanent. It is also less common than its fame implies: in a survey of 60 competitive gymnasts only five had stress-related change and four of those were minimal. Management is activity modification and rest, typically 3 months, with immobilisation if symptoms are severe.

Q: Which two features on a paediatric metaphyseal film should prompt an urgent full blood count and film?

A: Diffuse lucent metaphyseal bands at multiple sites, and permeative destruction with periosteal reaction — particularly in a child with bone pain, pallor, fever or refusal to walk. Acute lymphoblastic leukaemia and metastatic neuroblastoma both present this way and are commonly misattributed to juvenile idiopathic arthritis or osteomyelitis. Blood film and bone marrow aspiration are diagnostic.

Q: Which metaphyseal pattern indicates scurvy rather than rickets?

A: Scurvy produces a DENSE white metaphyseal line (the Frankel line, from failed matrix resorption) with a LUCENT band immediately beneath it (the Trümmerfeld zone), sclerotic ring epiphyses (Wimberger ring) and dense subperiosteal haemorrhage. Rickets does the opposite: it obliterates the dense metaphyseal line and produces cupping and fraying with generalised osteopenia.

Q: Rachitic-looking metaphyses, short stature, waddling gait, and completely normal calcium, phosphate and alkaline phosphatase. Diagnosis?

A: Metaphyseal chondrodysplasia, Schmid type — the commonest. An autosomal dominant COL10A1 disorder of type X collagen with normal biochemistry, normal epiphyses and a spared spine, often mistakenly treated as rickets for years. It presents at walking age with coxa vara and genu varum, and does not respond to vitamin D.

Q: You diagnose nutritional rickets in a toddler. What else does that oblige you to do?

A: Look beyond the patient. The global consensus frames nutritional rickets as a preventable public health problem rather than an isolated diagnosis, and ranks maternal and infant risk factors specifically — so check the siblings, ask about maternal vitamin D status during pregnancy and lactation, and consider the wider community and its access to supplementation or fortified food. Note also that the diagnosis is defined by clinical, biochemical and radiographic features together: a cupped, frayed physis is one component, not the diagnosis on its own.