A field-change effect could cause both an increase in local osteochondroma formation and growth disturbance. Hence local osteochondroma ‘burden’ might be associated with deformity without invoking ‘cause and effect’. A putative ‘post-axial’ (ulnar and fibular) preference for a ‘field-change’ effect would result both in greater osteochondroma volume and the genetic effect would then result in more exostoses and a shorter ulna. However this theory becomes more difficult to sustain if some patients are observed to have a ‘pre-axial’ preference and others a post-axial one. This is especially so of different preferences were to be observed in opposite limbs of the same patient; in this case a neoplastic pathogenesis for local growth disturbance becomes more likely.

Solitary osteochondromas are not hereditary, but they appear identical to osteochondromas arising in the multiple form. Several studies have suggested that bi-allelic mutations can be found in solitary osteochondromas, however this is not ubiquitous and perhaps other non-EXT pathways are involved in the development of these benign tumours [2]. Nevertheless, their clinical behaviour and pathological features are indistinguishable from those in MO. The clonal nature of neoplasia means that the formation of a solitary osteochondroma will initially involve a genetic change in a single cell of the chondral mesenchyme of the peripheral physis. A field change is unlikely to be responsible as there is no germline defect such as occurs in MO. Hence growth disturbance caused by a solitary exostosis cannot easily invoke a field-change effect to explain its occurrence. Consequently, studies which identify growth disturbance in solitary exostoses can shed important light on the same effect in MO.

When a child with MO presents, the parents wish to know what the future is likely to hold. Without an understanding of pathogenesis there can be no certain advice about preventing the growth disturbance which in some children can be severe. If evidence favours solely a neoplastic pathogenesis then the surgeon will choose to remove exostoses in association with deformity as they develop at key sites (eg distal forearm, distal tibia and fibula). He/she may even decide NOT to remove some exostoses if that decision might result in more balanced growth disturbance affecting paired bones. On the other hand, if evidence favoured a field-change effect, then removal of exostoses could not be justified on grounds of amelioration of the disease process, only in order to reduce pain, improve range of movement or cosmesis. Finally it is possible that there is a mixed aetiology for growth disturbance; in which a field-change effect might cause growth restriction at preferred sites in the absence of osteochondromas yet additionally a local effect of a large osteochondroma could modify that effect. In that situation advice to parents about the result of surgery would be more guarded, and allow for both possibilities. If it is believed that the excision of exostoses might reduce growth-disturbance effects, then the question of timing (early or late) becomes important since early exostoses are confluent with the growth plate, but later ones may have already resulted in significant deformity.