1. Spontaneous calcification of the rachitic callus in the later stages of healing has been described in detail, and has been shown to be responsible for the consolidation of fracture in rickets.
2. Spontaneous calcification of the callus has been defined, on the basis of observations upon the blood calcium and phosphorus, and upon undecalcified histological specimens which demonstrate the bone salt, as calcification which is progressive and limited to the fracture area. It is not accompanied by any change in the levels of the blood calcium and phosphorus. or in the existing state of the rachitic metaphyses. The calcium salts are laid down in the osteoid and cartilage of the tissues adjacent to the shaft in a characteristic pattern which is clearly distinguishable from calcification which follows administration of phosphate solution or vitamin D, and results in healing of the rickets.
3. The necrotic and uninjured portions of the section of the shaft which is enclosed in the growing callus have each been considered as possible sources of the calcium salts deposited in spontaneous calcification of the callus. The fact that the living cortical bone, by far the greatest portion of the length of the shaft enveloped in callus, becomes considerably rarefied when the callus reaches maximum size, and at the time when spontaneous calcification reaches its maximum distribution, suggests that this calcification represents local transfer of calcium salts from the shaft to the callus. Since the necrotic portion of the section of the shaft surrounded by callus is only a small fraction of the bone mineral stored in the cortex at the fracture area, it is believed that if it contributes to local transfer in the course of its absorption, the amount of bone salt thus liberated is relatively insignificant and cannot be regarded as an important source of the calcium salts deposited in the callus of healing fractures.
4. Because local implantations of devitalized bone or injections of colloidal calcium phosphate into the rachitic callus osteoid, prior to the advent of spontaneous calcification, fail to initiate calcification, it is concluded that these substances cannot be regarded as local sources of the bone salt. The differences in the mechanism of the resorption of living bone, as compared with the process of the absorption of dead bone or calcium salts, suggest that the local redistribution of the bone salts in the area of a healing fracture is brought about by the activity of the cellular elements of the bone, possibly the osteoclasts.
5. The phenomenon of local transfer of calcium salt may be regarded as indirect experimental evidence of local increase in concentration of dissolved calcium salt in the extracellular fluid of living bone undergoing resorption.