Acute bone decalcification is an essential part of a biological process which, in cases of fracture, leads to bone union. This temporary rare-faction is reflex in nature and proceeds from traumatic irritation of the nerve branches which supply the bone and the periosteum. When the irritation subsides, this process is brought to a standstill and is replaced by deposition of lime salts in the newly formed soft callus and the decalcified ends of the fragments. A soldering of the fragments is thus obtained. In some cases, this irritation of the nerve branches continues for a long period and prevents nature from carrying out the normal healing process. Local deficiency of lime salts causes delay in bone union and may even prevent consolidation.

The etiology of this condition may be ascribed to unusual involvement of the sensitive nerve branches, due to trauma, or to methods of treatment which tend to maintain the irritation of the afferent nerve conductors. Fractures of the forearm and leg are especially prone to non-union because of their profuse and diversified innervation. In cases of fracture of the forearm, disregard of the rules of reduction and immobiliztion is an important factor in the production of pseudarthrosis. The sensitive nerve branches which may be chiefly accused of sustainihg irritation and favoring non-union appear to originate in the upper part of the limb from the radial-nerve and ulnar-nerve cables. In the lower limb the corresponding sources are the obturator, saphenous, and peroneal nerves. A special branch of the peroneal nerve, located on the dorsum of the foot and known as the cutaneus dorsalis intermedius, has been found by the author to be especially prone to neuritis of a degree capable of producing marked decalcification. Another form of neuritis, associated with the treatment of fractures, arises from the modern free use of nail extension. Indiscriminate piercing of the bone in such profusely innervated regions as the inner side of the knee and the calcaneum frequently gives rise to stubborn neuritis with consequent wide-spread decalcification.

In the clinical examination of slowly healing fractures more attention should be paid to the possible involvement of the peripheral-nerve branches. Roentgenographic examination should not be limited to the immediate site of injury. Decalcification which extends toward the most distal part of the limb should be regarded as positive proof of existing traumatic neuritis.

Acute bone atrophy plays a conspicuous role in the general pathology of osseous tissue. The aid of physiology and physiological chemistry is needed in solving the problem of this complex process.