We shall next deal with the inflammatory changes occurring in the bones themselves, and shall consider them under (a): Rarefying or Rarefactive Ostitis, (b): Osteoplastic Ostitis, and (c): Caries and Necrosis.

Inflammatory changes occurring in the medulla we may pass without consideration, for in the bones of the foot the medullary cavity is so small, and the changes taking place in it of such minor importance, that we may do this without in any way seriously prejudicing our work.

(a) Rarefying or Rarefactive Ostitis. - By this term is indicated an inflammation of the bone attended by its absorption, the absorption being due to the action of certain cells, termed osteoclasts. This condition may be due to the pressure of tumours, may occur as the result of injury when a piece of bone is stripped of periosteum, or may be the result of an inflammation occurring in the periosteum elsewhere.

A piece of bone undergoing rarefactive ostitis is redder than normal, and the openings of the Haversian canals are distinctly increased in size. As a result a greater number of them become visible. Their increase in size is due to the inflammatory absorption of the bony tissue forming them, and in the larger of them may be seen inflammatory granulation tissue surrounding the bloodvessels. This enlargement of the Haversian canals is well seen when the bone is macerated, the whole then giving the appearance of a piece of very rough pumice-stone.

This process of rarefaction or absorption of bone tissue may be confined to quite a small portion, or it may be spread over the whole of the bone, rendering it more porous than is normal, but stopping short of complete destruction of the bone tissue (a condition which is sometimes known as inflammatory osteoporosis (see Fig. 118)). In this latter case the condition is a chronic one, and the bone tissue remaining often appears to be strengthened by a compensatory process of condensation. For an example of rarefactive ostitis as met with in cases of disease of the feet, we refer the reader to laminitis (see Fig. 118). The osteoplastic or condensing process that appears to exist simultaneously with it explains, no doubt, how it is that bones so affected do not more commonly fracture.

A further example of this process is illustrated in Fig. 133. The pressure of a tumour (in this case a keraphyllocele) has led to rarefactive changes in the bone, forming a neat indentation in the normal contour of the bone which serves to accommodate the tumour.

(b) Osteoplastic Ostitis, Osteosclerosis, or Condensation of Bone. - This, too, is essentially a chronic process. It may occur as a result of, or, as we have just shown, exist simultaneously with the condition of, diffuse rarefactive ostitis. In this case there is a formation of new bone in the connective tissue surrounding the vessels in the Haversian canals. As a consequence the bone affected is greatly increased in density, and many of the Haversian canals by this means obliterated. The end result is an increase in size of the bones in such positions as the horny box admits of it, and a peculiar ivory-like change in their consistence.

For an example of this, we again refer the reader to the changes occurring in chronic laminitis.

(c) Caries and Necrosis. - Caries is a word which appears to be used with a considerable amount of looseness. In addition to the meaning implied by necrosis (namely, 'death' of the part), caries is generally used to indicate that there is also a condition of rottenness, decay, and stench. It is particularly applied, in fact, when the death of the bone is slowly progressive, and is due to the inroads made upon it by putrefactive or septic matter.

Necrosis of bone may be the result of any injury, such as severe blows, or pricks and stabs. In such cases it would appear that it is loss of a portion of periosteum that is the starting-point. With death of a portion of this membrane the vascular supply to a portion of the bone is cut off, and necrosis ensues. It may also result from the extension of inflammatory affections of the structures adjoining it, as, for instance, the spread of the infective material in severe tread, or the encroaches made by pus in cases of quittor, suppurating corn, or complicated sand-crack.

When the necrosed portion of bone is small, and is free from infective properties, it is quite possible that it may, as is the case with small spots of necrosis in softer tissues, be removed by a process of absorption. It must be remembered, however, that where the necrosis has occurred as a result of septic invasion this cannot be looked for, for in every case such reparative changes are worked solely by healthy tissue. If the tissues around the necrosis are engaged in dealing with organismal invasion and the poisonous products thus poured into their working area, their state of health is so weakened that they are unable to successfully combat with the two conditions simultaneously. As a consequence, the necrotic piece of bone persists, and acts as a permanent source of irritation.

It must be remembered, too, that if the dead portion of bone - even though it be free from septic matter - is very large, that it may itself act as a continual irritant, in which case it again persists, and cannot by natural means be removed.

In our cases necrosis of bone may be met with in punctured foot, in severe cases of tread, in cases of complicated crack, and in suppurating corn. It is met with, too, in navicular disease, in the extension of irritating discharges in cases of quittor, and in cases of chronic laminitis where the solar margin of the os pedis has penetrated the sole. In this latter case the protruding portion of bone is quickly denuded of its periosteum. Its blood-supply is destroyed, and necrosis follows.