In its Causation, chronic ostitis is very varied. All sorts of irritants acting on the bones lead to it. Traumatic agents causing wounds, and more especially fractures, are a frequent cause. The processes concerned in the healing of fractures are essentially those of chronic inflammation. Necrosis, from whatever cause, leads to a chronic ostitis around the dead piece. Again, inflammations of joints, whether tubercular, traumatic, rheumatic, or other, lead to inflammations of the neighbouring parts of the bones, the agent which causes the inflammation in the joint acting also by absorption and in a diluted form on the bone. Syphilis and tuberculosis, although producing specific lesions, also lead to ostitis. Phosphorus produces a peculiar form of ostitis associated with necrosis. (See under Necrosis).

The chronic inflammation produces activity in the soft structures of the bones, with the consequence that as regards the bony tissue itself two opposite conditions, namely, destruction and rarefaction of the bone are, according to circumstances, produced. It is customary to speak in this sense of a rarefying and a formative ostitis, but these terma in reality refer to local processes and simply indicate the local results of the inflammation. It is quite common in the same case to have, in different regions, both a rarefying and a formative ostitis. The soft structures of the bone, whose relation to ossification has been referred to in the introductory section, become, under the influence of the inflammation, cellular so as to be converted into Granulation tissue. This occupies the various situations already referred to as those occupied by the active tissue of growing bones. It is present in the medullary spaces, in the Haversian canals, and on the surface of the bone beneath the periosteum. It is an active tissue and produces changes analogous to those of the similar tissue in growing bones. These changes consist in absorption of the existing bone on the one hand and new-formation of bone on the other.

The Rarefaction of bone (sometimes called rarefying ostitis) occurs by enlargement of the spaces and channels, such as the Haversian canals and medullary spaces. It is manifested chiefly in the shafts of long bones, where the dense bone may be converted into a loose cancellous tissue. There is usually at the same time new-formation of bone, so that the thickness of the shaft is increased. The granulation tissue acting on the bony trabeculse causes absorption of the bone, and it is believed that the giant-cells or myeloplaques are chiefly engaged in the process.

New-formation is a more constant and important effect. In all forms of inflammation there is liable to be thickening of the bones from new-formation on the surface. As this takes place under the periosteum it is generally ascribed to periostitis, and this membrane is generally credited with a special power of bone-formation. It is, however, merely the local circumstances which determine the situation of the new-formation, and there is not infrequently an encroachment on the medullary cavity as well as apposition on the surface. The new-formed bone has a rough tuberculated surface as shown in Fig. 272, p. 555. The new-formation may follow on the process of rarefaction so that a dense thickened bone may result (condensing ostitis).

The process of new-formation is similar to that in ordinary ossification. The granulation cells act as osteoblasts, surround themselves with osseous matrix, and remain buried in this as the bone-corpuscles.

Literature

Stanley, On diseases of bones, 1849; Klebs, Beitr. zur path. Anat. tier Schusswunclen, 1872; Rosenbach, Mikroorganismen b. d. Wundinfectionskr., 1884; Gabre, Fortschritte der Med., 1885; Ollier, in Internat. Encycl. of Surg., vi., 1886: Lannelongue et Achard, Annales de l'lnst. Pasteur, v. 1891.