Although it is highly probable that the medulla is the part in which all pathological plastic processes in bone originate, yet very little is known of its diseases. And upon this deficiency of information it no doubt depends, that, on the one hand, our opportunities of investigating the diseases of the medulla are almost entirely confined to very advanced cases - cases in which the whole bone is involved in the disease, - and hence that on the other hand, whilst studying the changes in the actual bony tissue, we are in the habit of paying less attention to the medulla.

Oftentimes, in consequence of hypertrophy, it is augmented in quantity, and its increase occasions dilatation of the Haversian canals, the cancelli, and the medullary cavities, in which it is contained. Such hypertrophy is unquestionably the cause, either by itself or in combination with other processes, of many of the osteoporoses, both those which are circumscribed, and those which extend throughout a bone. While increased in its quantity, it may retain or depart from its normal texture and composition. Thus instead of the jelly which fills the cells of the spongy tissue of some portions of hopes, of the diploe of the bones of the skull, for instance, actual medulla is sometimes found, even in the form of compact lobular masses.

Its excessive accumulation leads at length to atrophy of the spongy and reticular bony substance, and to expansion of the compact walls of the bone.

On the other hand, when the bone is affected with concentric atrophy, the medulla shrinks as well as the bony tissue, otherwise its place is taken by a gelatinous, fatty, or serous fluid.

In color and consistence it very frequently deviates from its usual condition, and so also in its texture and composition. The former changes are usually mainly dependent upon the latter in relation to their cause.

The color is sometimes unusually pale or white, sometimes it is a dark yellow; and it frequently acquires various hues of red, rusty brown, yeast-yellow, or chocolate, from mixture with blood; it is variously discolored when caries is going on in the bone.

In consistence it is sometimes too thin, being liquefied by serum, or oleaginous; in other cases it is unusually firm, it resembles suet or adi-pocere, and may be broken.

In reference to its texture, it is liable to congestion and to hemorrhage, by which it may be discolored, and assume a dark-red, chocolate, rusty brown, or yeast-yellow, hue.

The real seat of inflammation in bone is the membrane which lines its cavities. The inflammation of this membrane leads to an exudation which sometimes becomes organized into bone, and sometimes is converted into cellular or fibroid tissue, as may be seen after injuries of bone, or, more rarely, in consequence of spontaneous inflammatory processes; i. e., the medullary membrane and its prolongations undergo fibroid thickening: lastly, the products of the inflammation are sometimes purulent or ichorous, and in various ways destroy the structure in which they are deposited, and the bony tissue. The anatomical marks of these processes are self-evident; they may be recognized also by reference to what has been said about inflammation of bone and its consequences.

In dropsy, the place of the fat of the medulla is gradually taken by a thin, gelatinous, and finally serous fluid.

There are some remarkable changes already alluded to, which the marrow undergoes in osteoporosis and mollities ossium, but their exact nature is still unknown.

Finally, the medullary membrane is the structure in which all adventitious growths in bone originate. Tubercle and cancer afford easy proofs of this remark, especially many forms of the latter, such as encephaloid infiltration of bone, and the cancerous diseases named erosion by Otto, and osteolyosis by Lobstein.