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born child. Nor have I been able to discover epithelium overlying the cartilaginous surface: what Mr. Bowman took for that structure was, I believe, the superficial layer of cells as above described, which, in the yet unused joint, is finer than when it has been subject to wear and tear. The absence or presence of vessels upon the foetal cartilage is of importance, because if present it would establish the fact of a structure lining a cavity being nourished by its free surface. Besides, as it is clear that, at least during intra-uterine life, there is large provision for nutrition of the cartilage from the deep surface, the presence of such vessels would show that a structure having one free, one attached surface might be nourished from both. Moreover, it would prove that a cellular structure might be nourished from the surface towards which the cells grow. But the two first facts would be isolated, and the latter is hardly conceivable; and as others besides myself have failed to discover this arrangement, there must have been in the observation of such vessels some occult source of error.
Thus articular cartilage is not so dead and unorganized a material as is generally imagined, as is proved by the care taken to supply to it nutriment in finely divided streams-the most available form possible for use. The great vascularity of the parts, which furnish this supply (a vascularity consisting of dilated and dilatable vascular loops, which are not destined for the nourishment of the bone, since this structure has its own Haversian canals,) shows that the vital actions of cartilage must be active; and although we shall probably never be able to make experiments proving their rate of growth, yet have we on record one or two cases, which show that other changes may be very rapid, so as to confound the conventional idea of the inertness of articular cartilage. Mr. Arnott has reported a case of this sort.† A man was bled, and six days afterwards was attacked with phlebitis; six days after its commencement-i.e., on February 4th-pain in the left knee, with some swelling, was observed; on the 8th of the month the man died. The cartilages on the femur and tibia were over a large space so deeply eroded as to lay bare the bone. All which ulceration must have occurred in from 96 to 120 hours.
Mr. Mayo gives a less rapid case of a boy who had received an injury to the skull. Four days afterwards a joint of one of the fingers and one of his ankles became painful and swollen. He survived the accident only three weeks. Examination of the swollen joints showed that the cartilages had disappeared from them almost entirely.
Sir B. Brodies gives the case of a boy who had injured the knee, and died in twenty-two days; the account of the examination is as follows:
"The cartilage covering the condyles of the femur, and that covering the head of the tibia, were found in some parts entirely absorbed, so that the bone was exposed; while in other parts it was absorbed on the surface towards the cavity of the joint, the layer of it next to the bone retaining its natural
* Kölliker could not make out any vessels on the surface of fatal cartilage.
adhesion and its natural structure. The cartilage in these parts was formed into grooves, having an appearance as if the greater portion of it was removed with a chisel. There was no purulent or other effusion into the cavity of the joint."
A man fell on his head from a considerable height, and was brought insensible into St. Thomas's Hospital; the next day acute synovitis began in the right knee; on the fifth day he died. There were of course the signs after death of synovitis, but the cartilages were sound, except in a spot larger than a sixpence on the inner condyle of the femur, whence it had entirely disappeared; the edges of this ulcer were perfectly smooth, clean, and sharp.
Now the alterations which take place in cartilage are all dependent upon changes in the cells, for in every structure which consists of cells and an inter-cellular part, each cell has a certain district of the latter substance under its maintenance and control; hence the changes in texture or state of the hyaline substance of cartilage are all secondary; and the ordinary mode of classifying the structural changes in cartilages, according to the alterations of its inter-cellular substance, is as false as every classification built upon secondary facts must be. The error is one not of words merely, or it might well pass unchallenged, but is one of essentials, and confounds together certain forms of malady which should be kept distinct, and separates others which have no, or only accidental, differences. Thus the division of the diseases of cartilage into fibrous, fatty, and granular degeneration, according as the hyaline substance is split into fibres or studded with oily or granular matter, must be false, for both the latter changes are mixed with the fibrous transformation of the inter-cellular substance. In fact, fibrous degeneration, as Mr. Birkett and other writers have called it, is not itself a disease, but an accompaniment of almost every morbid process which takes place in articular cartilage.
The basis of a true division can only be laid in the changes taking place in the cells; and these may be divided into-1st. Alterations in their contents, or degenerations; and, 2nd. Alterations in their activity.
1st. Changes in the Contents of the Cells.-The degenerations which the cells undergo are albuminous or granular and fatty. Granular degeneration of the cells advances pretty far before it affects the hyaline matter; it begins by a deposit in the cells contained in one or more cartilage corpuscle, of fine opaque granules. The cells enlarge somewhat, but never develop other cells or nuclei; after a time the cartilage corpuscle bursts, and gives forth the cells, which in their turn let free the granules, but the nuclei entirely disappear, and do not come into view when treated by acetic acid. As this disease of the cells reaches a certain point, the hyaline substance becomes striated and splits into fibres.
Fatty degeneration is a much more frequent disease. Many joints of subjects brought into the dissecting room (no symptoms having been observable during life,) are found to have their cartilages ulcerated. These ulcerations are lined, and partly filled, with a fibrous structure, and many of them are due to fatty degeneration. The cells near the ulcer
are filled with fat globules, generally very small, which completely conceal, afterwards destroy, the nucleus, and render the whole cartilage corpuscle opaque and of a brown colour. The hyaline substance is likewise studded with fat granules, and has undergone a like change of hue; it becomes striated, and ultimately splits into fibres. appearance is well known, but it sometimes happens that in examining joints not otherwise diseased, the cartilage will be found in one or more slightly raised specks to have lost its lustre, its grey translucent appearance, and to have become of a dull yellowish hue. On cutting vertically through these spots, they are seen to be of a triangular shape, the base being at the free surface, the apex extending more or less deeply into the tissue. A thin section placed under the microscrope shows that below the point where the change in colour is perceptible, there is an accumulation of fat in the cells of one or more corpuscles; farther on, more such bodies are involved, and are more crowded with fat granules. When the cells are completely fatty, there will be seen proceeding from them rows of small oil globules, like strings of beads, separated from each other by bands of the hyaline substance, of various breadths, each such band being divided into fibrilla, among which an occasional oil globule is visible. This is, I conceive, the first stage of fatty degeneration, and serves to show that a fibrous condition of the hyaline substance is not to be considered as a disease apart from the other alterations of cartilage, since it follows both forms of cell degeneration.
2nd. Changes in the Activity of the Cells.-The activity of the cells may be either decreased or increased. Of the former little is known; but thinning of cartilage does certainly take place, and in such specimens I have found the cartilage corpuscles smaller than usual, and even close to the bony attachment, forming lengthened horizontal bodies, in which the cells are very small, with a hardly perceptible nucleus, and look already like the flattened scale of the free surface.
The morbid condition which originates in increased activity of cells is that to which I would more especially call attention, as taking place in all inflammatory disease of joints. The cartilage corpuscles in this state increase in size, and instead of possessing only from two to six nucleated cells, contain from twenty to sixty of all sorts-brood cells, young cells, and bare nuclei. The corpuscle subdivides also more frequently, thus giving rise to a greater number, and they often burst and discharge their contents freely into the hyaline substance; or if this takes place on the surface, they leave a depression at that spot. Mr. Redfern's third, fifth, sixth, and other observations are of this sort of disease. It may terminate either in simple erosion of the cartilage, that is, total disappearance at the spot of that structure, the edges of the cavity looking sharp and clean "as though cut with a chisel;"* or it may give rise to conversion of the hyaline structure into fibres previous to its disappearance. The former of these conditions is the most acute, the latter the more chronic form. That this increase of growth should be attended by loss instead of augmentation of sub
* Sir B. Brodie: Diseases of the Joints.
stance is to be accounted for by the excess of demand by the cells over the supply of nutriment, an excess which must be supplied by the inter-cellular substance. In the acute form of the disease, where the cell-generation is excessively rapid, the hyaline substance disappears bodily; in the less acute condition, alternate lines in the direction of the cell-force are absorbed and
left, whence fibre must result. The cells, as we have seen, tend to the vertical in the deep, to the horizontal in the superficial part of the cartilage; and the fibres, as they form, take the same direction (fig. 6). The great distinction to be observed between this form of disease and the cell-degenerations above mentioned is, that in the former rapid generation of cells takes place, brood cells giving birth to progeny, the nuclei dividing and forming fresh cells; and although at the latter stage of the process a few fat granules may be seen in the cell, they neither obscure nor destroy the nucleus. In the latter forms (degenerations), the cell becomes clogged with a material which destroys the generative power of the nucleus, and the cell dies without progeny; but in both the hyaline substance becomes fibrous.
Now, although by the cases quoted from Mr. Arnott and other writers we find that absorption of cartilage may be extremely rapid, and although by the examinations of articular cartilage we find that the processes are those of excessive action, it may seem bold to state that this latter form of disease is inflammation. It is true, that throughout, no vessel, nor any signs of a vessel, can be seen in cartilage, but if we enter into a study of all organs of the body, we shall find that every tissue is without blood vessels; the capillaries only skirt the organization, whatever it may be. Examine the grey portion of the brain, then the white, and it will be seen that the pieces of brainmatter between the enclosing meshes of vessel are much larger in the latter than in the former; then examine a piece of the dermis from the tip of the finger and another piece from about the loins, and again are the islets of tissue between the vascular streams larger in the latter than in the former; but shall it therefore be said that the grey matter of the brain is more capable of inflammation than the white, or the skin of the finger-tip more capable thereof than that of the loins? Take a wider example, and compare the vascularity of intestinal mucous
membrane with that of bone. A piece of that mucous membrane is so richly supplied with blood, that it is of a brilliant red hue, and if it be injected, it appears simply a mass of blood vessels. A piece of bone, on the other hand, is so sparingly supplied, that the islands between the vessels, whither no blood penetrates, are frequently half a line square, and even much larger in the longitudinal section; yet the mucous membrane is not more capable of inflammation than bone. Surely it would be very illogical to say that every vascular part, whether highly so or only slightly so, was equally capable of inflammation; but every non-vascular part (so called) was incapable of it. Surely, if this vascularization make the difference between capacity and incapacity, there would be degrees of capability from the part most supplied to that least supplied with blood; but we do not find this to be the case. Again, although in such a tissue as the brain the vessels lie very close together, yet there must be spaces, however small, wherein brain-matter lies and whither vessels do not penetrate, which are therefore non-vascular; and in cerebral inflammation it is these very spots, and not the vessels themselves, which are inflamed. Can any one presume to say that a non-vascular tissue of a certain size shall be capable of inflammation, but beyond that size incapable? In other words, can it be affirmed, that in order to render any issue capable of inflammation, it is necessary that blood should flow at a distance not exceeding a certain definite fraction of a line?
In endeavouring to explain the vascular phenomena of inflammation, recourse has been had to all sorts of theories; some have supposed that there is dilatation, others contraction of the capillaries, with increased or decreased rapidity of the blood-stream; others have imagined an actual stasis. Soon it came to be shown that capillary vessels are incapable of either contraction or dilatation, and the place of action was shifted to the finer arteries and to the nerves which may be supposed to control them. Here again, however, is difficulty without end, for we find all sorts of vascular states, which have been called passive and active, venous and arterial congestion, which, however, are not inflammation.
I lately saw a man, under the care of my friend Dr. H. Salter, who had chronic palpitations of such rapidity, that his heart beat over two hundred in a minute. If rapid vascular action be the cause of inflammation, the man ought to have been inflamed all over, through and through. Moreover, how does it happen that parts supplied by the same branch or twig of artery shall be inflamed in one point, and not in another?
Let us, to solve these difficulties, again go back to the affirmation that inflammation is an alteration in the nutritive function, and let us consider the conditions of that function. It is evident that in the support of various tissues the blood vessels are the mere passive carriers of nutriment—at least, no one, I imagine, would for an instant suppose that the nutritive function is forced upon a part by the blood; on the contrary, the tissues (all extra-vascular) draw from the blood pabulum as they want it. This demand of the tissue is so balanced with the