them as possible; perhaps change of air, scene, diet, and mode of life, may have much to do with this fact.

It is not, however, my desire to place before the reader an exaggerated idea of the benefit such treatment may afford. A spa supports a quantity of hotels, attendants, gamblers, &c., &c. ; we hear the successful cases quoted again and again; indeed if we could believe all that has been said and written about many mineral springs, we should only wonder why, with such waters on the earth, diseases should continue to exist. Although it must be acknowledged that many who resort to such places with the hope of coming back sound and healthy, only bring away with them disappointment and regret; yet others are decidedly benefited.

This disease is so slow, and extends over such a long period, that I refrain from giving any history of cases.

CHAPTER XIII.

INFLAMMATION AND DEGENERATION OF CARTILAGES.

MOST works on diseases of the joints contain a part devoted to those maladies, which have their especial seat in the cartilages; and yet nothing can be more sure than that of all the jointdiseases, which fall under the surgeon's notice, not one originates in the cartilage. It has been seen that an inflammatory action commencing in the synovial membrane or in the bone, will spread to the cartilage and set up an ulceration of that structure; it is also well known that in the dead-house and dissecting-room we frequently find breaches of continuity in various articular cartilages which were accompanied by no symptom during life. The joints in which such conditions are found have been perfectly free from any pain or any diminution of mobility, and the neighbouring tissues have been perfectly untouched by any disease whatever. Thus we come to the inevitable conclusion, that disease confined to the cartilage gives rise to no symptoms; and we must ask whether disease, which has commenced elsewhere and passes to the cartilage, may give any sign whereby we can tell whether or no the cartilage be diseased? To answer this question fully it is necessary to enter somewhat deeply into the physiology and pathology of cartilage; but as the subject has occupied some attention in each division of this work, it will be only necessary to revert to the points already treated, and the present chapter will rather be a résumé than a full exposition of the subject.

The questions resolve themselves into these :-Are there different sorts of ulceration of cartilage; one accompanied, the other unaccompanied, by any symptoms? If so, are either or both these ulcerations produced by some action of the tissue itself, or of some other tissue, absorbing the cartilage as a passive material ?

Sir B. Brodie has throughout all the editions of his work on

diseases of the joints adhered to his original view of active changes in the cartilages; in his earlier papers he ascribed these to the intervention of vessels; and he has even in his fifth edition some difficulty in getting rid of the idea, since he affirms that "in persons who have not yet attained their full growth, vessels penetrate into the articular cartilage." Mr. Aston Key, however, in 1833, saw some reason to doubt the possibility of any vital actions in cartilage, and attributed their absorption entirely to the "villous processes developed on the synovial membrane during inflammation of that structure." Sir B. Brodie, nevertheless, adhered to his original idea. In 1843 M. Richet,* of the Hôpital Bons-Secours, added his testimony to the idea of cartilage being a dead, an almost inorganic material. Dr. Ecker, † in 1844, published the first observations upon the actions and conditions of cartilage-cells in disease. One of Mr. Goodsir's 'Pathological and Surgical Observations' in 1845, also mentioned the growth and increase in the number and size of the cells. In 1848 Dr. Redfern published a series of careful and minute observations 'On the Abnormal Nutrition of Articular Cartilages,' carrying further the researches of Ecker and Goodsir, and disclosing many details which those authors had not mentioned. Yet the idea that cartilage is truly a living structure capable of vital action penetrated so slowly, that in 1853 M. Richet, in a paper on white swelling, § insists upon the inactivity of cartilage, and is at pains to prove that it is incapable of any independent action, saying, although he refers to Dr. Redfern's paper, "that the only direct manner of proving that cartilages are susceptible of inflammation would be to demonstrate vessels in their substance itself." Mr. Birkett || censures the use of the word ulceration, and desires to substitute disintegration."

66

Even so late as 1859, Mr. Bryant ¶ of Guy's Hospital, following too implicitly in this path, ascribed all the diseases of

* Richet, 'Sur les Tumeurs Blanches.' Annales de Chirurgie.

+ Ueber Abnützung und Zerstörung der Gelenkknörpel.' Archiv. für Physiologische Heilkunde, vol. ii. p. 235.

See my paper On the relation between Synovitis and Ulceration of Ar

| ticular Cartilages.' Edinburgh Medical Journal, February, 1860.

§ Mémoires de l'Académie Impériale,' tome xvii., 1853.

Guy's Hospital Reports,' 2nd series, vol. vi., p. 237.

'Diseases and Injuries of the Joints.'

cartilage to atrophy; degeneration and hypertrophy being only mentioned in order to throw doubt on the possibility of their

occurrence.

I believe myself to have been the first to have pointed out that those diseases of cartilage which accompany the inflammation of other tissues in the joint are, in reality, inflammation.* The whole view of the subject, and the arguments which irresistibly lead to this conclusion, have been already detailed (see Chapter II. and Chapter V.) Histologically cartilage belongs to the connective tissues, and we have seen abundant evidence of the fact that their inflammation essentially consists in a rapid multiplication of the cells, which form an essential part of their structure. We find this to be the case with the areolar, ligamentous † and osseous tissues; indeed, we find that the action of vessels in inflammation is but secondary; they appear only as bearers of an increased supply of nutriment to tissues making increased demands; hence the one necessary essential which renders it possible for a tissue to assume an inflammatory action, is not the presence of vessels actually in that tissue, but the presence of cells unoccupied by any material which might prevent their multiplication and generation. § Thus, histologically and pathologically, there is no reason why cartilage should not inflame, and in certain diseases of that structure we see the cells assuming a generative activity, which is the essence of the inflammatory act, as exemplified in all tissues of the connective class. || Wounds of the cornea, according to Mr. Bowman, ¶ produce an abundant generation of cells, which lead either to reunion or suppuration and destruction of the part. Dr. Redfern passed setons through the costal cartilages of dogs, and found that they invariably produced considerable generation of cells in the part next the silk. An examination of areolar tissue in the neighbourhood of a wound

* See my paper' On the Nutrition and Inflammation of Articular Cartilages,' in Med. Chi. Review, Oct. 1859.

† See my paper On Granulation.' Beale's Archives, vol. ii., No. 5.

See my paper On Osteitis,' in Med. Chi. Review, April, 1860; and Chap. XI. § From this fact a corollary may be drawn; one which on the face of it may appear utterly false, far-fetched, and even absurd; but which I nevertheless believe myself in a position to prove, namely, that no special tissue is capable

or ulcer, shows the cells of that structure in an active condition of generation; and the cells in the lacunæ of bone are actively employed in inflammation of that structure. When, therefore, an inflammatory disease of the synovial membrane spreads to the other constituents of the joint, and we find the cartilage and bone involved, we have no à priori reason for refusing the term inflammation to the disease of the cartilage, simply because that structure contains no blood-vessels.

A point of pathology cannot, however, be settled by mere reasoning: the morbid anatomy is the only true key to the argument. It is found, then, that multiplication of cartilage cells may occur to such an extent as to eat up or absorb the hyaline structure, producing ulcers commencing on the free surface of the cartilage. This process takes place when the surrounding structures are inflamed, and is similar to the inflammatory act in them.

But ulcerations of, i. e. breaches of continuity in cartilage, occur when the parts around are perfectly healthy. The existence of these lesions is not suspected during life; they are found in the dead subject, whose articular functions had been perfect. Such ulcers look to the naked eye more fibrous, rough, and are generally softer than those already described; sometimes the cartilage is converted into a set of parallel fibres, close together, and standing from the bone surface as the pile of velvet from the woof; and often that part of the cartilage is yellow. If sections of this material be examined microscopically, the corpuscles will be found increased in size, and the contained cells also are larger; but they are not increased in number. Those corpuscles, which contained two, three, or four cells near the attached surface, still continue, on approaching the other edge, to possess only an equal number of cells; the nuclei do not multiply; on the other hand, they become obscured by an accumulation of minute globules of oil around them, between the cell wall and the nucleus; in a further advanced stage, and nearer the free surface, the corpuscle itself gets filled with the oil, which lies around the cells. The fibrification of the hyaline substance commences by the appearance of thin faint striæ; in some instances there may be seen between these a row of oil globules, and the stria become more numerous and more open, until the substance is split into fibres.