The New-formation of epithelium is an essential part of the process of the conversion of a granulating wound into a cicatrix. To some extent the cells at the margins of the granulating wound are derived from the epidermic cells, and these will develop into epidermis. The new epithelium, however, is derived to a large extent more directly by karyomitosis from the surrounding epidermic cells. Hence this part of the process occurs usually at the margins of the wound, and will only take place in the midst of the wound if epithelial structures such as hair follicles or glands survive there. A certain limited amoeboid movement is asserted by which the young epithelium passes into its proper place. The newly-formed epithelium is translucent and delicate, so that the granulations beneath show their colour through it. The epithelium remains somewhat translucent, like that of the stratum lucidum of the epidermis, and there is not in the cicatrix a formation of a proper Malpighian layer. Living epithelium may be transplanted from a distant part or from another person to the surface of a wound where it may multiply. (See under Transplantation).
(b) Other inflammatory new-formations present processes which in their elements are similar to those just described. For new-formation to occur the inflammation must be prolonged for a considerable time, and it must not be too severe, hence usually a chronic inflammation. As it is connective tissue which is chiefly concerned in this process, the result is in most cases an increase of existing connective tissue. In such cases the process does not go through such definite stages as in the case of the granulating wound, but the various steps are present side by sid,e. The tissue shows leucocytes, formative cells, and fully-formed connective tissue.
A brief consideration of the distribution of the connective tissue will indicate the general characters of the inflammatory new-formation. Membranes, such as serous and mucous membranes, undergo great thickening of their connective-tissue structures. As serous membranes are essentially composed of this tissue there is simply a thickening of these. (See under Chronic Pleurisy and Chronic Peritonitis.) The same applies to the endocardium of the heart and the intima of vessels, which are connective-tissue membranes and, in chronic inflammations, undergo thickenings. (See under Chronic Endocarditis and Atheroma.) Mucous membranes contain glandular structures, and the thickening and shrinking of the connective tissue may cause atrophy of the former, and actual thinning of the mucous membrane as a whole. (See under Chronic Bronchitis.) On the other hand, there may be a great thickening of the mucous membrane, especially where the glands are few or simple in structure. This inflammatory thickening may occur irregularly, and there is sometimes a localized formation of tissue which projects from the surface and forms tumour-like out growths, the so-called Mucous polypi, such as are found in the uterus, nares, larynx, intestine, etc. In some cases there is a new-formation of gland tissue along with connective tissue, and the polypi may thus be more complex in structure.
In parenchymatous organs, such as the liver and kidney, there is a stroma of connective tissue supporting the proper tissue, and carrying blood-vessels, lymphatics, and ducts. In chronic inflammations this undergoes increase, and often leads to atrophy of the proper tissue and shrinking of the whole organ.
Foreign bodies, or dead pieces of tissue, frequently give rise to inflammatory new-formation. A foreign body introduced among the living tissues, if not very virulent in its own nature, sets up a mild chronic inflammation, with the result of producing a vascular rudimentary tissue like granulations. If the foreign body be permeable by this tissue, then the granulations grow into it, and, as it were, devour it, replacing it first by their own rudimentary tissue, which afterwards gives place to connective tissue. As this connective tissue is comparatively small in bulk, and tends to contract more and more, the result of the whole process is an absorption of the foreign or dead substance and the gradual disappearance both of it and of the tissue which has replaced it. But if the foreign body is not permeable, or only partially so, then the inflammation results in the production of a layer of connective tissue around it, and so the body becomes encapsuled.
Many instances of this might be given. If a piece of dead animal tissue be introduced into the body, as, for instance, a piece of liver previously hardened in chromic acid solution, or a piece of prepared catgut used to ligature a vessel, then the dead tissue is first replaced by rudimentary tissue which gradually shrinks away. Again, if a piece of a tissue or organ dies, then, if severe inflammation is kept off, it is replaced by rudimentary tissue and absorbed. In fractures of bones it often happens that a piece is entirely separated and dies. Such a piece of bone may lie exposed in the wound in a compound fracture, and it has frequently been seen how it has been eaten into by the granulations and absorbed by them.
The encapsuling of foreign bodies is frequently seen. A parasite such as the trichina or echinococcus obtains a connective tissue capsule. Dead material in the body which is not permeable by the granulations is similarly treated, such as dried-in inflammatory products, which have formed first a caseous and then a calcareous mass. We frequently find such calcareous material surrounded by a fibrous capsule in the lungs and elsewhere.
Attempts have been made to limit the use of the term Inflammation to the phenomena described as those of the earlier periods, and which are concerned especially with the vessels and their contents. The new-formation of tissue is thus excluded, mainly on the ground that it is reparatory, and that it often occurs without any of the phenomena of acute inflammation. Whilst it may be acknowledged that increase of connective tissue may occur as a consequence of atrophy of the proper parenchyma, and without any indication of inflammation, yet it must be added that, if we include the etiological factor in our definition of inflammation, much of fibrous new-formation is inflammatory. Taking inflammation as the ordinary phenomena which result from the action of agents which directly damage the tissues, we must include those cases in which there is a prolonged action, slight at its onset, as well as those in which the onset is abrupt and the influence severe. Moreover, if we are to separate as non-inflammatory the processes which are reparatory, then this principle must be applied to all stages of the process. It will be found impossible, in regard to such typically inflammatory phenomena as active congestion and exudation, to say to what extent restorative processes are involved, as, for example, in the emigration of leucocytes. Discussion has mainly arisen on the question of the so-called chronic interstitial inflammations of the liver and kidney, and the decision has been made to hinge on the question whether degeneration of the parenchymatous tissue precedes the new-formation of connective tissue or not. To the author it appears that this is a wrong issue. The question is rather, whether or not the diseases are due to chronic irritation of these organs by noxious agents. If the irritant act characteristically on both tissues, or if it act primarily on one, it is none the less inflammatory. The author decidedly inclines to the view that cirrhosis of the liver, which occurs in a form characterized by great and evidently primary new-formation of connective tissue is inflammatory and he has come to the same conclusion as to the corresponding disease of the kidney.