CHRONIC NON-TUBERCULAR

ARTHRITIS.*

PATHOLOGY AND CLASSIFICATION.

JEWETT V. REED, M.D. INDIANAPOLIS, IND.

Diseases of joints have been subject to all possible forms of classification, either according to their etiology, pathology, clinical features, or a combination of these. A satisfactory classification is extremely difficult for several reasons. From the standpoint of etiology it is impossible to base a classification because many etiological factors may produce the same pathological condition, while in other instances a certain single cause may produce a variety of morbid changes in the joints. In fact, the gonococcus is capable of producing almost every known form of arthritis.

A classification of the arthritides based upon the pathological changes produced is the most rational, but this is difficult because our knowledge of these changes, especially in the early stages of the disease, is very imperfect. Moreover, one form of joint inflammation may gradually change into another form, while in many other cases, two or more of the so-called primary changes may be present in the same joint. Perhaps there are no structures of the body, the diseases of which are so poorly understood as the joints. Any discussion of these diseases at the present time must be considered provisional, and subject to many changes when we have gained more knowledge regarding the etiology and pathology of these conditions. In order to study joints from a pathological standpoint, it will be necessary to render obsolete the term "rheumatism," except perhaps in the single instance, acute articular rheumatism. To diagnose a chronic joint

disease as "rheumatism" is worse than useless. It serves only as a shield behind which we hide our inability to determine the true pathological condition in the joint.

At present an attempt will be made to classify the various forms of arthritis, based upon the primary and secondary pathological changes occurring in the joints, and at the same time to show the relations between these joint changes and their etiological factors.

According to Hoffa, who classifies according to etiology, all forms of arthritis may be divided into the tubercular and the non-tubercular. The latter group may be subdivided into the traumatic, infectious, toxic, neuropathic and constitutional.

* Read at the Annual Meeting of the Indiana State Medical Association, Oct. 8, 1909.

This last division includes those joint changes that occur in gout, scurvy, hemophilia, purpura and angio-neurotic edema.

The forms of arthritis due to trauma, infections and toxic conditions help to make up that great group of chronic joint affections generally classed as arthritis deformans, rheumatoid arthritis, osteo-arthritis, chronic rheumatism, etc.; and it is this group of joint diseases that an attempt will be made to classify on a working basis. The forms of arthritis due to gout, tuberculosis, purpura, etc., have a fairly definite and distinct pathology peculiar to each form, and as a rule there is comparatively little difficulty in recognizing these. Still even in these more definite joint lesions, the late pathological changes may closely resemble those changes seen in the rheumatoid arthritis and osteo-arthritis groups.

The chief etiological factors of the joint affections under consideration may be grouped under three headings, namely: trauma, infections and toxic conditions. Under trauma may be mentioned contusions, sprains, chronic strains and gross injuries to the joints. The chronic joint changes following the various forms of trauma are due to the persistence of the effusion, and to the roughness or irregularities of pressure over the articular surface.

One form of trauma should receive special mention, as it is fairly common and is often unThis recognized-that is the chronic strain. occurs whenever the line of pressure passing through a joint becomes deflected. This is fairly common in the knee and ankle joints, occurring secondarily to flat-foot and badly reduced fractures of the leg. There is a constant strain on the lateral ligaments of one side of the joint, and at the same time there is an inequality of pressure exerted over the articular cartilages. The result is a constant pain in the joint, followed by an effusion and later by a partial pressure atrophy of the cartilages. In fact, any factor that tends to produce an unequal distribution of pressure between the articular surfaces, leads to an atrophy of the cartilage at the point of greatest pressure, with a subsequent irregularity of the articular surfaces. This condition is also seen in cases of loose cartilage, in joints with a lax capsule and in villous arthritis. The Charcot's joint of tabes and syringomyelia is now considered by several neurologists to be due primarily to trauma. trauma. The primary injury of the joint is allowed to go unprotected and untreated on account of the loss of the sensation of pain. A chronic joint hydrops forms, which is followed by atrophy of cartilage, and finally by marked deformity of the joints.

The second group of etiological factors, the most important cause of chronic arthritis, includes the infections. Bloodgood writes: "In spite of the absence of a definite bacteriological proof, more and more investigators are inclined from clinica! and pathological studies to the view that the majority of forms of both acute and chronic arthritis are of infectious origin."

The various organisms and infections that may produce both acute and chronic arthritis are as follows:

1. The gonococcus. This organism takes precedence over all others on account of the frequency, seriousness and variety of joint lesions it can produce.

2. The staphylococcus and streptococcus. These seldom attack the joints except in general pyemia and in penetrating wounds.

3. The pneumococcus. This organism may produce a mild degree of acute arthritis as a complication of pneumonia, but the condition rarely becomes chronic.

4. The diplococcus rheumaticus. This is the probable cause of acute articular rheumatism, and very rarely leads to permanent joint changes.

5. The typhoid and paratyphoid bacilli. A general infection with these organisms may be complicated by a mild degree of acute arthritis which generally subsides, leaving a normal joint. More important, however, is the infection of the ligaments of the spinal column with these organisms, producing the so-called "typhoid spine," which frequently results in a spondylitis deformans.

6. Influenza. An attack of this infection is the starting point of a chronic synovial arthritis,

or "arthritis deformans."

7. Syphilis. This may produce almost any form of arthritis, but with the exception of the arthralgia and stiffness of the early secondaries, joint syphilis is comparatively rare. Occasionally it may simulate acute articular rheumatism or villous arthritis, and in cases of gummatous deposits about the joint it may give the general appearance of tuberculosis.

8. Unknown and unrecognized bacteria. This is the last and most important group of infectious agents that cause the greater number of forms of chronic arthritis. While the organisms themselves are often difficult or impossible to demonstrate, their source of supply, or the primary seat of infection can generally be found on thorough examination of the mucous membranes. In this connection Bloodgood says: "The tonsils stand first as a portal of entrance of non-tubercular arthritis, except the gonorrheal." Next in importance to diseased tonsils are the chronic infections of the pharynx, middle ear, frontal,

ethmoidal and maxillary sinuses. Carious teeth and pyorrhea alveolaris may also serve as a portal of entrance. At the other end of the alimentary tract may be found fissures and fistulæ in ano, and ulcerating hemorrhoids that may furnish a chronic infection to the joints. Again, while it cannot always be determined definitely, the gonococcus probably plays an important part in the production of chronic arthritis, especially of those cases of apparently cured gonorrhea, where there is in reality a low grade of prostatitis, vesiculitis, endometritis, etc. While it may be impossible in many cases to trace a direct relation between the primary infection of the mucous membrane and the progressive joint lesions, nevertheless it has been a common experience to find that, with the treatment of these primary infections, the joint symptoms improve, or at least come to a standstill.

The third group of etiological factors consists of the toxic conditions. These toxins are not understood, but are probably elaborated in metabolic disturbances, in chronic gastro-intestinal diseases, and in very chronic cardiac and pulmonary conditions. These toxins frequently lead to the various osteo-arthropathies.

We will next consider the pathological changes that result from the above-mentioned etiological factors.

The morbid changes occurring in the various forms of arthritis may be classed under two chief groups, depending upon the stage to which the joint lesion has progressed. First, there are the primary pathological changes, the first joint changes that occur following the initial insult. Clinically, these primary changes may appear either as acute or chronic, depending largely upon the etiological factor.

The secondary and late pathological changes are those that follow the primary, and are due either to the healing of the primary inflammation, or to a constant but slight trauma resulting from an altered mechanism of the joint.

In all forms of arthritis the seat of active inflammation is in the synovial membrane, the joint capsule and the periarticular tissue. The articular cartilages may become injured, necrotic, or may atrophy, but they always play a passive part in the production of the morbid changes in the joints.

The Primary Pathological Changes. These primary pathological changes may be divided into the acute and chronic. The acute group contains the joint hydrops, serofibrinous effusion, purulent effusion or joint empyema and periarticular induration.

Hydrops or serous effusion into the joint cavity may result from any form of trauma, from the bacteria of acute infections, from the toxins of acute infectious diseases and as a manifestation of angioneurotic edema.

Serofibrinous effusion is generally due to an infection of the synovial membrane with the gonococcus, pneumococcus and typhoid bacillus, or it may occur as an early stage of joint empyema. Empyema of a joint is generally the result of an infection with the gonococcus or other pyogenic bacteria.

Periarticular induration occurs in its most typical form in acute articular rheumatism. It may also occur about a joint containing a serofibrinous or purulent effusion. In all of these conditions the periarticular tissue returns practically to normal. But there is another form of acute periarticular induration that occurs secondary to chronic infections of the mucous membranes. Clinically, this condition may look very much like acute articular rheumatism. There may be one attack or more commonly, repeated acute attacks, but, unlike acute articular rheumatism, each acute attack leaves the joint permanently swollen and stiffened, due to deposits of scar tissue in the periarticular tissue. The final result is identical with that seen in the chronic synovial arthritis.

Chronic Primary Pathological Changes.Under this heading belong all of those forms of chronic arthritis, generally classed as "arthritis deformans" and "osteo-arthritis." In many cases these two forms are distinct; in others both forms may be present in a single joint. Both the arthritis deformans and the osteo-arthritis lead to an enlargement of the joint with impairment of motion. In the former the enlargement is due mainly to inflammatory deposits in and about the soft tissues of the joint, while in the latter it is due chiefly to a proliferation about the ends of the bones. Arthritis deformans and osteo-arthritis are respectively designated by Goldthwait as atrophic and hypertrophic arthritis. Hoffa calls the former the synovial form of chronic arthritis, the latter the osseous form of chronic arthritis.

We can therefore divide all the forms of primary chronic arthritis into two great groups: First, the synovial or atrophic form of chronic arthritis; second, the osseous or hypertrophic form of chronic arthritis.

The synovial form is due, probably in the greater number of cases, to a low grade of gonorrheal infection. Next in importance are the other chronic infections of the mucous membranes. Less frequent causes are influenza, typhoid and syphilis. Any of these above factors can produce a

chronic inflammation of the synovial membrane, joint capsule and periarticular tissues. All three of these tissues are probably involved in every case, but as a rule one tissue suffers more than the others. In a certain group of cases the chief inflammatory reaction involves principally the synovial membrane and its vascular fatty capsule, the results being a proliferation of the synovial fringe within the joint, forming the so-called villous arthritis. In another group of cases belonging to the synovial form of chronic arthritis, the inflammation attacks chiefly the joint capsule and periarticular tissue. Thus the synovial form of chronic arthritis may be divided into two distinct groups, depending upon whether the inflammation attacks principally the inner or outer layer of tissues about the joint. When the inflammation attacks chiefly the inner layer the result is a villous arthritis. When the outer layer is chiefly involved, a chronic periarticular thickening is the result.

With the formation of a villous arthritis, the joint cavity is more or less distended, with a great number of soft pedunculated fatty masses covered with a normal endothelium. Occasionally these fatty villous projections become fibrous or even cartilaginous. A chronic or intermittent form of hydrops is generally present in these joints. Villous arthritis leads to a swollen joint, with more or less constant pain and impairment of motion. Crepitation is generally marked, and the hypertrophied villi can often be palpated through the capsule.

The periarticular type of the synovial form of chronic arthritis shows a gradual increasing thickening of the joint capsule and adjacent tissue. This is due to the accumulation of scar tissue following a low grade of chronic inflammation, or to repeated acute attacks. This leads to a progressive limitation of the range of motion of the joint, which may finally result in absolute fixation. There is a decrease in the synovial fluid of the joint, otherwise its cavity remains unaltered. This form of pathological joint changes includes those joints commonly designated as arthritis deformans or rheumatoid arthritis.

Spondylitis deformans of the fibrous type, which is generally due to the gonococcus or to a typhoid or paratyphoid infection, also belongs in the class of chronic synovial arthritis. In this condition the lateral ligaments of the vertebra become infiltrated with scar tissue, producing a condition similar to the periarticular thickening about a joint.

The second primary form of chronic arthritis is the osseous type, the hypertrophic form, or the so-called osteo-arthritis. This form occurs most

11. Unrecognized bacteria from chronic infections.

Synovial form of chronic arthritis "atrophic." (a) Villous arthritis. May be caused by (2-4-11). (b) Periarticular thickening. May be caused by

Loose joint bodies and Chronic hydrops

}

Atrophy of cartilage.

(4-8-9-10-11-E).. Fibrous anchylosis about joint.

Type of joint closely resembling the osseous form of chronic arthritis.

Osseous form of chronic arthritis. "Hypertrophic."

(lax

(2-4-8-9-11-13).. Large deformed joints or "Osteo-arthritis" monarticular or general. Morbus coxae senilis. Heberden's nodes.

locked from irregularities of surface.

Spondylitis deformans. Charcot's joint.

Pulmonary osteo-arthropathy

frequently in old people, especially those suffering from chronic intoxications and metabolic disturbances. The osseous, like the synovial form, may also occur as the result of gonorrhea, chronic infections of the mucous membranes, typhoid and syphilis.

As stated above, the synovial form of chronic arthritis involves mainly the soft tissues about the joints. The osseous form involves chiefly the articular ends of the bones and cartilages. It must be remembered that the capsule of the joint blends with the periosteum of the bone at the epiphyseal line, and it is at this line that the arteries enter the bone to supply the epiphysis and articular cartilage. The first change that occurs in the formation of an osteo-arthritis is a chronic proliferative periostitis about the ends of the bones. This leads to the formation of new bone that extends beyond the edges of the articular surface in the form of osteophytes or bony, lip-like projections. At the same time the presence of a periostitis about the epiphyseal line. constricts the blood-vessels as they enter the bone. This results in an anemic atrophy of the cartilage and a rarification of the ends of the bones. This allows the cartilage and later the underlying bone to become eroded with use. This erosion is seldom regular, which leads to marked changes in the articular surfaces.

Thus the principal changes occurring in the osseous form of chronic arthritis are, first, an hypertrophy of the bone about the edges of the joint; second, an atrophy and wearing away of the articular surfaces. The entire joint is enlarged, deformed, and its mechanism is greatly interfered with. Occasionally, complete immobility may occur, due to the deformity of the articular surfaces, or to the interlocking of osteophytes. A true bony ankylosis, however, never occurs.

The various types of joint lesions that belong under this heading of chronic osseous arthritis are as follows: The Heberden's nodes, which are probably the mildest form of this condition, the monarticular and generalized osteo-arthritis, the hip-joint disease of old people and the osseous form of spondylitis deformans. In the lastnamed condition the ligaments binding together the bodies of the vertebræ become transformed into bone. The bone and joint changes occurring in long-standing pulmonary and cardiac diseases, the so-called hypertrophic pulmonary osteoarthropathy, also belong to the group of osteoarthritis. Also many of the Charcot joints probably belong under this division.

Secondary Joint Changes.-The secondary and late joint changes are those that follow any of

the above forms, either as the result of a healing process, or from the altered mechanism of the joint.

To begin once more with acute hydrops of the joint, this condition, which may not be serious in the beginning, may, if not relieved, lead to marked secondary changes. An acute hydrops may become either chronic or intermittent, which will lead to a looseness of the capsule. This lax joint will allow the articular surfaces to glide over each other in an irregular manner, and a certain degree of atrophy of the cartilages will result. These joints resemble to a certain degree those of the osteo-arthritic group, except that there is little if any bony proliferation about the ends of the bones. Many Charcot joints are an example of an extreme degree of this form.

Serofibrinous, and more especially purulent effusion into joint cavities, may lead to the most serious secondary changes. If the joint is not promptly drained before necrosis of the cartilage or destruction of the endothelial lining takes place, a permanent impairment of the joint will invariably result. With the destruction of the endothelium of the synovial membrane, even over small areas, there is a granulation tissue formation, which binds together adjacent surfaces, the final result being a true fibrous ankylosis. With necrosis of the articular cartilages, there will result a true bony ankylosis.

The acute periarticular induration, when due to the diplococcus rheumaticus, as a rule completely disappears, but when it is due to other organisms, a more or less permanent thickening results, producing a condition identical with the primary chronic periarticular thickening.

A joint suffering from villous arthritis receives more or less constant trauma from the friction of the villi. The result will be a chronic hydrops, a lax capsule and finally a wearing of the articular surfaces. This is more marked when the villi are of the fibrous type. Frequently the villi are torn loose from their slender attachments and lie free in the joint cavity. The rice bodies or "joint mice," commonly considered to be the result of tuberculosis, are in reality detached fibrous villi.

The periarticular form of the chronic synovial arthritis, and also the osseous form, show no secondary changes except a gradual progression to complete immobility. In these cases the immobility must be distinguished from a true ankylosis, which occurs only in joints which have suffered an acute destruction of the cartilage or synovial membrane, as seen in intra-articular fractures, tuberculosis and empyema of the joint. The immobility in the chronic periarticular form is due to a thickening and loss of elasticity of the