Degenerative joint disease (DJD) is a common disorder of humans and animals. It is generally regarded as a noninflammatory condition of articular cartilage resulting from natural aging, trauma, or disease. Many names have been applied to the condition; however, osteoarthritis and degenerative joint disease are two of the most common and will be used interchangeably in this chapter.
DJD has been recognized in animals for a long time. Paleopathologic examination of dry-bone preparations has shown lesions comparable to those of DJD in fossil reptiles from the Mesozoic period.(36) Although caution must be used in the interpretation of these findings, they point out that articular disease has affected animals since animals have walked on earth.
DJD has been classified in many ways. One classification describes DJD as either primary or secondary.(16,28) Primary DJD is that which occurs in diarthrodial joints in which there has been no known previous trauma or disease. This primary condition is best exemplified by the Joint changes seen in older animals. Primary DJD is generally regarded as an aging phenomenon (4,16,28) in which deterioration of the articular cartilage occurs, leading to the characteristic joint changes.
As the name implies, secondary DJD is the result of some insult to the affected joint. Usually it is a local phenomenon rather than a systemic disease, although some systemic diseases that affect joints may ultimately lead DJD. Local insult with resulting degenerative changes is best exemplified by cranial cruciate ligament rupture.
Two major categories of articular disease are described; noninflammatory and inflammatory.(16,28) DJD is placed in the noninflammatory category although an intermittent inflammatory component is recognized. Other conditions of so-called noninflammatory articular disease include traumatic arthritis, mechanical abnormalities such as torn menisci, aseptic necrosis, neuroarthropathy, and neoplasia. The inflammatory category is subdivided into an infectious section, which includes articular disease caused by bacterial, fungal, viral, and protozoal organisms, and a noninfectious section, which itself is further divided into two subcategories: immunologic and nonimmunologic. The immune-mediated articular diseases, such as rheumatoid arthritis and systemic lupus erythematosus, and nonimmune inflammatory conditions such as crystal-induced arthritis, (i.e., gout, pseudogout) and chronic hemarthrosis will be dealt with in other sections of this text.
Mature articular cartilage is a unique tissue in that it does not incorporate its own direct blood supply. The usual tissue response to insult is one of inflammation, which relies on intrinsic vascularity. Without vascularity, articular cartilage response to insult is different than that of other tissue. DJD is a sequel to cartilage insult, but because cartilage lacks intrinsic vascularity it does not become inflamed, thus the designation of DJD as a noninflammatory condition.
However, DJD is not a condition of articular cartilage alone. The synovial membrane lining the affected joint cavity is also involved. This tissue, with its high degree of intrinsic vascularity, exhibits inflammatory change. The intensity of these changes varies with the extent of the insult to the joint and the duration of the condition. The inflammatory changes of DJD are also reflected in the cellular constituents of the synovial fluid. Total cell counts need not be high, but certain cell types will be seen, confirming the inflammatory nature of DJD. Thus, a classification system for canine articular disease was developed to reflect these inflammatory changes and is presented in Table 87-1.
|TABLE 87-1 Classification of Articular Disease|
The characteristic structural changes that typify DJD are disorganization and loss of articular surfaces and proliferation of tissues in and adjacent to these surfaces. The precise sequence of histologic change in affected articular tissues is not known with absolute certainty. For instance, in primary DJD it is not known whether synovial membrane changes precede articular cartilage changes. Much of the sophisticated histologic and biochemical research into DJD has concentrated on articular cartilage. DJD has been observed in human autopsy specimens from persons who reportedly were asymptomatic during life. This has led to the hypothesis that these lesions may be considerably different than those seen in the joints of symptomatic patients.
Advancing age is important in the pathogenesis of DJD but is probably not the primary cause of the disease. While cartilage breakdown is more frequent in older humans and animals, all joints are not affected concomitantly, and it is evident that local factors play a major pathogenic role. With advancing age a considerable number of chemical, biologic, and mechanical alterations occur in normal articular cartilage. It has been stated that if aging itself is considered normal, so then too should these changes.(4) Load bearing is important in the normal biology of joints. (26) As described in Chapter 86, the nutrient transport to articular cartilage via the synovial fluid is dependent on joint motion and weight bearing. In fact, degenerative changes of articular cartilage have been demonstrated in studies in which limbs were immobilized for varying periods of time.(9) The affected joints were allowed no motion or weight bearing. At the end of 5 weeks, definite changes in articular cartilage, some indistinguishable from DJD, were noted. Conversely, heavy use of well aligned joints rarely contributes to cartilage breakdown. (15)
The placement on joints of abnormal physical stresses that accompanies such conditions as chronic subluxation, hip dysplasia, slipped epiphyses, and aseptic necrosis' plays a vital pathogenic role in the development of DJD. Studies have shown that joint remodeling normally occurs with advancing age, thus changing joint contour and articular surface congruity. Joints normally are not entirely congruous but rather have areas of "contact" and "noncontact."(15) With increased loads on joints, the areas of contact increase in size, and greater joint surface congruity is achieved. With advancing age, minor alterations in cartilage allow greater congruity with smaller and smaller loads, thus bringing areas of normal noncontact in the intact joint into contact. Such alterations in congruity lead to erosive and osteophytic changes. These lesions of "limited progression" have been observed in human autopsy specimens from persons who were thought to be asymptomatic during life. While the gross appearance and location of these lesions differ somewhat from those seen in patients with clinically symptomatic joint disease, the biochemical characteristics of' the lesions differ little from those of the clinical condition. (15)
The classic morphologic changes of osteoarthritic articular cartilage begin with fibrillation,(4,15,43) a local surface disorganization involving a splitting of the superficial layers of the cartilage. The early splitting is tangential with the cartilage surface, following the axes of' the predominant collagen bundles. Horizontal flaking of cartilage occurs along with the development of shallow pits or clefts perpendicular to the cartilage surface. Eventually, the splitting extends deeper, altering the normal arrangement of the collagen bundles. As the disease progresses, the clefts extend entirely through the cartilage to its junction with subchondral bone.
With disease progression, fibrillation continues and is accompanied by synovial hyperplasia and adjacent osteophyte formation. Continued deterioration of articular cartilage leads to exposure of subchondral bone and a more generalized synovial change. Severe end-stage DJD is characterized by extensive subchondral bone exposure and tremendous deformity in joint surface contour, often leading to luxation.
While fibrillation is generally accepted as the first significant change in articular cartilage readily identifiable by light microscopy, molecular, chemical, and other physical changes precede fibrillation. Thus, fibrillation should be considered as a common microscopic endpoint of' both normal and abnormal occurrences that lead to cartilage failure.(4)
To understand the processes leading to cartilage failure, it is important to look at the cellular processes and biochemical structure of normal cartilage. Hypocellulanty of normal articular cartilage as compared with other tissues is a striking feature. The greatest portion of articular cartilage mass is composed of a macromolecular extracellular matrix surrounding the chondrocytes. Because of their appearance under light microscopy, articular cartilage chondrocytes were once thought to be rather inert or inactive. It is now well recognized that the maintenance and production of the extracellular matrix by the chondrocyte is an active and continuing process.
Normal mature articular cartilage is divided histologically into four distinct zones based on the arrangement and orientation of its cellularity.(43) The most superficial zone, that closest to the articulating Surface, is the tangential zone. Here the flattened cells have their long axes parallel to the articular surface. The ultrastructural appearance of these cells has suggested to some that they are fibroblastic in nature.(43) Immediately beneath the tangential zone, the cells are more rounded and are randomly oriented. This is the transitional zone. The chondrocytes in this area are metabolically active, producing collagen and proteoglycan. Beneath this region is the radial zone in which cells are arranged in short columns perpendicular to the articular surface. These cells are smaller than those immediately above and appear less active. The calcified zone, with its pyknotic cells surrounded by calcifying matrix, resides deep to the radial zone.
Cartilage matrix is a gel-like substance composed of water and the macromolecular polyanionic substances, proteoglycan and collagen.(15,43) Although produced separately, proteoglycan is linked to collagen extracellularly. Proteoglycans are elastic molecules that expand in solution and strongly resist compression into a smaller volume. Proteoglycan consists of a protein core or backbone to which are attached side chains of glycosaminoglycans (GAGs). Three distinct GAGs have been identified: chondroitin 4-sulfate, chondroitin 6-sulfate, and keratin sulfate. Because of their repelling negative charges, the GAGs are attached to the protein core at nearly right angles. In the matrix, the proteoglycan is arranged in high-molecular-weight aggregates formed by noncovalent association between proteoglycan subunits, hyaluronic acid and linkage protein.
With normal aging the ratio between the various GAGs changes. In immature cartilage the ratio between chondroitin 4-sulfate and chondroitin 6-sulfate is nearly 1:1, and there is very little keratin sulfate. As aging progresses the ratio becomes 1:4, and by middle age the concentrations of the keratin sulfate and chondroitin 6-sulfate are nearly equal and account for almost 90% of the GAG content of articular cartilage.
Proteoglycan of normal articular cartilage is constantly degraded and resynthesized; its half-life has been estimated at 150 days.(43) The remodeling system appears to be enzyme dependent. Lysozymes such as cathepsin-D and arylsulfatase are thought to be two of the primary enzymes responsible for proteoglycan degradation.
Like proteoglycan, collagen makes up about 50% of the dry weight of articular cartilage.(43) Collagen is composed of fibers and fibrils the structures of which are complex helices of linearly arranged amino acids. Collagen of skin differs from that of articulating surfaces as a result of different amino acid arrangements.(19,27,31) In early studies it was discovered that collagen of skin and tendon was composed of three intertwined amino acid chains, two of which were found to be identical. The two identical chains were designated alpha-1 and the dissimilar chain was designated alpha-2. On further examination of articular cartilage, the alpha-1 chains were shown to be of two types that differed from each other by alteration in amino acid sequence. It was further discovered that collagen of articular cartilage was composed of three identical alpha chains differing from the alpha-1 of other tissues by various amino acid substitutions. Thus, two types of alpha-1 chains were recognized: alpha-1 (I) present in skin, tendon, bone, and cartilage and alpha-l (II) present only in articular cartilage. These two types of collagen were designated types I and II respectively. The major distinctions between the two types are the differences in amino acid composition and the absence of an alpha-2 chain in type II collagen. In addition, there are differences in the pattern of intramolecular and intermolecular cross linkages. Eight other types of collagen are known to exist. Type III is found in skin and the walls of the uterus and arteries, and types IV and V are found in basement membranes of various organs.(27)
The arrangement of collagen fibers within canine articular cartilage is similar to that in human articular cartilage, with various and distinct zones noted.(45) The most superficial layer is the lamina splendens, composed of fine fibrous material. Beneath this is the tangential layer in which tightly packed collagen fibers are parallel with the articular surface. These fibrous bundles are at random angles to each other, but their uniform orientation is parallel with the surface. In the transitional zone, the fibers assume a more random orientation, although in the vicinity of the chondrocytes the fibers sweep in almost capsular fashion about the lacunae. A distinct line of demarcation is not seen between the transitional zone and the deeper radial zone. However, collagen fiber orientation becomes less random and more perpendicular to the articular surface in the radial zone.
Generally speaking, the number of collagen fibrils per unit area decreases with increasing distance from the articular surface. In addition, the diameter of the collagen fibrils increases with increasing distance from the surface.(45)
Excessive or abnormal use and direct injury such as fractures or ligamentous disruptions have always been the obvious explanation for DJD development. Yet it has been shown in humans that what may be considered greater than normal use does not necessarily lead to degenerative changes. In a study comparing former runners with a control population of nonrunners, the runners had less DJD of the primary type.(15) Evidence has not yet been produced that shows that excessive use without injury leads to DJD.(4)
While the etiology of DJD may be multifactorial and the rate of morphologic changes variable, the end result is a decrease in joint motion and function, an increase in deformity, joint instability, and pain. DJD is commonly seen in varying degrees associated with hip dysplasia, cranial cruciate ligament rupture, ununited anconeal process, ununited (fragmented) coronoid process, osteochondritis dissecans, ligamentous injuries, and as a sequela to articular fractures.
Tissues respond to insult in a characteristic manner, with the magnitude of responsive change comparable to the extent of insult. The degree of articular cartilage response to injury likewise will vary with the degree of damage. It should be recognized that the following description of the morphologic and biochemical changes of articular cartilage in response to insult and the subsequent development of DJD is presented more as an overall review of these changes and not as a definitive sequence of events that occurs in every instance of DJD.
DJD changes are first recognized as a focal area of dullness on the articular cartilage surface.(28) This is accompanied by a color change from the more normal glistening white to a mottled gray or yellow. Fibrillation, as described above, is occurring in these regions. Because of alteration in the matrix composition, these areas also become softer than normal. Chondrocytes adjacent and superficial to the softened areas become more numerous, while those within the Softened areas decrease in number. In experimentally induced DJD, chondrocyte density increases in areas adjacent to the splits or clefts and the number of lacunae with two or more nuclei also increases.(17) As the fibrillation continues, clones of two or more cells are particularly abundant around severely fibrillated sites. This response of increased numbers of cartilage cells at the initial site of injury has been viewed by some as an attempt at intrinsic cartilage repair (Fig. 87-1). (28)
As the clefts and splits in the collagen deepen, abrasion of the fibrillated cartilage continues, eventually exposing the underlying subchondral bone. With continued disruption of the osteochondral junction, hemorrhage and bone necrosis occur. Osteochondral repair takes the form of granulation tissue and fibrocartilage. With continuing loss of the cartilage surface and increased bone exposure, the bone becomes sclerotic. In severe cases of DJD the exposed bone may actually become well worn, smooth, and polished. Such bone is described as eburnated. (28,36)
|FIG. 87-1 Fibrillation of articular cartilage. Clefts and splits begin on the cartilage surface parallel with the articular plane. They then extend deeper into the cartilage substance becoming perpendicular to the joint surface. (H & E x 60)|
Areas of bone rarefaction, or "cysts," may appear beneath the eburnated surfaces. These spaces formed by the loss of trabeculae are a fibromyoid degeneration of the marrow. On occasion, fragments of dead bone, cartilage, and amorphous material may also be found within these areas. Because these lesions only rarely contain pockets of mucoid fluid and do not have a fibrous border or capsule, they are not considered true cysts. (36)
Another bony change that often accompanies DJD is that of exophytic growth at the margins of the articular surface. Marginal osteophytes occur at the junction or interface between the articular cartilage and synovial membrane. They may appear as protuberances into the joint space or develop within capsular or ligamentous attachments at the joint margins. The direction of osteophyte formation is governed by the line of mechanical force imparted to the area of growth.
Osteophyte formation begins as a deposition of mineral outside the existing bony cortex.(6) Further deposition of new bone, resorption, and remodeling ultimately produce a mature osteophyte. Capped by a hyaline or fibrocartilage surface, mature osteophytes communicate freely with the marrow spaces of the bone from which they arose (Figs. 87-2 and 87-3).
In experiments in which the anterior cruciate ligament of dogs was severed to produce DJD, beginning osteophyte development was detected by microangiographic techniques 7 days after ligament transection Macroscopically and radiographically, osteophytes could be seen at 2 weeks and 5 weeks respectively following ligament transection.
While in itself the presence of osteophytes (i.e., without cartilaginous defects) is probably not evidence for a diagnosis of DJD, it is indicative of abnormal activity within a joint.
A third significant bony change of DJD is the development of sclerosis in the subchondral area. The bone in this area becomes more dense with increasing loss of the articular cartilage above. This sclerosis has been described as being the result of increased loads placed on the bone because of the articular cartilage loss.(4,28)
|FIG. 87-2 Osteophytes on lateral aspect of lateral femoral condyle. Osteophytes develop at the interface of articular cartilage and synovial membrane Vascularity of the synovial membrane can be seen (arrow).|
|FIG. 87-3 Osteophytes on the proximal aspect of the femoral trochlea.|
For the most part, biochemical alterations in articular cartilage undergoing changes associated with DJD precede the characteristic macroscopic changes.(4,18) While there are some conflicting reports regarding the changes in water content, production and type of collagen present, and the ratio of proteoglycan constituents, the general consensus is that water content increases along with an initial increase in chondrocytic synthesizing activities. With progression of DJD and continued loss of articular cartilage substance and therefore loss of the chondrocytes themselves, it is obvious that chondrocyte activities decrease.
The water content of normal articular cartilage is between 72% and 78%.(15) In DJD not only is the water content increased but the water is more tightly bound and therefore less freely exchangeable with the joint space. (15,43) It is suspected that owing to proteoglycan depletion, larger amounts of water become more avidly bound to collagen. The loss of water-transfer capabilities may have a deleterious effect on chondrocyte nutrition, articular cartilage elasticity, and joint lubrication.(43)
While the total collagen content of osteoarthritis articular cartilage is similar to that of normal cartilage, the composition and orientation of the collagen fibrils are changed.(43) in the upper region of degenerative cartilage the total number of collagen fibrils remains nearly the same as normal cartilage; however, there is a decrease in the number of large-diameter fibrils.(45) As might be expected, fibril orientation is severely altered. Rather than remaining in tightly packed bundles parallel with the articular Surface, the fibrils are in a looser arrangement with a random orientation. These findings of a higher proportion of small-diameter collagen fibrils and random orientation of the fibrils are also characteristic of the deeper layers of the affected cartilage.
In addition, the type of collagen fibril found in osteoarthritis articular cartilage is different than that found in normal cartilage. Several reports have shown that osteoarthritis chondrocytes produce not only type II collagen but substantial amounts of type I collagen, that which is usually found in skin and bone.(l5,39,43) While evidence to the contrary has also been reported," it is generally believed that the changes in the type of collagen fibrin and the alterations in their size and orientation serve to after the mechanical properties of arthritic cartilage.(43)
It is generally accepted that the total proteoglycan content of osteoarthritis articular cartilage is decreased and that the decrease is directly proportional to the disease severity. (15) However, while total GAG content of affected cartilage is diminished, not all GAG components are affected equally. When compared with normal cartilage, there is a relative decrease in keratin sulfate and an increase in chondroitin 4-sulfate such as is found in normal young or immature cartilage. Thus, chondrocytic synthesizing activity continues in affected cartilage but the products produced are different.(14,18) What triggers this alteration in production is not known, but it has been suggested that it may be an attempt to heal the cartilaginous defects.(15)
It must be noted that these changes are found only in areas of cartilaginous lesions such as fibrillation. In intact areas of cartilage from the same joint surface, GAG content is normal. (39) In addition, GAG content is increased in areas of osteophytic activity.
In later stages of DJD, there is a continued decrease in GAG synthesis and a relative decrease in chondroitin sulfate compared with keratin sulfate.(40) These decreases correlate well with the histologic severity of the disease.
CELLS OF ARTICULAR CARTILAGE
There is ample evidence to show that in the early stages of DJD there is an increase in the number of chondrocytes adjacent to the splits in the cartilage. The rate at which new cells are produced has been found to be proportional to the severity of the disease based on a histochemical grading system for early and moderate lesions.(15) These cells, particularly near the articular surface, have a microscopic appearance suggestive of fibroblasts. Ultrastructurally, they have an increase in rough endoplasmic reticulum, mitochondria, and Golgi apparatus, which are the organelles associated with increased matrix production.(43) In addition, some of these cells are found to have a decrease in stored glycogen, also suggestive of increased cellular activity.(45)
In advanced severe lesions, new cell production is decreased and the cells present appear to be undergoing degenerative changes.(43) Thus it seems as if the increased synthesizing activity of GAG and production of new cells cannot keep pace with the forces and activities responsible for cartilage destruction. This has been described as a failure" or breakdown in the reparative mechanism that accompanies increasing disease activity.(l5)
Lysosomal activity and enzymatic degradation are also factors in the osteoarthritis process and may in fact explain how there can be a loss of matrix components in the face of increased matrix synthesis. While the initiating factors for enzyme release are not known, there is no doubt that they are present in increased amounts in osteoarthritis cartilage. Acid phosphatase, arylsulfatase A and B. and cathepsin B and D have been found in greater amounts than normal in cartilage from affected joints.(3,5,34) These enzymes affect the matrix in various ways, but in general they cause a degradation of proteoglycan. As mentioned above, some of these enzymes are necessary for the normal turnover of proteoglycan. What causes their increased production or decreased removal is not known. However, it is known that their activity contributes to the breakdown of the proteoglycan structure and subsequent loss of matrix substance.
Protease inhibitors are known to be present in articular Cartilage, and it has been hypothesized that an impaired ability of the chondrocytes to synthesize these substances leads to the loss of matrix components. (39) In this theory, the degradative enzymes normally present in articular Cartilage are held in check by other enzymes produced by the chondrocytes. But in DJD, for some unknown reason, the protease production is decreased and therefore the check held on the degradative enzymes is lost. While this hypothesis has not been proven to date, it remains an interesting concept, especially in light of what is known of other regulatory biologic mechanisms.
CHANGES IN SYNOVIAL MEMBRANE
The connective tissue that surrounds diarthrodial joints is designated the joint capsule. Its outer part, composed of dense connective tissue reinforced by tendons and aponeuroses, is termed the fibrous capsule. The inner part is termed the synovial membrane. The synovial membrane has several components. Its inner layer, which is immediately adjacent to the joint surface, is a glistening tissue composed of synoviocytes two to three cells thick. Beneath this is the subsynoviocytic tissue, a loose connective tissue that vanes in depth, vascularity, and amount of interspersed adipose tissue. Within the subsynoviocytic layer are collagen and elastic fibers, as well as fibrocytes, occasional histiocytes, macrophages, and mast cells.
Just as the earliest changes of articular cartilage in primary DJD have not been identified, likewise the earliest changes of synovial membrane are not well described. This is due to the inaccessibility of the tissues. The insidiousness of primary DJD makes it all but impossible to produce experimentally or to gain knowledge from biopsy specimens blithe spontaneous disease. Information about synovial membrane changes in DJD comes from tissues taken after the spontaneous disease has been present for some time or from experimental models of DJD, which more accurately reflect the changes of secondary DJD.(46)
Tissue taken from human patients with primary DJD seen 1 to 16 years following the onset of symptoms shows three overlapping stages of synovial membrane inflammation.(37) In the initial stages, slight to moderate synoviocyte hypertrophy is noted. There is also an increase in the number of synoviocytes, thus thickening the inner synovial membrane layer. Within the subsynoviocytic zone, fibroblastic proliferation is noted, along with a moderately hyperemic change due to blood vessels. The vessels are thinly surrounded by infiltrates of lymphocytes and plasmocytes. Focal aggregations of similar cells are seen occasionally. Edema, although present, is only moderate.
In the progressive stages of the disease, synoviocyte hyperplasia is more prominent, with the layer now being three to five cell layers thick. Increases in fibroblastic activity are noted in the subsynoviocytic layer, in which the fibroblasts are more numerous. In addition, an increase in collagen fibers is seen as well as a significant increase in the subsynoviocytic vascularity (Fig. 87-4).
|FIG. 87-4 Synovial membrane from the stifle of a dog in whom the cranial cruciate ligament was experimentally transected 8 weeks previously. The synoviocytic layer is 5 to 7 cells thick. Superficial cells are perpendicular rather than parallel with the joint space (J). Beginning fibrosis of the normal adipose subsynovial tissues is apparent (arrow). ( H & E x 60)|
The advanced stage is characterized by a maintenance of the synoviocytic hypertrophy and hyperplasia and a marked hypercellularity of fibroblasts in the superficial and deeper regions of the subsynoviocytic layer. In several places broad collagen fibers are noted. Also, in several layers the subsynoviocytic tissues with their complement of collagen, fibroblasts, and vessels are thrown into folds or villi extending above the adjacent flat synoviocytic surface and protruding into the joint space. While some villi are normally present in the synovial membrane, especially in those areas of the joint capsule that undergo a great deal of stretching during joint motion, these villi are abnormal because of the altered architecture of the synoviocytic and subsynoviocytic layers.
Inflammation of the synovial membrane, characterized by synovial cell hypertrophy and hyperplasia, plasma cell and lymphocyte infiltration, and increased vascularization of the subsynovium, are prominent features of experimentally produced DJD in the dog. Subsynovial fibrosis is also a common finding.(46)
The increased fibrosis of the synovial tissue and the progressive formation of villi could easily contribute to the joint stiffness and painful symptoms often associated with advanced DJD.
Primary DJD is an insidious progressive condition that most commonly affects older animals, whereas secondary DJD may be more acute in onset and occurs in the young or old patient. Once the pathologic transformation of the tissues begins, the general signs and symptoms are similar.
Dogs with DJD are usually presented with a complaint of lameness or gait change.(10) In some cases the owner will state that the animal has difficulty in performing certain acts that heretofore were performed readily. Most commonly, the animal is no longer able to jump with as much vigor as he had previously or now has difficulty in climbing a flight of stairs that previously were easily negotiable. The astute clinician knows there are many afflictions and conditions that produce lameness and/or gait abnormalities in the dog, and one must keep an open mind when performing a physical examination on such patients. Every older German shepherd presented with hindlimb lameness and weakness does not have DJD secondary to hip dysplasia, nor does every young giant breed dog presented with foreleg lameness have osteochondritis dissecans of the shoulder.
Since the majority of cases of DJD that occur in the dog are the result of another condition, the primary condition must be diagnosed and treated in order to curtail the degenerative processes that are occurring in the affected joint. In addition, there are many conditions that produce lameness or gait changes in the dog that do not affect the joints.(32) One must be able to differentiate these problems from those that are articular diseases. A carefully taken history and thorough physical examination, including a neurologic assessment of the patient, are necessary in evaluating lameness. The animal's breed and age are combined with the information gleaned from the history and physical examination and are central in reducing the list of differential diagnoses. Also, animals may be presented with concomitant conditions, and it must be kept in mind that both problems may be contributing to the patient's lameness. Such a situation may occur in old German shepherds who have degenerative myelopathy of the spinal cord and DJD secondary to hip dysplasia. A partial list of conditions that may manifest as lameness and/or gait abnormalities and therefore may be mistaken initially for articular disease is presented in Table 87-2.
|TABLE 87-2 Nonarticular Conditions That May Cause Lameness or Gait Abnormalities|
Physical examination of the animal should include all body systems and especially a neurologic examination; it should not be confined solely to the apparently affected limb. Examination of the affected limb should include palpation of the musculature and joints and a comparison with the opposite normal limb.(32) Severe pain on joint palpation and manipulation is unusual in the dog with DJD. However, pain may be elicited in such conditions as osteochondritis dissecans of the shoulder. The affected joint should be manipulated gently through its full range of motion and the vibratory sensations of crepitus should be noted if present. Crepitation is usually indicative of articular cartilage wear or osteophyte formation. In addition, ligamentous and tendinous structures of the joint should be assessed for integrity and laxity. Joint range of motion should be measured with a goniometer, compared with the same joint on the opposite normal limb, and the results noted in the patient record.
Extensive joint effusion is not a prominent feature of DJD although slight increases in joint fluid volume are not unusual. In chronic cases the effusion is usually less severe and may not be readily detectable by palpation. However, as mentioned in Chapter 86, significant changes are present in the cellular constituents of the synovial fluid from osteoarthritis joints, and synovial fluid analysis should be an integral part of the diagnostic evaluation of the patient.
Joint enlargement is most frequent in the more chronic cases and varies with the degree of periarticular soft tissue fibrosis, joint capsule thickening, and osteophyte formation.
Although DJD is an inflammatory disease of articular tissues, a palpable increase in temperature of the tissues overlying the affected joint may not be readily detectable even in the acute condition. Thermographic studies, however, may show increases in tissue temperatures. Such techniques have been used in humans and in horses.(42) it should be noted that most inflammatory conditions are associated with increases in tissue temperatures and that thermography cannot be used to any significant degree in differentiating degenerative joint disease from other inflammatory conditions of joints.
In addition to the usual complete examination of all body systems, it must be determined whether the animal has a local or systemic condition, although a localized condition may affect multiple sites. (16) Careful questioning of the owner should accompany the actual examination of the patient. It must be determined when the lameness was first noticed and under what circumstances. Was there a "traumatic" incident or an unusual experience such as overuse? The pattern of involvement, if any, should be determined. In what order, if any, did the joint involvement occur? Is the lameness more noticeable after rest or after exercise? Does the patient "warm" in or out of the lameness? Is the involvement self-limited, migratory, or progressive?(16) Migratory means that the process subsides in one joint only to manifest itself in another. Progressive means that the first joint remains involved but additional joints become affected as well.
Previous treatment should be determined. What was given, for how long, and what effect did the therapy have on the condition? In addition, any side-effects produced by the medication must be noted.
All animals suspected of having articular disease of any type must have the appropriate joints radiographed. The usual tenets of good radiographic technique and protocol must be followed. These include accurate patient positioning, at least two standard views of the affected ,joint or joints, sedation or general anesthesia of the patient to ease patient positioning and prevent motion on the film, the use of proper film and screens for the area of the body to be radiographed, and proper exposure of the film.
It has been stated that there are two types of signs of articular disease: the clinical and the radiographic.(25) Animals with clinically obvious articular disease may have few radiographic abnormalities, while those with extensive radiographic changes may show few clinical abnormalities. Therefore, radiography is but one diagnostic tool; just because a joint appears free of radiographic change does not mean it is free of articular disease. Radiographic findings must be interpreted and integrated with the other diagnostic information, especially with the findings of physical examination and synovial fluid analysis.
Characteristic radiographic features of DJD include sclerosis of subchondral bone, subchondral bone cysts, osteophyte formation, subluxation, narrowing of the joint space, and intra-articular or periarticular calcification (Fig. 87-5 and 87-6).(21)
Sclerosis of subchondral bone is seen in more chronic cases of DJD and suggests that bone beneath the cartilage is being subjected to increased stress that normally is borne by the articular cartilage. Sclerotic subchondral bone appears radiographically as a homogeneous, radiodense area beneath the articular surface of the affected joint.
As mentioned above, the so-called subchondral bone cysts of DJD are not truly cysts but fluid- or mucoid filled spaces in the subchondral bone probably created by microfractures of subchondral trabeculae. Because they lack a definite capsule, these areas are not true cysts. Their presence in dogs and cats with DJD is unusual, although they are frequently found in the horse and other large animals.(21) When present, they appear as rounded, lucent areas surrounded by a thin layer of sclerotic subchondral bone.
|FIG. 87-5 Lateral radiographic view of the elbow of a dog with DJD. Osteophytes are seen on the cranial (1) and caudal (2) aspects of the joint. Sclerosis of the radial head (3) and proximal ulna (4) is also present.|
|FIG. 87-6 Lateral (A) and cranial-caudal (B) radiographic views of the stifle of a dog with DJD. Osteophytes are present on the proximal aspect of the femoral trochlea (1), proximal and distal aspects of the patella (2), femoral condyles (3), and proximal tibia (4). Sclerosis of the proximal tibia (5) is also present.|
Osteophytes are commonly seen radiographically in more chronic cases of DJD, especially in the stifle, hip, shoulder, and elbow joints. They appear as periarticular spurs or outgrowths of bone arising from the margins of the articular surface. Correlations have not been made between the presence of osteophytes and the presence of articular cartilage breakdown or disease. In other words, does the radiographic finding of osteophyte formation automatically mean the presence of DJD? While it is true that osteophytes are common in joints affected with DJD, ,joints that have osteophytes may not have the other features of DJD.(24) To date, this controversy has not been resolved. It is safe to say that osteophytes alone probably are not pathognomonic of DJD but their presence does indicate some abnormal activity within or adjacent to the affected joint.
Subluxation has been described as a radiographic feature of DJD of the stifle of the dog. (20) Although probably due more to concomitant ligamentous and/or meniscal injury than to anything else, the subluxation is demonstrable in many cases when the radiographs are taken with the patient in a weight-bearing position. Abnormal joint laxity due to the loss of supporting structures plays a significant role in the perpetuation of DJD. The abnormal stresses to which the joint tissues are subjected because of supporting structure loss continually feed the fire of inflammation, resulting in joint tissue destruction. Whether the laxity preceded the degenerative changes and therefore resulted in secondary DJD or whether the laxity occurred as a result of the ligamentous destruction in the ongoing process of primary DJD is, at least for this discussion, immaterial. What is important is that subluxation can be seen radiographically in DJD. In the hip it is often seen in the DJD of hip dysplasia.
Joint laxity may also be demonstrated radiographically by obtaining "stress" views of the affected joint. Stress views are obtained by applying abnormal medial or lateral pressure to a joint that is being radiographed. Likewise, the joint may be radiographed in hyperflexion or hyperextension.
Changes in radiographic appearance of the joint space in DJD or other articular diseases must be judged and interpreted with care. Narrowing or collapse of the joint space is said to be a fairly consistent feature of chronic DJD.(21) This is due to the loss of significant amounts of articular cartilage, allowing subchondral bone, which is more radiodense than articular cartilage, to come in closer contact, therefore giving the appearance of a narrow joint space. This in fact is the case, but the radiographic appearance of the joint space will also be affected by patient positioning, assumption of a weight-bearing or non-weight-bearing position when the radiograph was taken, joint effusion, and integrity of the ligamentous structures of the affected joint. As noted above, dogs with hip dysplasia and DJD of the coxofemoral joint have joint effusion that affects the interface between the femoral head and the acetabulum.(l2,13) In these animals the joint space will appear quite different if radiographs are taken before and after arthrocentesis. True assessment of changes in the width of the joint space are best made with the patient in a weight-bearing position.
Calcification of the supporting soft tissues of a joint, whether intra-articular or periarticular, is rarely seen in the dog. This finding has been associated with DJD of long duration. However, soft tissue calcification alone, without other radiographic signs, is probably a poor indication of the presence of DJD.(21) Synovial chondromatosis is a condition in which chondrification and mineralization of the synovial membrane occur. Although rare in the dog, the patient presents with lameness and mineralized densities within the joint. The etiology of the condition is unknown in humans and in dogs, and the joint inflammation that ensues is secondary to the original problem.
Intra-articular mineralization can also be seen with osteochondritis dissecans. Loose bodies form from the dislodged cartilaginous flap. The cartilage is nurtured by the synovial fluid and remains viable. In some cases the free flap becomes embedded in the synovial membrane. Once again, this unusual finding is not characteristic of DJD; it is just an odd finding in the occasional case of osteochondritis dissecans.
There are no specific laboratory findings characteristic of DJD. Results of a hemogram, urinalysis, and blood chemistry determinations are usually within normal limits. Results of rheumatoid factor tests and lupus erythematosus (LE) clot tests are negative, as is the search for antinuclear antibodies.
Examination of the synovial fluid will usually confirm the presence of a low-grade intra-articular inflammatory processes in the acute condition or in secondary DJD associated with common conditions such as osteochondritis dissecans, hip dysplasia, or ruptured cranial cruciate ligament, synovial fluid volume is often increased. Synovial fluid color ranges from pale yellow to straw color and is usually clear. Haziness or flocculence may be seen in some cases of secondary DJD, especially those in which there is an articular cartilage defect. Viscosity is usually normal and the mucin clot test rated flair to good.
Total white cell count rarely exceeds 5000 cells/ mm3; the predominant cells are lymphocytes and monocyte-macrophages. Phagocytic vacuoles may be seen on close examination of the macrophages. Neutrophils are rarely encountered.
Osteoarthritis is not a condition that can be cured in the sense of returning the patient to complete normalcy. In most cases, some residual abnormality will remain in the affected joint or joints, and this abnormality is often of such a nature as to continually produce difficulties for the patient. The goals in the treatment of DJD are to alleviate the animal's discomfort, to prevent the occurrence of further degenerative changes, and to restore the affected joint or joints to as near normal and pain-free function as possible.
Compared with the treatment of other conditions such as a bacterial infection, treatment of DJD is rather symptomatic and nonspecific. Rest and physical therapy are employed to initially decrease inflammation of the affected joint and then to strengthen the supporting structures of the joint. Medical therapy includes a wide variety of compounds and medicaments, each with essentially the same purpose-to reduce inflammation and act as an analgesic. Surgical treatment in concert with medical and physical therapy may prove beneficial in some cases.
Excessive use of the joint may aggravate the symptoms of DJD and accelerate degenerative changes. Rest plays a significant role in the management of DJD in humans and should also in the dog. Too often this important aspect of therapy is overlooked. It may be argued that dogs rest most of the time, in that except for the true working or racing animal most dogs have little true physical activity. Indeed, this may be so. This does not, however, prevent owners from expecting their more sedentary pets to perform certain acts or games that involve running or jumping. While exercise may be a valuable portion of the treatment regime, it must be controlled and specifically tailored to each situation and animal. Just as rheumatologists would counsel their patients on the type and extent of exercise, so too should the veterinarian counsel the client who has a dog with DJD.
In the acute stages of DJD, when joint effusion is present and the inflammatory process is at its peak, exercise should not be allowed. Our patients are at somewhat of a disadvantage in that even the act of moving from one spot to another may involve use of an affected joint, whereas a person may use a crutch or cane to aid in reducing the stress.
Once the joint effusion has subsided and the analgesic anti-inflammatory medications have been given, controlled exercise is advisable. Stressful activity should be kept to a minimum and the animal's tolerance to activity judged carefully. Walking on a leash several times a day for short distances is advisable initially. As the patient responds to this and there are no untoward effects such as reluctance to take the walk, stiffness or soreness several hours following the activity, or changes in gait patterns, the walking should increase in length. More strenuous activities can be introduced as the animal gains strength.
While the relationship between obesity per se and DJD in humans remains controversial, reduction to ideal weight appears prudent, since degenerative changes are initiated or aggravated by excessive or abnormally directed pressures on articular cartilage.(22) Weight reduction by dietary control should be considered for the overweight dog as well. This is often difficult to accomplish owing to the reluctance of owners to feed their animals less and owing to the limited activity of the patient. Caloric requirements should be calculated for the animal based on ideal body weight and amount of activity; a dietary plan can then be established for the owner to follow.
There are no drugs or combinations of drugs that will consistently prevent or reverse the pathologic changes of DJD. Drugs are administered to DJD patients primarily as analgesics and anti-inflammatories for symptomatic relief of clinical signs.
Acetylsalicylic acid (aspirin) is an analgesic and anti-inflammatory as well as an antipyretic and is the basic drug for the treatment of DJD. It is the basic drug in a class known as nonsteroidal anti-inflammatory agents. Used properly it can be quite effective and free of side-effects. Aspirin has an impact on a wide variety of metabolic processes and enzyme systems. Mild to moderate peripheral pain is relieved by its ability to block the effects on pain endings of inflammatory mediators such as bradykinin.(2) In contrast to the opiates, aspirin acts peripherally rather than centrally as an analgesic. Aspirin's actions as an anti-inflammatory agent are due primarily to its abilities to inhibit prostaglandin biosynthesis. (15)
As with any drug, sufficient dosages must be taken to obtain adequate effects. A dosage of 25 mg/kg three times per day is given initially and the therapeutic results observed.(2,35,47) If the desired effects have not been obtained in 4 to 5 days, the dosage may be increased slightly. Dosages reaching 50 mg/kg may produce emesis.(45) Vomiting can occur at lower doses as well and may be prevented by administering the drug with food. Patients with gastric intolerance to plain aspirin may find it well tolerated when taken with oral antacids such as magnesium-aluminum hydroxide.
When taken at therapeutic levels, aspirin is virtually free of serious side-effects. Gross overdoses may produce hyperthermia, severe acid-base and electrolyte disturbances, renal damage, hemorrhage, convulsions, and coma.(2)
Treatment for such acute and severe problems includes gastric lavage to remove any unabsorbed drug, urine alkalinization with sodium bicarbonate to enhance renal excretion of salicylate, and peritoneal dialysis to remove salicylate from plasma.(2)
Less life-threatening toxic manifestations include skin eruptions, edema, gastrointestinal bleeding and ulceration, hypoprothrombinemia, vomiting, and deafness. In the dog, the most common of these are vomiting and melena. Withholding the medication will alleviate these problems.(2)
Phenylbutazone has been used with a good deal of success in the symptomatic treatment of chronic DJD. It has been quite valuable in some cases of DJD that were unresponsive to aspirin. Because of the bone marrow depression it may cause, phenylbutazone has not been used as widely in humans as it has in animals. When properly administered and monitored, it can be a most valuable drug for the symptomatic treatment of DJD in the dog.
Phenylbutazone is a nonsteroidal anti-inflammatory drug with a mechanism of action similar to that of aspirin.(35) It is given in dosages ranging from 0.5 mg to 1.0 mg/kg of body weight three times per day. Bone marrow depression may be the most serious of its side-effects. Peptic ulcers, malaise, pruritus, rashes, renal dysfunction, and other problems have also been reported in humans.
Other Nonsteroidal Anti-inflammatory Agents
Within recent years a variety of agents have been introduced for treatment of articular disease. There is a category of nonsteroidal anti-inflammatory agents that are commonly referred to as aspirin-like. These drugs also are anti-inflammatory, analgesic, and antipyretic, and their mode of action is the inhibition of prostaglandin synthesis or release. The drugs of this type presently approved in the United States for use in humans include fenoprofen, ibuprofen, indomethacin, nefanamic acid, naproxen, oxyphenylbutazone, sulindac, and tolmetin.(23) Meclofenamic acid has been approved for use in the horse. The efficacy of many of these drugs in the dog has yet to be established. On a clinical basis, meclofenamic acid has been as effective as aspirin in some cases of DJD in the dog.*
Ibuprofen given orally in a total dose of 15 mg/kg body weight divided into three doses daily and indomethacin in an oral dose of 1.00 mg to 1.25 mg/kg divided into two or three doses daily have been suggested for the treatment of DJD in the dog.(28) With chronic use both drugs may cause gastrointestinal problems.
To date, there is little convincing data that show that any of the newer compounds are superior to aspirin in effectiveness when the objective of therapy is an immediate anti-inflammatory effect.(44) The compounds do, however, have fewer side-effects, and for that reason alone have found great acceptance by the physician and the general public. Well-designed and well-executed studies will be needed before their effectiveness in the dog and the cat can be determined.
It is important to note that as of this writing many of these newer drugs have not been approved by the appropriate authorities for use in the dog. Therefore, one cannot legally administer or prescribe them.
* Wallace LJ: Unpublished data
Corticosteroids are potent anti-inflammatory drugs that may be of benefit in some cases of DJD. Their mechanism of action is related to retardation of leukocyte migration, decreased permeability of microvasculature, inhibition of prostaglandin release, and stabilization of Iysosomal membranes. (7,35) Corticosteroids should not be considered as the agent of choice in the treatment of DJD. They are reserved for those cases that are unresponsive or slowly responsive to the previously mentioned agents. Corticosteroids are most commonly administered orally or parenterally in low doses and given for short periods of time. Prednisolone may be given parenterally at a dose of l mg to 2 mg/kg followed by an oral maintenance dose of 0.5 to 1.0 mg/kg once daily. The lowest possible maintenance dose should be established, such as alternate day or every third day administration of 0.5 mg to 1.0 mg/kg. Corticosteroids have been used in combination with nonsteroidal anti-inflammatory drugs. Aspirin and corticosteroids are administered concomitantly in the doses mentioned above. Each subsequent day, smaller doses are given so that by the fifth or sixth day corticosteroids are no longer administered and the aspirin is being given in low maintenance doses. While some patients respond to this regime, they may be prone to gastrointestinal hemorrhage.
Intra-articular instillation of corticosteroids has been used in humans and in animals for the treatment of DJD. Effects of the drug last for varying periods of time and are often repeated on an "as needed" basis. It has been suggested that the beneficial effects of such treatment are due to absorption and systemic distribution of the drug.(22) The practice of intra-articular corticosteroid injection is not without complications. Postinjection flare, a synovitis induced by corticosteroid crystals, may occur. In addition, the injected joint may be more susceptible to infection. Experimental work in animals and clinical observations in humans show that intra-articular corticosteroids have a deleterious effect on cartilage that is already damaged by disease.(22) To date, sufficient studies in the dog and cat have not been recorded that confirm or deny that these animals are as susceptible or as prone to the complications of intra-articular corticosteroids as are humans. Intra-articular corticosteroids in the dog and cat should be used with great discretion until such information is available.
Intra-articular injection of hyaluronic acid is presently under investigation as a treatment for DJD in humans and in animals. A healing effect on traumatic lameness in the horse has been reported. (33) However, clinical trials in human osteoarthritic knee joints have so far shown either no beneficial effect or varying degrees of improvement of symptoms.(22) Until further reports are available, this drug should probably not be considered a part of the treatment regime for DJD.
Orgotein is another drug that may have potential in the treatment of DJD; to date it has not been studied in sufficient depth or length to be recommended. Orgotein is a superoxide dismutase that exerts its effects by membrane stabilization, promotion of leukocyte chemotaxis, and, most importantly, by inhibition of certain enzyme functions that promote inflammation.(35)
Injection into osteoarthritic hips and knees of humans produced sustained improvement, and such treatment has been used in the horse with some success.(22,35)
Acupuncture has been shown to be effective in the reduction of certain types of pain. However, reports of its efficacy in humans with DJD are conflicting.(22) While it may be of some benefit in animals with DJD, controlled studies are lacking. Until such reports are available. acupuncture will remain a controversial and curious phenomenon.
The main purposes of surgery in the treatment of DJD are to increase joint function and reduce or eliminate joint pain. The two may not be compatible. For instance, arthrodesis is done most commonly to reduce joint pain and return a limb to use, but obviously the affected joint will no longer be functional. The majority of small animals who are operated upon for joint disease have secondary osteoarthritis. Osteochondritis dissecans of the shoulder and ruptured cranial cruciate ligament of the stifle are good examples. Each condition, especially if it is of several weeks duration, is almost always associated with changes of secondary DJD. By appropriate surgical treatment of each, the primary condition is eliminated, thus ending the cause of the secondary DJD.
Orthopaedic procedures related to joint disease may be categorized as articular, juxta-articular (immediately adjacent to the joint), and para-articular (near a joint).(8)
Synovectomy, the surgical removal of synovial membrane, is usually performed in cases of immune-mediated arthritis such as rheumatoid arthritis. Removal of the active proliferative synovium often causes remission of symptoms and return to function for long periods of time. It is not a procedure recommended for DJD. Fusion of a joint, or arthrodesis, as noted above, is used to stabilize a severely painful and/or deformed joint in hopes of increasing use of the entire limb. In the dog, the carpus, hock, and stifle are the joints fused most frequently. On rare occasions, the elbow and shoulder may also be arthrodesed.(41)
Arthroplasty is rebuilding a joint and includes the insertion of a total prosthesis, as is done for the severe DJD of hip dysplasia, or a trochleoplasty of the distal femur for patellar luxation. Resection arthroplasty is rebuilding by removing the adjacent ends of bone making up the joint and allowing a pseudoarthrosis to develop. This is the rationale for femoral head and neck excision in cases of severe hip dysplasia.
Other examples of resection arthroplasty in the treatment of conditions resulting in secondary DJD include removal of ununited (fragmented) coronoid and ununited anconeal processes from the elbow joint.
Surgery may be performed on structures next to rather than directly inside a joint. Capsulorrhaphy procedures for patellar luxation or extracapsular stabilization techniques of the stifle for anterior cruciate ligament rupture are examples.
Osteotomy is a surgically induced fracture that allows a then realigned bone to heal so that different forces are imparted to the adjacent joints. Osteotomies are done to correct distal radial and ulnar growth deformities, which if uncorrected may lead to DJD of the carpus and elbow joints. Pelvic osteotomies are now performed in selected cases of hip dysplasia to prevent further degenerative changes from occurring in the coxofemoral joint.
Tendon surgery may be of benefit in certain cases of DJD. Transsection of the pectineus muscle is used in select cases of hip dysplasia to reduce pain in the affected joint.
It must be remembered that the surgical procedures mentioned here are not meant to be specific treatments of DJD. Rather they are part of a treatment plan designed to decrease pain and increase joint and limb function.
The treatment of primary and secondary DAD is essentially the same except that the initiating cause of secondary DJD must be treated as well. Controlled exercise and physiotherapy are important to the animal's well-being, and the owner should be given specific instructions in this regard. Diet must also be discussed with the owner, particularly for the obese animal.
Drug therapy usually begins with aspirin. Favorable response to the drug often takes 2 to 3 days to occur. If less than favorable results are seen at this time and the patient has not shown intolerance to the drug, the dosage should be increased from 25 mg/kg three times daily to 35 mg to 40 mg/kg three times daily. Another 2 to 3 days of therapy may be required before results are seen.
Owners often expect immediate results after they administer medication to their pets. They must be counseled regarding the difficulties in the treatment of osteoarthritis and be made aware of its incurability. Frank discussion between the owner and the veterinarian will ultimately result in better treatment for the patient.
Once a favorable response is obtained with the exercise program and the aspirin administration, the total daily dose of drug should slowly be reduced. As improvement continues, the drug may then be given on an "as needed" basis.
Those animals who do not respond well to aspirin may be given phenylbutazone or corticosteroids. Our best success with phenylbutazone has been in dogs with severe coxofemoral DJD that was unresponsive to aspirin. As noted above corticosteroids are used after aspirin and phenylbutazone have proven unsatisfactory or in cases of acute inflammation. Concomitant use of aspirin and corticosteroids in decreasing dosages may be of benefit. Once the newer nonsteroidal anti-inflammatory drugs have been approved for use in the dog, they may prove to be even better than aspirin in the treatment of DJD. The goal in treating DJD is to enable an animal to be as active and pain-free as possible while at the same time taking the lowest possible dosages of medication.
Traumatic arthritis is a joint disease resulting from direct or indirect injury to a joint. It may include any or all of the following: soft tissue injury of the synovium or supporting structures, partial-thickness cartilage depression, fissuring or laceration, full-thickness cartilage defects, or tears into the subchondral bone. The extreme of trauma can lead to an intra-articular fracture.
Traumatic arthritis as a distinct entity is diagnosed infrequently in veterinary medicine. This is either because it is so minor as to be unrecognized or because it is merely a transient intermediary step leading to DJD, which is the major problem presented for diagnosis. Figure 87-7 illustrates how trauma influences the cycle that leads to DJD.(52) As demonstrated by the figure, trauma may incite synovitis or chondrocyte death with resultant protein release or may change a joint biochemically. Any one factor or all can lead to DJD.
|FIG. 87-7 The vicious cycle of DJD. (Chrismall OD: Biochemical aspects of degenerative joint disease. Clin Orthop Rel Res 64:77, 1969)|
Minor trauma to joints associated with bumps, bruises, or penetrating objects may injure only the synovium and fibrous joint capsule, sparing the cartilaginous surfaces. Such trauma can lead to the classic signs of inflammation, but they are usually more subdued. Therefore, swelling is only mild to moderate, discoloration is mild, and local temperature is probably not markedly elevated to touch.
Histologically, a synovitis can be seen to occur, resulting in mild edema of the synovium, vasodilation, and slight focal increases in the number of synovial lining cells. Such a change may result in very mild changes in the synovial fluid. There may be a few more red blood cells and a slight increase in mononuclear leukocytes. Fluid volume may be slightly increased, but the increase is transient.(54) The discomfort to the animal is probably due more to intra-articular increase in fluid pressure than to the synovitis itself.
Assuming no additional trauma occurred, this problem should be transient and should respond well to analgesics and enforced rest. The entire clinical course should not exceed 7 to 10 days. There is no rationale for surgical intervention.
Partial-thickness cartilage injury presupposes that soft tissue injuries above have occurred also. Generally this injury arises from axially loading a joint and compressing or denting the articular cartilage or from blunt trauma to the articular surface. The extent of the injury, as it relates to subsequent disease, is more severe if it involves weight-bearing surfaces as opposed to non-weight-bearing areas.
Direct cartilage injury generally results in fissuring and local chondrocyte death. Following Iysis of dead chondrocytes, chondroitin sulfate and other cartilage debris are released into the synovial fluid, which eventually results in synovitis. Of greater significance is the loss of cartilage elasticity due to loss of protein polysaccharide. This results in further fibrillation of cartilage and further destruction.(48)
The above mechanism is circuitous and causes the process to repeat, eventually leading to further mechanical problems and DJD. Were it possible for partial thickness cartilage injuries to correct themselves and heal, the process could be healed and stopped; unfortunately, the later healing process does not occur (Fig. 87-8).
Clinically, the animal is presented with a painful swollen joint. There is chemical synovitis, signs of increased fluid, and pain on joint manipulation. Synovial fluid characteristics are reflected in Figure 87-9.
Many of these animals whose arthritis has traumatic origin show the early bony changes of DJD on presentation. Only if the underlying injury to the cartilage is eliminated can the progress of DJD be eliminated or stopped.(50) Salicylates may help prevent continued degeneration.
|FIG. 87-8 The role played by trauma in DJD. A, soft-tissue injury alone; B. partial-thickness cartilage injury; C. full-thickness cartilage injury; D, intra-articular fracture.|
|FIG. 87-9 Synovial fluid abnormalities in traumatic arthritis. (Miller JB, Perman V, Osborne CA et al: Synovial fluid analysis in canine arthritis. J Am Anim Hosp Assoc 10:392, 1974)|
Trauma sufficient to cause full-thickness cartilage injury also produces the biologic changes discussed in the previous two sections. In addition, there is gross fissuring into subchondral bone and probably hemorrhage. Of major concern, however, is the chondrocyte death and the release of chondroitin sulfate, cathepsin, and other cartilage debris as described in the preceding section.
Full-thickness lacerations may actually be less of a problem than partial-thickness injury because the cartilage can heal from the subchondral defect and may eventually return to nearly normal.(49)
Of greater importance is the biochemical changes that such a defect or defects cause if they are sufficient to cause abnormal joint wear; further chondrocyte wear and tear will again begin the cycle of partial-thickness injury and lead to DJD.
Clinically the animal with lull-thickness cartilage injury appears similar to animals with partial-thickness cartilage injury, with increased synovial fluid volume, normal mucin, and probably normal numbers of white blood cells but increased numbers of red blood cells.
The problem does not correct itself unless the joint is normal biomechanically and the full-thickness defects heal. The layers of such full-thickness defects heal in the following sequence: (1) fibrin, (2) granulation tissue, (3) connective tissue, (4) cartilage cells in connective tissue (connective tissue cartilage), (5) fibrocartilage, and (6) new hyaline cartilage.(5) In some cases this sequence may stop at fibrocartilage. Continued motion of the affected joint during healing enhances the likelihood of hyaline cartilage formation.(53)
Fracture of a portion of a joint produces all the symptoms discussed and leads to total dysfunction due to severe internal derangement.
Synovial fluid should be the same as in full-thickness injury but may have considerably more hemorrhage and probably some free fat. Should the dog or cat walk on such fractures for any period of time, there will be cartilage destruction, release of enzymes as in partial and full-thickness injuries, and resulting synovitis. This undoubtedly leads to some DJD even if treated very quickly. If not treated shortly after injury, considerable DJD will result.
Many older animals with chronic DJD, which they tolerate well, may be acutely lame following a traumatic episode. Usually the new trauma is from prolonged vigorous activity or a fall. The new trauma commonly results in fracture of proliferative marginal bone spurs or tears of the thickened, chronically inflamed joint capsule. If these conditions are managed as an acute traumatic arthritis, the animal will return to the same function it had prior to the additional trauma. Such animals remain painful for 10 to 14 days and respond to treatment of the acute trauma. Treatment should include a 7- to 10-day course of a decreasing dose of corticosteroids. It is not necessary to attack the chronicity of the DJD, since it is very unlikely that treatment will affect the old problem.
DEGENERATIVE JOINT DISEASE
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