by Fred Lanting
The knee is an engineering marvel, extremely complicated and concise, able to move in multiple combinations of direction, and normally able to withstand considerable torque forces. The structure is encased in an exquisite joint capsule with ligaments connecting three large longbones, tendons running into and over it and connecting bone with muscle, as well as muscle to muscle via the sesamoids and patella. The capsule is lubricated by synovial fluid.
The most common joint disorder in the stifles, other than ruptured cruciate ligaments, is luxated patellas. The patella, or “knee cap” is a small bone (the body’s largest sesamoid bone) that seems to “float” outside of a joint. In actuality, it normally is securely attached to the area and the muscles by means of ligaments and tendons. It can be considered a localized ossification center in the tendon connecting the quadriceps muscle in the upper thigh to the tibia in the lower leg. You should be able to feel it somewhat above the slight indentation along the front of your dog’s rear leg, where the breed standards like to refer to the “bend of stifle”; this is where the upper and the lower thighs meet. In motion, the patella will normally slide down into a groove between the condyles of the femur. The quadriceps muscle group acts to extend (straighten) the limb; because the patella is enclosed in the lower tendon of that muscle group, the knee cap is more in front of the joint when the muscle is relaxed, and slides upward in front of the lower femur when contracted. That’s when the major discomfort occurs in dogs with defective stifles, with the patella missing the center of the groove in which case it is referred to as being luxated. Almost all dogs with patellar luxation have some other structural abnormality related to it; thus, in order to improve the individual’s life and prevent passing the defect to others, a regime of early evaluation and detection is important.
The alignment of muscle and tendon insertions or the relative positions of the leg bones may be such that the patella is pulled more to one side and hence misses that groove. The biomechanics are easily described by what we call the “bowstring effect”, in which the muscle fiber group on one side works better than the other side, and puts tension on the patellar tendon and associated bone structures. In so doing, the kneecap is pulled toward the dog’s centerline (medial displacement) and if the force is strong enough it will slide out of the groove running between the femoral condyles. This wears away the ridge of that “trochlea” so the effect is to slip out of the groove more easily as time goes on. Meanwhile, the underside of the patella also abrades, becoming less V-shaped and less likely to stay in the track where it belongs. In the more severe cases, the abnormal strain on the muscles and joint caused by forces being misdirected in this manner results in pain. It is usually considerable and almost always leads to a very noticeable change in gait, such as skipping or perhaps even a refusal to walk at times. Mild cases can go undiagnosed by a vet and, to some extent, unnoticed by the owner. Most pups can be diagnosed only after 4 to 6 months of age. If the luxated patellar bone is offset toward the centerline of the dog, the condition is called medial luxation or displacement. If the bone moves on the “outside”, or away from the centerline, it is called lateral luxation. A method you can use to keep these terms straight might be to think of the “median strip” in the middle of a divided highway. Medial patellar luxation is almost undoubtedly inherited.
We know that in limbs with two bones, such as the lower thigh and the lower foreleg, there are frequently small differences in the growth rate or eventual length ratios between tibia and fibula or between ulna and radius. It may well be that a disruption in growth rate of one of such a pair causes a twist or misalignment of both hard and soft structures in joints such as the wrist, elbow, knee, and hock. On the other hand, slightly abnormal muscle-fiber type or ratios might cause more tension on one side than on another. Some have tried to solve to solve the puzzle of the chicken-or-the-egg with explanations of one sort, and others have proposed the other. Whichever happens, and it could be that either is involved in any specific case, we are more concerned here with the “after-the-fact” condition, and how it relates to a dog’s gait, health, and value as a show or breeding animal. Whatever is the reason for a specific abnormality, sometimes all I can do in this book is describe it. Where possible, I shall try to explain it.
In some individuals of achondroplastic breeds such as Bassets and Dachshunds, luxation might be more a result of “breeder-selected” abnormal shape and position (curvature) of tibia and femur. The lateral deviation of the distal femur and the medial deviation of the proximal tibia seem to have similar results as found with luxation caused by muscle abnormalities.
This is the most common form. Most cases of medial patellar luxation involve toys and other small breeds, many of which are rather “straight in the stifle” such as the Shar Pei, but there may not be more than coincidence in that. Small (Toy and Miniature) Poodles, perhaps because there are so many of them indiscriminately bred, seem to be the most “visible” to the casual observer, but there is evidence that indeed, there is a 4 to 8 times greater predisposition in the miniature and toy breeds in general, and “the incidence of medial luxations is high in toy poodles”. Dr. Priester, the same man who did a study on breed, sex, and other factors in relation to HD, also studied these factors and their connection to canine patellar dislocation. Medial luxation in larger dogs is far less common, but does occur.
experienced dog show observer can often spot the more severely afflicted dogs,
usually while watching the Pomeranian, Lhasa Apso, Peke,
Four grades of medial luxation are used to describe the disorder. Grade 1 is for the dog that usually has a normal condition, but which can be luxated by minor trauma or pushing firmly with the thumb and fingers. In Grade 2, the patella can be manually displaced by adequate finger pressure or can slip out when the leg is fully extended, though it can be pushed back by the owner or a vet. With the next two grades it is difficult (grade 3) or impossible (grade 4) to put the patella back in place. Other signs are progressively worse, too, of course. Older dogs with Grades 1 or 2 may seem O.K. until a sudden onset that may be triggered by trauma or arthritic change that the dogs no longer fully tolerate; nevertheless, it is a genetic problem.
Grade 1 dogs occasionally skip or carry a leg, sometimes only for one stride in a twenty- or thirty-foot stretch of gaiting. Pain might be barely or not noticed, even when the cap is luxated slightly with finger pressure. Grade 2 dogs will more frequently to usually “carry” a leg, and occasionally bear weight on it; crepitus might be felt and heard, depending on the dog’s age. Surgery is recommended for Grades 2 to 4, earlier for the worse degrees. In Grade 3, a little weight bearing might be possible, but there is permanent dislocation; you can push the patella back into the shallow groove, but it will ride out as soon as you ease up on the pressure. Most dogs will stand bowlegged or crouched. In Grade 4, the affected leg will always be carried so that weight is not transmitted to the ground. The luxation is permanent and surgery will have to address other surfaces in the joint as well.
When the patella is displaced toward the “outside”, it is said to be luxated laterally. This condition is not as common, accounting for less than 24% of patellar dislocations. While it can be found in any size dog, it is more commonly found in large breeds. Any misalignment in the quadriceps muscles, the trochlear groove between the condyles of the femur, the tibia (larger of the two lower leg bones), and the ligaments early in life will abnormally shape the cartilage and, as it ossifies into bone, this legacy will solidify. Other puns aside, though, it has been seen that changing the directions or vectors of the muscle contraction forces will give unbalanced strains on the growth plates and other cartilaginous tissues in the young pup, and this means permanent deformities in the bone structures they will have developed into. It only takes a couple of weeks of misdirected stresses to produce this permanent deformation.
Coxa valgum, the condition in which the femoral head is inserted into the acetabulum at a greater-than-normal angle, tends to force the lower part of the femur toward the midline, which changes the relative position of the trochlear groove in which the patella should slide without pressure on one side of the groove or the other. An increase in the anteversion angle between the femur and the acetabular portion of the pelvis carries with it a corresponding torsional force on the whole femur, and another tendency for medial displacement of the distal femur as well. A vet school professor I consulted years ago felt that there was a cause-and-effect relationship between patellar luxation and hip dysplasia, but admitted there was disagreement on which caused what. Others have mentioned that lateral luxation can cause deformation of the femoral head in large, fast-growing breeds.
What happens when the stifles are brought closer together in this “knock-kneed” condition known as genu valgum? The dog’s weight is applied unevenly to one of the femoral condyles, and as the puppy is subjected to this, the development of the growth plate on that (lateral) side is inhibited while the medial condyle continues to grow and ossify normally. The change in the height of the lateral trochlear ridge, plus the fact that the patella rides atop it instead of next to it in the groove, makes for a shallow groove. In addition, if luxation started early, there were little or no developmental forces to even create a normal groove in the first place. All this presents an easy escape for the patella into an increasingly bad position. With every step the dog takes, the abrasion continues, cartilage is destroyed, ligaments are stretched, and pain probably increases. At almost infinitesimally small increments, to be sure, but progressively nonetheless.
The same sort of “bowstring effect” exists as in medial luxation, but bowing the femur inward instead, and rotating the tibia laterally (outward) while displacing the developing tuberosity on the tibia where the patellar tendon is inserted. The vastus medialis part of the quadriceps muscle is supposed to act as half of the couple (an engineering term meaning balanced rotational forces) and insure the patella rides in the groove and transfers the quadriceps’ force to extend the lower leg in a straight fashion.
Lateral luxation of the patella can begin with a hypoplastic muscle called the vastus medialis. It is the part of the quadriceps muscle group that is the last to develop and is the first muscle to undergo atrophy following injury or disuse. Hypoplasia means underdevelopment, with fewer cells and myofibers, so the muscle doesn’t stretch properly. It is probably not clinically identifiable in many or most cases. If it is not working properly, it does not balance the force of the vastus lateralis, which is then able to exert too much pull toward the “outside” (laterally). The vastus lateralis may also cause or contribute to the femur and tibia being twisted out of alignment with each other. This compounds the problem, sending the forces of the contracting quadriceps into a slightly (but importantly) different direction. The whole joint capsule is abnormally stressed and there is a possibility that a ruptured cruciate ligament so often seen in sporting and working breeds might be genetically related. Some 15 to 20% of luxated patella cases have accompanying (or resultant?) cranial cruciate ligament rupture. It could be that the genes for one muscle’s hypoplasia give cruciate ligament damage if combined with genes for certain characteristics, and patella luxation if combined with those for other characteristics.
Causes for lateral patellar luxation are often unproven, partly because there are so few cases. Willis in his excellent work on the German Shepherd Dog, says that he has only seen two cases in the breed, and Priester reported Saints but no GSDs in his 1972 study, despite the fact that the latter breed is the most populous in the world and was one of the five or six most popular breeds in the USA at the time. I hold the premise that almost everything has a genetic base, and that the reason some dogs are afflicted by an apparently environmental occurrence is that they are genetically more susceptible than others, be it rupturing a cruciate ligament, having gastric volvulus, heat stroke, or whatever. However, the low incidence makes it hard to convince some people. Just how such a genetic weakness is expressed, that is, its etiology and pathogenesis, can easily and understandably be a point of disagreement. Thus, such “causes” have been proposed as estrogen imbalance or trauma while in the uterus; both have been pretty much discounted as possibilities.
In lateral luxation, the lateral condyle of the femur, because its growth plate has been subjected to excess pressure and growth has been altered, is misshapen. The trochanteric ridge is lower, sort of like riding on one of those compact spare tires, and the trochlear groove is more shallow. Thus the patella does not have a nice, deep, secure groove to ride in, and it is easy to pull it out of normal direction, especially since the force to one side is so persistent (every time the dog flexes or extends the knee). The groove becomes even more shallow due to wearing away faster than the dog can rebuild with new cells. Still, symptoms of lateral luxation usually are slower to develop than medial luxation signs. The dog may be over 5 years old by the time clinical signs of Grade 1 or 2 appear. The affected dog may be knock-kneed, cowhocked, or toed-out, but then, many non-affected dogs may show these traits, so do not base a diagnosis on those alone. In sudden-onset cases involving both rear limbs at once (perhaps brought on by strenuous exercise), the dog might not be able to stand and the condition may appear to be a neurological disorder.
Surgical correction (not cure) generally is aimed at re-establishing or creating a deeper groove and repositioning the muscle vectors. If surgery is postponed, osteoarthritis may be a problem of varying severity, with osteophytes and a thickened, swollen knee joint capsule making correction more difficult. Steroids are often prescribed (they are as commonly resorted to as Valium for adult humans or Ritalin for kids) but given the dangerous and unpleasant side-effects of such medication, your best recourse is probably surgery, which sometimes is very extensive. Since patellar luxations are progressive, the earlier you detect and treat, the greater the success will be.
It’s part of my usual soapbox to point toward genetic origins for almost everything, and this is no exception. Noted geneticist Frederick Hutt flatly said of patellar luxation, “It is inherited and polygenic”. However, as Olmstead says, the heredity of lateral patellar luxation is difficult to substantiate because the condition does not occur as often as, say, HD or many other more frequently seen orthopedic disorders. While the role of trauma is easy to see, the “primary pathophysiology” is not. Just how and why the genes express themselves in luxated patellas, whether medially or laterally, is not all that clear. But perhaps it need not be, as long as we follow the wise breeder’s rule: don’t breed defective dogs, whatever the defect or supposed cause.
NOTE: A well-respected AKC and Schaferhund Verein judge, Mr. Lanting has judged in more than a dozen countries, including the prestigious FCI Asian Show hosted by Japan Kennel Club, the Scottish Kennel Club, a Greyhound specialty in England, and more. National Specialties: 1994 GSD Club of America National; 1991 Tibetan Mastiff National; 1990 Shiba National; Fila Brasileiro Nationals (several times), Dogo Argentino National, Pyrenean Shepherd National. Numerous Chinese Shar Pei and Australian Shepherd specialties; regional Anatolian Shepherd specialty. Numerous GSD, Rottweiler, & Boxer specialties worldwide. He is also the author of several ‘must read’ books, including THE TOTAL GERMAN SHEPHERD DOG, CANINE HIP DYSPLASIA, CANINE ORTHOPEDIC PROBLEMS. A former professional all-breed handler in the US and Canada, he has lectured in over fifteen countries on Gait-and-Structure (Analytical Approach), Canine Orthopedic Disorders, and other topics, as well as being a Sr. Conf. Judges Ass’n (SCJA) Institute instructor. WV Canine College instructor & member, advisory board. His full Curriculum Vitae is very impressive and we are grateful to him for sharing that knowledge on this site.