1| mini; This is to certify that the thesis entitled The Measurement of Canine Coxofemoral Joint Laxity presented by Stephen Mark Belko f f has been accepted towards fulfillment of the requirements for M. S . Mechanics degree in W Major professor Date 11/ 14/ 86 0-7639 MS U is an Wank Action/Equal Opportunity Institution LIB AR MM ' R n SIG“ “MAKE 9 Win nil“ \/ MSU LIBRARIES .m— RETURNING MATERIALS: Place in book drop to remove this checkout from your record. FINES will be charged if book is returned after the date stamped below. mam: THE MEASUREMENT OF CANINE COXOFEMORAL JOINT LAXITY By Stephen Mark Belkoff A THESIS Submitted to Michigan State University in partial fulfillment of the requirements for the degree of MASTER OF SCIENCE Department of Metallurgy, Mechanics, and Material Science 1986 4.373103% ABSTRACT THE MEASUREMENT OF CANINE COXOFEMORAL JOINT LAXITY By Stephen Mark Belkoff The purpose of this research is to develop an instrument to measure laxity in the coxofemoral joints of anesthetized canines. Animals of various sizes and ages were tested and a quantitative measurement of the laxity in each hip joint was obtained for each animal. The measurements were then converted to a laxity index which would allow the clinician to compare joint laxity for normal, bilaterally lax and unilaterally lax animals regardless of their age, sex, breed or size. The test protocol is non-invasive and non-injurious and the results obtained from the test were reproducible. The effectiveness of present joint laxity diagnostic techniques is considered and a correlation is drawn between joint laxity and morphological abnormalities of the joint connective tissue. To my parents, for their love and support. ii ACKNOWLEDGEMENTS The author wishes to express his deepest appreciation to the following people for making the completion of his Master of Science degree possible: To Dr. Robert Wm. Soutas-Little, his major professor, for his encouragement, friendship, and invaluable assistance in the preparation of the manuscript. To the Orthopedic Foundation for Animals, for their generous funding of the project. To Dr. Ulreh Mostosky, for his assistance in the project. To Robert E. Schaeffer, for his amazing technical assistance and his invaluable instruction in the finer points of the design process. To Jane Walsh, for her assistance with the project and her warm friendship. To Lisa Stewart and Mark Jones for their assistance with the project and, more importantly, their invaluable friendship. iii TABLE OF CONTENTS Page LIST OF TABLES ............................................ v LIST OF FIGURES ........................................... vi LIST OF SYMBOLS ........................................... vii Section I. INTRODUCTION ..... i ................................... 1 II. SURVEY OF LITERATURE ................................ 5 III. EXPERIMENTAL METHODS ................................ 11 IV. RESULTS AND DISCUSSION .............................. l9 BIBLIOGRAPHY .............................................. 37 iv LIST OF TABLES Table Page I. Overlap Ratios and Normalized Loads ...................... 20 2. Laxity Indexes........... ...... ............. ............. 24 3. Correlation of Post Mortem Observations and Laxity Indexes .................................................. 27 4. Result Reproducibility .............................. ..... 32 5. Joint Stiffness .......................................... 33 LIST OF FIGURES Figure Page 1. Coxofemoral Joint ........................................ 2 2. Preliminary Test Results ................................. 12 3. OFA Radiographic Position ................................ 14 4. Testing Setup ............................................ 15 5. Measurement Diagram ...................................... l6 6. Load Radiograph - Case 2 ................................. 22 7. Load Radiograph - Case 10 ................................ 23 8. OFA Radiograph - Case 11 ................................. 28 9. Load Radiograph - Case 11 ................................ 28 10. OFA Radiograph - Case 3 .................................. 29 11. Load Radiograph - Case 3 ................................. 3O 12. OFA Radiograph - Case 1 .................................. 31 13. Load Radiograph - Case 1 ................................. 31 vi LIST OF SYMBOLS Definition Femoral head diameter, left Femoral head diameter, right Distance between the left and right cranial effective acetabular rims Overlap distance, left Overlap distance, right Overlap ratio, left Overlap ratio, right Laxity index, left Laxity index, right Normalized load, left Normalized load, right Applied load Joint stiffness, left Joint stiffness, right vii I. INTRODUCTION Canine hip dysplasia is thought to be a non-congenital, polygenetically inherited and usually progressive disease of the hip. It was first reported in veterinary medicine, in 1935, and it is still considered to be one of the major orthopedic problems in many breeds of dog. In some breeds as many as 47% of the animals (1) may be affected by it. There is no known cure, and the only accepted means of controlling the disease is through selective breeding. The term hip dysplasia literally means any malformation of the hip. When used in reference to small animals, particularly canines, the term denotes an abnormality characterized radiographically by remodeling of the femoral head and neck, a shallow acetabulum, coxofemoral subluxation and secondary degenerative joint disease. In order to understand the abnormality, one must be familar with both the anatomical and biomechanical functions of the hip joint. The joint is joined by the ligament of the femoral head, a strong strand of collagenous tissue which runs from the acetabular fossa to the fovea capitis and the articular capsule (see Fig. 1). Early in life, the ligament of the femoral head appears to stabilize the joint as well as to supply blood to the femoral head. After 3 - 4 months of age, however, the ligament of the femoral head lengthens and the articular capsule, which encloses the joint space, assumes the role of joint stabilizer. If the tissues of the articular capsule are lax or overly compliant, the femoral head will probably move laterally or subluxate 13 femoral head--- _ ,_ Trans. acetabulorv ligament Ligament of Figure 1. Coxofemoral Joint (Reproduced by courtesy of the W.B. Saunders Company, Phil.) from the acetabulum. When the femoral head is in this subluxated position, it no longer lies in intimate contact with the cranial acetabular edge and the load paths between the femoral head and the acetabulum become altered. These altered load paths may induce joint remodeling, especially in young developing animals. The abnormal remodeling is characterized by osteoarthritic spurs on the cranial effective acetabular rim, and flattening of the cranial acetabular edge. Radiographs are the most acceptable means of diagnosing hip dysplasia, but they become limited as a tool for diagnosing the condition in young animals. Although dysplastic changes have been evident in animals as early as 14 days of age in post mortem examinations, these changes are not normally radiographically apparent before 6 months of age. For animals which eventually develop dysplasia, the changes are usually apparent by two years of age. For this reason, the Orthopedic Foundation for Animals (OFA), which analyzes radiographs for dysplasia, will not certify an animal as having normal hips before the animal is 2 years old. The use of radiographs for the diagnosis of hip dysplasia is totally subjective. Even though the OFA uses a minimum of three veterinarians to review the radiographs for certification, conflicting diagnostic opinions often occur in borderline cases. In order to incorporate joint laxity into the diagnostic process, a palpation technique and "stress radiography" have been employed. The amount of lateral displacement of the femoral head was determined by palpation, and, although the method is still used by some clinicians, subjectivity made it less than desirable for widespread use. Stress radiography is a method to exhibit the joint laxity by forcing laterally both femoral heads from the acetabula by means of a medial force at the stifles. During this loading configuration, a fulcrum is placed between the femurs, distal to the hip joints, the femurs are loaded medially at the stifle joint, and a radiograph is taken. Although the displacement of the femoral heads from the acetabula can be measured from the radiographs, the applied load remains unknown. Without knowing the effective load at the joint, the test cannot be controlled and is therefore limited as a diagnostic tool. In human medicine a luxation examination, similar to the palpation technique in veterinary medicine, has a large degree of acceptance. This acceptance is due, however, to a large extent to the fact that human medicine does not have to contend with the wide variety in breed and patient size. To measure joint laxity as an aid in the diagnosis of hip dysplasia, an instrument and accompanying test protocol were developed. This would enable the clinician to quantitatively measure connective tissue laxity of the coxofemoral joint and to objectively compare test results with other animals regardless of size and breed. II. LITERATURE SURVEY Although Hippocrates (460-370 BC) reported hip dysplasia in hunans, more than 2000 years elapsed before hip dysplasia was first observed in canines. Since this first reporting by Schnelle (2), in 1935, hip dysplasia has become perhaps the most common and frustrating problem facing modern veterinary orthopedics. During the ensuing decades, several investigations were undertaken in search of the cause of the disorder while simultaneous efforts were made to develop more accurate diagnostic techniques. The first major contribution to diagnosing hip dysplasia came in 1955 when Schnelle (3) classified canine hip dysplasia into four catagories according to its radiographic appearance. His criteria for diagnosing dysplasia were the femoral head fit with the acetabulum and whether the acetabulum showed any shallowness or flattening. These criteria were later redefined and reevaluated. In 1961 the American Veterinary Medical Association asked a panel of ten veterinarians to report on hip dysplasia (4). The panel suggested that the radiographic positioning be standardized. They also suggested a grading system ranging from slight deviation from the norm (grade I) to flat acetabulum and dislocation of the femoral head (grade IV). This grading system was not changed until several years later. In 1972, the Orthopedic Foundation for Animals held a symposium on hip dysplasia (5), which resulted in a redefinition of the radiographically apparent characteristics of hip dysplasia. This definition included a shallow acetabulum, femoral head flattening, coxofemoral subluxation and secondary degenerative joint disease. These characteristics have remained the radiographic diagnostic criteria of hip dysplasia to date. The diagnostic criteria were made from observations developed mainly from older dogs whose joints had already undergone some secondary degenerative changes. Young dogs examined radiographically may not have developed degenerative changes and as a result may be mistakenly diagnosed as normal. Therefore, for young animals, the radiographic examination may be inconclusive, and other diagnostic methods are needed. Bardens and Hardwick (6) suggested a palpation technique to predict hip dysplasia in young animals. The technique depends upon the assumption that hip dysplasia is caused by lax hip joint connective tissue. With this technique, the puppy is placed under deep anesthesia and laid on its side. Standing directly behind the patient, the clinician places the first joint of the right index finger on the ischiatic tuberosity with the thumb of the same hand placed lightly on the greater trochanter. With the left hand, the femur is approached caudally, grasped in the middle third and lifted upward while the puppy is held down with the index finger on the ischiatic tuberosity. The amount of displacement at the greater trochanter is indicative of the degree of laxity, and allegedly predictive of dysplasia. Wright and Mason (7) used this technique and reported in 1977 that he found a definite relationship between laxity diagnosed by palpation and later development of hip dysplasia. His claim was further supported by Bardens in 1979. By this time, Bardens (8) had palpated 6,000 puppies and claimed a diagnostic accuracy of 85%. He reported that all the puppies he predicted would develop hip dysplasia did and 15% of those that he felt were normal later developed hip dysplasia. None of the puppies predicted to be dysplastic, however, ever became normal. Some of the subjects radiographed in the standard position appeared normal yet when palpated showed pronounced joint laxity, Bardens devised the wedge technique to show this laxity on the radiograph. This was done by placing a fulcrum, such as a roll of cotton, between the femurs and as close to the rectum as possible. The tibias were then grasped distal to the stifles and a medial force was applied forcing the femoral heads to translate laterally, at which time the subject's joint was radiographed. Bardens reported that those animals who were radiographically normal (OFA radiograph) but had dysplastic offspring had been determined previously to be lax using stress radiography. To supplement the radiographic diagnosis, radionuclide joint imaging was used by Allands, et a1. (9). The major advantage of this method was the information gained about the bone metabolic activity unattainable using normal radiographic procedures. It did not, however, aid significantly in diagnosing hip dysplasia. A comprehensive study on the developments in diagnosing hip dysplasia, by Van Der Velden in 1983 (10), claimed that all of the present methods of diagnosis were too subjective and could not be used as a selective criteria for breeding. His opinion underscored the need for the development of an objective quantitative diagnostic method. Paralleling the development of diagnostic techniques was the investigations of the cause of hip dysplasia. These investigations began in 1956 when Schales (11), using information on human hip dysplasia as a model for canines, speculated that hip dysplasia was a dominant genetic trait. Henricson and Olsson (12) examined some 750 German Shepherd dogs during the years 1957 and 1958. Their criterion for radiographically diagnosing hip dysplasia was abnormal shallowness of the acetabula. They did not consider subluxation or luxation to be correlated with acetabular dysplasia and doubted that "acetabular dysplasia should be only a sequela to luxation or subluxation caused by an insufficient ligament and joint capsule." They also reported secondary changes such as spur formations to be credited as sequelae to subluxation. Based on their investigation, dysplasia did not appear to be inherited as a regular monogenic characteristic, thus contradicting the speculations of Schales. Smith et al (13), contrary to Henricson and Olsson, hypothesized that the ligament of the femoral head and articular capsule played an important role in maintaining the integrity of the hip joint. For their study, the investigators used 15 four-week-old puppies. In seven of the puppies (Group I) they excised the posterior, anterior and superior portions of the capsule of the right hip and left the contralateral hip intact as a control. In the other eight, (Group II) a similar capsulectomy was performed and a complete surgical removal of the ligament of the femoral head was performed. The animals in group I showed slight lateral displacement and mild acetabular obliquity within seven weeks. Within four weeks, five of the group II puppies showed complete dislocations. Six of the animals, including the five with dislocations, demonstrated acetabular dysplasia. The ligament cfl’ the femoral head appeared to play a vital role in joint integrity in animals at a very young age. These investigators also demonstrated that "acetabular dysplasia is the result of the dislocation rather than the cause. Secondary changes in the head and neck of the femur such as varus deformity of the neck, flattening of the head and some reduction of the angle of anteversion were also observed as to result from experimental dislocation". This result was supported by research done by Riser and Shirer (14) who felt that the femoral head ligament served to stabilize the femoral head. In 1966, Henricson et a1. (15) compared congenital hip dysplasia in man to that in canines and found that canine hip dysplasia cannot be diagnosed at birth, is apparently non-congenital, and the primary cause is joint laxity occurring very early in life. As it became generally accepted that joint laxity was associated with hip dysplasia, researchers began to investigate the cause of joint laxity. Riser and Shirer, in 1967 (16), correlated pelvic muscle mass in canines with the incidence of hip dysplasia. He found that the more muscle mass the animal had, the lesser the incidence of hip dysplasia. Other investigators, Pierce et a1. (17), found a higher occurrence of hip dysplasia in dogs which had been injected with estrogen in early life. In 1973, Lust (18) embarked on an investigation monitoring the growth rate in puppies. He found that puppies which were Cesarean delivered and reared at a reduced growth rate exhibited a lower incidence of canine hip dysplasia than normally born puppies which were allowed to grow at optimal and suboptimal rates. In 1974, Cardinet et a1. (19), performed a study to see if pectineal myectomy had any effect on the development of canine hip 10 dysplasia. They found that there was no significant difference between the side to which the pectineal myectomy had been performed and the contralateral control side. Lust et al. (20,21) also investigated the relationship between the synovial fluid volume and joint stability. He found that increased synovial fluid volume, increased volume of the ligament of the femoral head, degenerative cartilage lesions, and mild non-supportive synovitis accompanied canine hip dysplasia. He first thought that the increased synovitic volume might have been the cause of the joint instability, but he later concluded that it was probably a secondary result of joint laxity. His study also showed that mild intraarticular abnormalities found on the necropsied animals did not show up on the radiographs, which emphasizes the limitation of radiographic diagnoses. In 1984, Schoenecter et a1. (22) did a dynamic study on growing puppies in which one hind leg was cast in extension and the other was left uncast as a control. In the cast leg they observed decreased blood flow to the femoral head through the ligament of the femoral head, progressive subluxation of the femoral head, and eventual dislocation. The continuous pressure resulted in acetabular dysplasia. There was a clear correlation between load distribution on the joint and dysplastic changes. III. EXPERIMENTAL METHODS It has become generally accepted there is a correlation between joint laxity and hip dysplasia. Although several subjective methods have been developed to determine joint laxity, they are less desirable than quantitative measures. In order to quantify joint laxity measurements, a special device and an accompanying test protocol had to be developed. Before laxity testing could occur, it was necessary to determine the load level required to cause the hip joint to exhibit abnormal laxity, but a level low enough not to damage connective tissue. Initial testing used a lateral load between 6 and 10 lbs. applied to several medium sized (40-50 lbs.) animals in order to place the connective tissue of the hip joint in tension. A 15 1b. load was reported (13) to be necessary to begin tearing of the joint capsule, so the 6 1b. load was initially chosen as a safe upper limit for medium sized animals. During the preliminary testing, animals appeared to be in two distinct groups based on their hip joint's response to loading. Figure 2 shows typical results for this preliminary stage of testing. For ease in locating the no load and positive load data points for each dog, a line was drawn between them. It is important to note that this line does not describe the relationship between the normalized displacements and normalized load, but it is simply an aid for displaying the data end points. The normalized displacement is the distance between the medial most surfaces of the femoral heads divided by the normalizing distance 11 12 muadmom ummH mumcweflaoum .N ousmwm 2020 003 03:05.02 0.9 0.9 0.0 0.0 . . _ . . _ . _ . . . . _ _ _ . mm.O 3.. a N l m 05.0 m ml 0 Av. eulllla I In mud .mlomd W! l x o .. mmd > Bill umou umwszLoz .m> EmEmomfimE UmwszLoz Lo camew (um/we) ruewaoeldsgg pazueuuoN 13 between the cranial effective acetabular rims. The normalized load is the 6 lbs. applied load converted into Newtons and divided by the femoral head diameter in centimeters. The normal group showed the femoral heads seated well within the acetabular fossa, indicating normal or desired coxofemoral articulation, whereas the femoral heads of the lax group were subluxated from the acetabula. As preliminary testing progressed, animals outside of the medium sized group were used, and it became apparent that a scaling of applied load would have to be made to account for the variation in animal size. It was assumed that the ability of the hip joint to resist load was directly proportional to the cross-sectional area of the articular capsule. The capsule thickness could not be determined non-invasively but the circumference of the capsule was assumed to be related to the diameter of the femoral head. Therefore, the normalized load P1 = L/¢1 where P1 is the normalized load, L is the applied load and ¢l is the femoral head diameter. The subscript 1 denotes the left side. Once the data were normalized, the results for animals of different sizes could be compared. There was a reduction in data scatter, which also supported using the femoral head diameter as the scaling factor. It was noted that in all cases tested thus far, a distinct division existed between the lax and normal animals at a normalized load of 10 N/cm; that is, no fUrther significant laxity information was obtained when the animals had greater than 10 N/cm loads applied. Thus, the 10 N/cm load became the maximum allowable applied load for the test protocol. The following test protocol was used on all further experiments. All animals were tranquilized and anesthetized until palpebral reflexes 14 were lost. The animal was then placed in dorsal recumbancy on the device platform and a standard OFA radiograph was taken as shown in Figure 3. Still in dorsal recumbancy, leg cuffs were attached to the Figure 3. OFA Radiographic Position animal's thighs and then connected to the load measuring instrument. By translating the load measuring instruments laterally, the connected leg cuffs pulled the animal's legs laterally, thereby placing the connective tissue of the hip joint in tension. The load applied to the animals legs was transmitted into the load measuring instruments via a length of Thompson* ball-groove shaft to a Sensotec model 11 (i 25 lbs.) load cell. The load cell signal was processed using a Sensotec** SA—4 amplifier and displayed digitally. Once the load reached the normalized 10 N/cm magnitude, a ventral dorsal radiograph was taken of the joint * Thompson Industries, Inc., Port Washington, NY ** Sensotec, 1200 Chesapeake Ave., Columbus, OH 43212 15 area. This radiograph was referred to as the radiograph taken under load. The animal was then released from the device and returned to the kennel. Figure 4 shows the test set-up and the load measuring instrument attached to the animal. Figure 4. Testing Setup Each animal tested was assigned a case number for identification and reference purposes. Those animals which were tested more than once were assigned an additional letter. For example, case 10b was the tenth case tested and was tested at least twice, b signifying the second time. Several measurements were taken from the radiographs to analyze the extent of joint laxity and are shown in Figure 5. The left and right femoral head diameters, £5. and 0%, were measured along the epiphyseal line of the femoral head. These values are used to normalize the applied load. The width of the hip was defined as the distance between the left and right cranial effective acetabular rims, and was l6 cranial effective acetabular rim 4:. v i / ' 5 NA\ ' “‘——D——— Figure 5. Measurement Diagram 16 cranial effective acetabular rim \ ' O /"[C\