The Journal of Bone and Joint Surgery 79:447-52 (1997)
© 1997 The Journal of Bone and Joint Surgery, Inc.
The Role of Access of Joint Fluid to Bone in Periarticular Osteolysis: A Report of Four Cases*
THOMAS P. SCHMALZRIED, M.D. ,
KENNETH H. AKIZUKI, M.D. ,
ALEXANDER N. FEDENKO, M.D. and
JOSEPH MIRRA, M.D. , LOS ANGELES, CALIFORNIA
Investigation performed at the Joint Replacement Institute at Orthopaedic Hospital, Los Angeles
 |
Introduction
|
|---|
In 1976, Harris et al. reported on four patients who had extensive, localized osteolysis after a total hip replacement14. This erosive or cavitary form of bone resorption has become a major problem that threatens the survival of otherwise successful total hip and knee replacements. Osteolysis has been associated with prosthetic arthroplasties since their introduction. Various etiologies of osteolysis have included infection5 and a foreign-body inflammatory reaction to particulate bone cement25, metal particles32,42, or polyethylene particles37.
While there is substantial evidence that small particles and activated macrophages play an important role in osteolysis, the pathophysiology of this condition has been incompletely defined. The mechanism needs to account for osteolysis that occurs in the absence of a discernible periprosthetic particulate burden32, that develops around femoral endoprostheses inserted without cement27, and that occurs around metal-on-metal total hip replacements38,43. The lesions described in the present report are examples of a defined pathological entity know as osteoarthrotic cysts, or geodes3,35. This periarticular, cavitary form of bone resorption occurs in the absence of prosthetic implants. The findings presented here, combined with a review of the related pathology and pathophysiology, demonstrate that the most fundamental factor in the development of osteolysis in association with osteoarthrosis and total joint arthroplasty appears to be the access of joint fluid to bone.
 |
Case Reports
|
|---|
CASE 1. In 1990, radiographs of a seventy-four-year-old man demonstrated multiple cysts in the right femoral head (Fig. 1-A). Radiographs made in 1994 demonstrated dramatic enlargement of these cysts (Fig. 1-B). Pain gradually increased, and the patient had a total hip replacement. Examination of the femoral head revealed extensive full-thickness loss of articular cartilage and focal loss of subchondral bone; a thin fibrous membrane covered the entrance into the large cysts (Fig. 2-A). Serial sections of the specimen confirmed the presence of multiple cysts, which were communicating with the intra-articular surface (Fig. 2-B). Histological examination of the cysts revealed a lining composed predominantly of fibrovascular tissue with occasional lymphocytes. The margins of the cysts were characterized by a mix of necrotic and viable bone with focal regions of scalloped erosions into necrotic bone. In other regions, multinuclear cells (osteoclasts) were actively resorbing lamellar bone (Fig. 3).

View larger version (177K):
[in this window]
[in a new window]
|
Figs. 1-A through 3: Case 1.
Fig. 1-A: Anteroposterior radiograph of the right hip, made in 1990, demonstrating multiple cysts in the femoral head. The arrows indicate two of the larger cysts.
|
|

View larger version (134K):
[in this window]
[in a new window]
|
Fig. 1-B: Anteroposterior radiograph, made in 1994, demonstrating dramatic enlargement of the cysts (arrows).
|
|

View larger version (135K):
[in this window]
[in a new window]
|
Fig. 2-A Photograph of the femoral head, demonstrating full-thickness loss of articular cartilage and a surface defect (arrow) that was communicating with the cysts.
|
|

View larger version (115K):
[in this window]
[in a new window]
|
Fig. 2-B Section of a specimen with multiple periarticular cysts, which were communicating with the intra-articular surface.
|
|

View larger version (143K):
[in this window]
[in a new window]
|
Fig. 3 Light photomicrograph of the margin of a cyst, demonstrating fibrovascular tissue with several multinuclear cells (osteoclasts) actively resorbing lamellar bone (hematoxylin and eosin; original magnification x 250).
|
|
CASE 2. Post-traumatic osteoarthrosis developed in the right hip of a forty-five-year-old man. Radiographs demonstrated loss of superior articular cartilage, a large Eggers supra-acetabular iliac cyst8, and cysts in the femoral head (Fig. 4-A). An arthrogram demonstrated free flow of contrast medium into, and accumulation of medium within, the supra-acetabular cyst (Fig. 4-B). Increasing pain led the patient to have a total hip replacement. A thin fibrous membrane partially covered the base of the supra-acetabular cyst, which was filled with fluid and a friable yellow-tan material that was grossly similar to that seen in osteolytic lesions after total hip arthroplasty. Sections of the femoral head confirmed the presence of a large cyst that communicated with the intra-articular surface. Histological examination of the contents of the supra-acetabular and femoral cysts demonstrated a mixture of necrotic and fibrotic tissue with rare lymphocytes and histiocytes.

View larger version (128K):
[in this window]
[in a new window]
|
Figs. 4-A and 4-B: Case 2.
Fig. 4-A: Anteroposterior radiograph of the right hip. There is a large supra-acetabular iliac cyst and cysts in the femoral head (straight arrows). There is also an apparent absence of a portion of the acetabular dome (curved arrow).
|
|

View larger version (131K):
[in this window]
[in a new window]
|
Fig. 4-B: Arthrogram made after exercise. The contrast medium has filled the joint space (small arrow), has passed through a defect in the acetabular dome (curved arrow), and has pooled in the supra-acetabular cyst (large arrows).
|
|
CASE 3. A sixty-nine-year-old woman had pain in the right knee for eight years. Radiographs demonstrated varus alignment with loss of articular cartilage in the medial compartment. A large cyst was noted in the medial femoral condyle. It appeared to originate from the articular surface (Figs. 5-A and 5-B). The distal and posterior femoral cuts for total knee replacement transected the cyst, which was filled with a friable yellow-to-green-gray tissue. Gross examination of the cut surfaces showed full-thickness loss of cartilage as well as a defect in the bone leading to the cyst (Fig. 6). Histological examination of the cyst revealed findings similar to those of the previous patients.

View larger version (110K):
[in this window]
[in a new window]
|
Fig. 5 Case 3. Anteroposterior and lateral radiographs of the right knee. A large cyst, which appears to originate from the articular surface, occupies most of the medial femoral condyle (arrows). There is complete loss of the joint space.
|
|

View larger version (116K):
[in this window]
[in a new window]
|
Fig. 5 Case 3. Anteroposterior and lateral radiographs of the right knee. A large cyst, which appears to originate from the articular surface, occupies most of the medial femoral condyle (arrows). There is complete loss of the joint space.
|
|
CASE 4. Post-traumatic osteoarthrosis developed in the right knee of a fifty-five-year-old man. Radiographs demonstrated a valgus deformity with loss of articular cartilage in the lateral compartment. A large cyst, measuring 3.0 by 1.7 millimeters on the anteroposterior radiograph, was noted in the lateral aspect of the proximal end of the tibia. The cyst appeared to extend as far as the proximal tibial articular surface. At the time of total knee replacement, a punctate lesion in the posteromedial aspect of the lateral tibial plateau was found to communicate with the cyst. The cyst contained friable yellow-green tissue. The histological findings were similar to those of the other patients.
 |
Discussion
|
|---|
The lesions described in this report are striking examples of periarticular, cavitary bone resorption, which has been called osteolysis3,14. The term geode has been applied to these periarticular erosions, which are a defined pathological entity noted in association with several joint abnormalities, including osteoarthrosis and rheumatoid arthritis3,35. In osteoarthrosis, geodes occur in areas of degenerated cartilage, often in a paired, or so-called kissing, position on both sides of the joint. Frequently, a defect in the articular surface is found to communicate with the cyst. The cyst may be filled with fluid but also may contain variable amounts of fibrovascular tissue and fragments of articular cartilage. A sclerotic margin is characteristic, but osteoclastic bone resorption may be seen at the margins of the cavity3,36.
Two fundamental theories have been proposed for the etiology of geodes: intrusion of synovial fluid (the hydrodynamic theory) and osseous contusion (the mechanical overload theory)35. Freund10 appears to have been the first to suggest that elevated intra-articular fluid pressure could lead to intrusion of joint fluid into cancellous bone through gaps in degenerated articular cartilage. Landells28 suggested that osteoarthrotic cysts always originate from a communication with the joint space and that they are not due to primary degenerative changes in the bone. Landells proposed that the pressure of the joint fluid leads to progressive bone resorption, and he cited the increase of synovial fluid that is seen in association with osteoarthrosis and the rounded outlines of the cysts as being indicative of the role of fluid pressure. Landells also proposed that the relatively low compliance of the capsule of the hip compared with that of the knee could predispose the hip to larger (and more frequent) cysts. Mechanical overload sufficient to cause osteonecrosis may be critical for the initiation of geodes. Regardless of the primary event, our observations as well as those of other investigators support the roles of fluid pressure and intrusion of joint fluid in the enlargement of geodes.
Intracapsular fluid pressure is a function of many variables, including capsular compliance, fluid compartmentalization, joint position, and muscle action29. The compliance of the joint capsule is reduced in association with osteoarthrosis. Conversely, joint-fluid pressures are increased in association with osteoarthrosis and vary with use of the joint. During gait, cyclical variations in intra-articular pressures of the normal knee are subatmospheric. In contrast, the osteoarthrotic knee has consistently positive pressures that increase with contraction of the muscles9,18,20-22,29,30,34. Intracapsular increases in fluid pressure may be transmitted to geodes, and transmitted pressures of as much as 250 millimeters of mercury (33.33 kilopascals) have been recorded22. Failure of the pressure to return to the baseline level suggests a one-way valve that maintains the elevated pressure, which in turn could contribute to enlargement of the cyst22.
In normal synovial joints, such as the hip or the knee, bone is not exposed to joint fluid. The joint boundaries are defined by the capsule, and within the capsule bone is covered by cartilage or synovial tissue31,39. In disease processes, such as osteoarthrosis, the normal anatomical and physiological compartmentalization of a synovial joint can be disrupted. Degradation of articular cartilage can allow direct communication of joint fluid with bone, resulting in an extension of the joint space. Inflammation of the joint is accompanied by an effusion12. The effusion, either with or without decreased capsular compliance30, results in increased intracapsular fluid pressures18,20,34. There is evidence that the combination of the access of joint fluid to bone and the transmission of elevated joint-fluid pressures contributes to the enlargement of geodes3,8,10,22. Increased fluid pressures may disrupt the local circulation. Necrosis in geodes has been reported previously3,19,35 and was a consistent feature of the specimens in the present report.
A similar process appears to occur in association with prosthetic arthroplasty. The normal anatomical and physiological compartmentalization of the joint is disrupted during the implantation procedure. Operative exposure is accompanied by variable disruption of the capsule and the synovial tissue. Resection of the native articular surfaces and preparation of the bone for attachment of the prosthesis results in a variable degree of communication between the initial joint space and bone. In joint arthroplasty, the so-called effective joint space can be quite extensive37. Further, periprosthetic inflammation is accompanied by an effusion as well as fibrosis of the pseudocapsule37. The pathophysiology of geodes indicates that the transmission of elevated joint-fluid pressure to bone can have a physical effect that results in the erosion of bone22. Through a similar mechanism, the expansile nature of osteolytic lesions adjacent to prosthetic joints may, at least in part, be due to a physical effect resulting from the transmission of elevated joint-fluid pressures1,16,37. A difference in the pathological findings in the region around geodes and those in the area of localized bone resorption around prosthetic joints is activated macrophages; geodes develop without this foreign-body response to prosthetic particles.
On the basis of the pathophysiology of geodes and the findings of investigations of osteolysis in total joint arthroplasty, we propose that joint-fluid pressure has a role in the pathophysiology of osteolysis. Wear particles are released into joint fluid and are distributed variably throughout the effective joint space37. These particles cause inflammation and contribute to the development of an effusion. Chronic inflammation causes fibrosis and decreased capsular compliance, which can result in the elevation of intracapsular joint-fluid pressures. In patients who have prosthetic joints, intracapsular fluid pressures may exceed 750 millimeters of mercury (99.98 kilopascals)16 and can be transmitted to regions distant from the articulation. A fluid pressure of 198 millimeters of mercury (26.39 kilopascals) has been measured in an osteolytic cavity in the femoral diaphysis1. The flow of joint fluid is an active process driven by fluctuations in joint-fluid pressures that occur with activities of daily living16 and that can contribute to progressive expansion of the effective joint space37. In contrast to an osteoarthrotic joint, a well fixed and otherwise well functioning prosthetic joint may not be associated with symptoms; as a result, the patient remains active and maintains the driving forces for osteolysis, which may account for the progression and extreme size of some osteolytic lesions associated with total joint arthroplasty.
The effective joint space can expand into soft tissue as well as bone2,6,15,17,33,40. This expansion into soft tissue is recognized less frequently, at least in part because imaging of the soft tissues is not routinely performed. Increased joint-fluid pressures may be painful and may result in rupture of the joint capsule or the formation of synovial cysts12,23. Synovial cysts may have a protective function; specifically, by accommodating fluid volume and limiting the increase in intra-articular pressure, such cysts may protect bone from damage due to pressure. An inverse relationship has been demonstrated between the occurrence of periarticular bone cysts (geodes) and that of synovial cysts11. The natural hip joint can communicate with the iliopsoas bursa4. Pressure-driven synovial fluid may be pumped into the bursa; this causes distension, which may be symptomatic2. Similar events can occur after total hip arthroplasty17,33. In the effective joint space, joint fluid seeks the path of least resistance; this path is variable and includes soft tissue as well as bone37.
Soluble factors capable of directly or indirectly effecting bone resorption have been identified in joint fluid; these factors include prostaglandins, interleukins, and matrix metalloproteinases7,13,26,41. Elevated levels of these factors may play a central role in rapidly destructive arthropathy of the hip26. Cytokines and matrix metalloproteinases have been identified in interfacial and pseudocapsular tissues from around loose total joint replacements7,13. While proteolytic enzyme activity in interfacial tissue contributes to local bone resorption, pseudocapsular tissues also release bone-resorbing factors into joint fluid41. Levels of cytokines and matrix metalloproteinases can be elevated in the fluid around total joint replacements7 and could effect bone resorption at distant sites. There are similar cytokine profiles in osteoarthrotic cysts and in osteolytic lesions around total joint implants24.
In summary, these observations suggest that a fundamental factor in the development of geodes in association with osteoarthrosis and of osteolysis in association with total joint arthroplasty is access of joint fluid to bone. A limitation of current prosthetic arthroplasty is the variable disruption of the anatomy and physiology of the joint that occurs as a result of the implantation procedure. In addition to the physical effect of pressure as seen with geodes, the fluid around prosthetic joints also carries wear particles and increased levels of soluble factors that are capable of stimulating bone resorption at distant sites. While a reduction in the particulate burden is desirable, we believe that limitation of access of joint fluid to bone is necessary to prevent osteolysis.

View larger version (107K):
[in this window]
[in a new window]
|
Fig. 6 Case 3. Gross specimen showing the distal (left) and posterior (right) femoral cuts made at the time of a total knee arthroplasty. There is full-thickness loss of cartilage and a defect in the bone leading to the cyst (arrow).
|
|
 |
Footnotes
|
|---|
*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. Funds were received in total or partial support of the research or clinical study presented in this article. The funding source was the Los Angeles Orthopaedic Foundation.
Joint Replacement Institute at Orthopaedic Hospital (T. P. S.) and Department of Pathology (A. N. F. and J. M.), Orthopaedic Hospital, 2400 South Flower Street, Los Angeles, California 90007.
Harbor/University of California at Los Angeles Medical Center, 1000 West Carson Street, Torrance, California 90509.
 |
References
|
|---|
-
Anthony, P. P.; Gie, G. A.; Howie, C. R.; and |and |Ling, R. S. M.: Localised endosteal bone lysis in relation to the femoral components of cemented total hip arthroplasties. J. Bone and Joint Surg., 72-B(6): 971-979, 1990.
-
Binek, R., and |and |Levinsohn, E. M.: Enlarged iliopsoas bursa. An unusual cause of thigh mass and hip pain. Clin. Orthop., 224: 158-163, 1987.
-
Bullough, P. G., and |and |Bansal, M.: The differential diagnosis of geodes. Radiol. Clin. North America, 26: 1165-1184, 1988.[Medline]
-
Chandler, S. B.: The iliopsoas bursa in man. Anat. Rec., 58: 235-240, 1934.
-
Charnley, J.; Follacci, F. M.; and |and |Hammond, B. T.: The long-term reaction of bone to self-curing acrylic cement. J. Bone and Joint Surg., 50-B(4): 822-829, 1968.
-
Coventry, M. B.; Polley, H. F.; and |and |Weiner, A. D.: Rheumatoid synovial cyst of the hip. Report of three cases. J. Bone and Joint Surg., 41-A: 721-730, June 1959.[Abstract/Free Full Text]
-
Dorr, L. D.; Bloebaum, R.; Emmanual, J.; and |and |Meldrum, R.: Histologic, biochemical, and ion analysis of tissue and fluids retrieved during total hip arthroplasty. Clin. Orthop., 261: 82-95, 1990.
-
Eggers, G. W. N.; Evans, E. B.; Blumel, J.; Nowlin, D. H.; and |and |Butler, J. K.: Cystic change in the iliac acetabulum. J. Bone and Joint Surg., 45-A: 669-686, 722, June 1963.[Free Full Text]
-
Eyring, E. J., and |and |Murray, W. R.: The effect of joint position on the pressure of intra-articular effusion. J. Bone and Joint Surg., 46-A: 1235-1241, Sept. 1964.[Free Full Text]
-
Freund, E.: The pathologic significance of intra-articular pressure. Edinburgh Med. J., 47: 192-203, 1940.
-
Genovese, G. R.; Jayson, M. I. V.; and |and |Dixon, A. St. J.: Protective value of synovial cysts in rheumatoid knees. Ann. Rheumat. Dis., 31: 179-182, 1972.[Free Full Text]
-
Goddard, N. J., and |and |Gosling, P. T.: Intra-articular fluid pressure and pain in osteoarthritis of the hip. J. Bone and Joint Surg., 70-B(1): 52-55, 1988.
-
Goldring, S. R.; Schiller, A. L.; Roelke, M.; Rourke, C. M.; O'Neill, D. A.; and |and |Harris, W. H.: The synovial-like membrane at the bone-cement interface in loose total hip replacements and its proposed role in bone lysis. J. Bone and Joint Surg., 65-A: 575-584, June 1983.[Abstract/Free Full Text]
-
Harris, W. H.; Schiller, A. L.; Scholler, J.-M.; Freiberg, R. A.; and |and |Scott, R.: Extensive localized bone resorption in the femur following total hip replacement. J. Bone and Joint Surg., 58-A: 612-618, July 1976.[Abstract/Free Full Text]
-
Hattrup, S. J.; Bryan, R. S.; Gaffey, T. A.; and |and |Stanhope, C. R.: Pelvic mass causing vesical compression after total hip arthroplasty. Clin. Orthop., 227: 184-189, 1988.[Medline]
-
Hendrix, R. W.; Wixson, R. L.; Rana, N. A.; and |and |Rogers, L. F.: Arthrography after total hip arthroplasty. A modified technique used in the diagnosis of pain. Radiology, 148: 647-652, 1983.[Abstract/Free Full Text]
-
Howie, D. W.; Cain, C. M. J.; and |and |Cornish, B. L.: Pseudo-abscess of the psoas bursa in failed double-cup arthroplasty of the hip. J. Bone and Joint Surg., 73-B(1): 29-32, 1991.
-
Jayson, M. I. V., and |and |Dixon, A. St. J.: Intra-articular pressure in rheumatoid arthritis of the knee. I. Pressure changes during passive joint distension. Ann. Rheumat. Dis., 29: 261-265, 1970.[Free Full Text]
-
Jayson, M. I. V., and |and |Dixon, A. St. J.: Intra-articular pressure in rheumatoid arthritis of the knee. II. Effect of intra-articular pressure on blood circulation to the synovium. Ann. Rheumat. Dis., 29: 266-268, 1970.[Free Full Text]
-
Jayson, M. I. V., and |and |Dixon, A. St. J.: Intra-articular pressure in rheumatoid arthritis of the knee. III. Pressure changes during joint use. Ann. Rheumat. Dis., 29: 401-408, 1970.[Free Full Text]
-
Jayson, M. I. V.; Dixon, A. St. J.; and |and |Yeoman, P.: Unusual geodes ('bone cysts') in rheumatoid arthritis. Ann. Rheumat. Dis., 31: 174-178, 1972.[Free Full Text]
-
Jayson, M. I. V.; Rubenstein, D.; and |and |Dixon, A. St. J.: Intra-articular pressure and rheumatoid geodes (bone `cysts'). Ann. Rheumat. Dis., 29: 496-502, 1970.[Free Full Text]
-
Jayson, M. I. V.; Swannell, A. J.; Kirk, J. A.; and |and |Dixon, A. St. J.: Acute joint rupture. Ann. Phys. Med., 10: 175-179, 1969.[Medline]
-
Jiranek, W. A.; Dalury, D. F.; Qui, J.-Y.; and |and |Cardea, J.: Bone resorption in osteoarthritic cysts demonstrates a similar cytokine profile as osteolytic lesions around joint implants. Trans. Orthop. Res. Soc., 22: 159, 1997.
-
Jones, L. C., and |and |Hungerford, D. S.: Cement disease. Clin. Orthop., 225: 192-206, 1987.
-
Komiya, S.; Inoue, A.; Sasaguri, Y.; Minamitani, K.; and |and |Morimatsu, M.: Rapidly destructive arthropathy of the hip. Studies on bone resorptive factors in joint fluid with a theory of pathogenesis. Clin. Orthop., 284: 273-282, 1992.
-
Kozinn, S. C.; Johanson, N. A.; and |and |Bullough, P. G.: The biologic interface between bone and cementless femoral endoprostheses. J. Arthroplasty, 1: 249-259, 1986.[Medline]
-
Landells, J. W.: The bone cysts of osteoarthritis. J. Bone and Joint Surg., 35-B(4): 643-649, 1953.[Abstract/Free Full Text]
-
Levick, J. R.: Joint pressure-volume studies. Their importance, design and interpretation. J. Rheumatol., 10: 353-357, 1983.[Medline]
-
Lloyd-Roberts, G. C.: The role of capsular changes in osteoarthritis of the hip joint. J. Bone and Joint Surg., 35-B(4): 627-642, 1953.
-
McCarty, D. J.: The physiology of the normal synovium. In Joints and Synovial Fluid, edited by L. Sokoloff. Vol. 2, pp. 293-314. New York, Academic Press, 1980.
-
Maloney, W. J.; Jasty, M.; Harris, W. H.; Galante, J. O.; and |and |Callaghan, J. J.: Endosteal erosion in association with stable uncemented femoral components. J. Bone and Joint Surg., 72-A: 1025-1034, Aug. 1990.[Abstract/Free Full Text]
-
Matsumoto, K.; Hukuda, S.; Nishioka, J.; and |and |Fujita, T.: Iliopsoas bursal distension caused by acetabular loosening after total hip arthroplasty. A rare complication of total hip arthroplasty. Clin. Orthop., 279: 144-148, 1992.
-
Myers, D. B., and |and |Palmer, D. G.: Capsular compliance and pressure-volume relationship in normal and arthritic knees. J. Bone and Joint Surg., 54-B(4): 710-716, 1972.
-
Resnick, D.; Niwayama, G.; and |and |Coutts, R. D.: Subchondral cysts (geodes) in arthritic disorders. Pathologic and radiographic appearance of the hip joint. AJR: Am. J. Roentgenol., 128: 799-806, 1977.[Abstract]
-
Rhaney, K., and |and |Lamb, D. W.: The cysts of osteoarthritis of the hip. A radiological and pathological study. J. Bone and Joint Surg., 37-B(4): 663-675, 1955.[Abstract/Free Full Text]
-
Schmalzried, T. P.; Jasty, M.; and |and |Harris, W. H.: Periprosthetic bone loss in total hip arthroplasty. Polyethylene wear debris and the concept of the effective joint space. J. Bone and Joint Surg., 74-A: 849-863, July 1992.[Abstract/Free Full Text]
-
Schmalzried, T. P.; Szuszczewicz, E. S.; Petersen, T. D. and Amstutz, H. C.: Osteolysis in metal-metal bearing total hip replacements. Read at the Annual Meeting of The American Academy of Orthopaedic Surgeons, San Francisco, California, Feb. 13, 1997.
-
Simkin, P. A.: Physiology of normal and abnormal synovium. Sem. Arthrit. and Rheumat., 21: 179-183, 1991.
-
Svensson, O.; Mathiesen, E. B.; Reinholt, F. P.; and |and |Blomgren, G.: Formation of a fulminant soft-tissue pseudotumor after uncemented hip arthroplasty. A case report. J. Bone and Joint Surg., 70-A: 1238-1242, Sept. 1988.[Free Full Text]
-
Takagi, M.; Konttinen, Y. T.; Lindy, O.; Sorsa, T.; Kurvinen, H.; Suda, A.; and |and |Santavirta, S.: Gelatinase/type IV collagenases in the loosening of total hip replacement endoprostheses. Clin. Orthop., 306: 136-144, 1994.
-
Urban, R. M.; Jacobs, J. J.; Gilbert, J. L.; and |and |Galante, J. O.: Migration of corrosion products from modular hip prostheses. Particle microanalysis and histopathological findings. J. Bone and Joint Surg., 76-A: 1345-1359, Sept. 1994.[Abstract/Free Full Text]
-
Walker, P. S.; Salvati, E.; and |and |Hotzler, R. K.: The wear on removed McKee-Farrar total hip prostheses. J. Bone and Joint Surg., 56-A: 92-100, Jan. 1974.[Abstract/Free Full Text]

CiteULike Connotea Del.icio.us Facebook Technorati Twitter What's this?
This article has been cited by other articles:

|
 |

|
 |
 
K.-P. Gunther, A. Hartmann, P. Aikele, D. Aust, and J. Ziegler
Large Femoral-Neck Cysts in Association with Femoroacetabular Impingement. A Report of Three Cases
J. Bone Joint Surg. Am.,
April 1, 2007;
89(4):
863 - 870.
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
C. Heisel, M. Silva, and T. P. Schmalzried
Bearing Surface Options for Total Hip Replacement in Young Patients
J. Bone Joint Surg. Am.,
July 3, 2003;
85(7):
1366 - 1379.
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
T. P. SCHMALZRIED and J. J. CALLAGHAN
Current Concepts Review - Wear in Total Hip and Knee Replacements
J. Bone Joint Surg. Am.,
January 1, 1999;
81(1):
115 - 136.
[Full Text]
|
 |
|
|