A 10-year-old Quarter Horse gelding (horse 1) used for trail riding was examined because of lameness of several months' duration (exact timeframe unknown). There was no specific history of trauma. Physical examination revealed marked left gluteal muscle atrophy and severe effusion of the left femoropatellar and medial femorotibial joints. The horse was lame at a walk on the left hind limb (grade 4/51) and showed signs of severe pain after upper limb flexion. Radiographic examination of the left stifle joint, including standing caudocranial, lateromedial, and caudal 60° lateral-craniomedial oblique views, revealed periarticular osteophytes on the proximomedial aspect of the tibia and distomedial aspect of the femur and narrowing of the medial femorotibial joint. Additionally, as measured on the caudocranial view, SCLs were evident in the left medial femoral condyle (1.2 × 0.7 cm [width × height]), the left medial tibial condyle (1.4 × 1.9 cm), and the left proximal tibial metaphysis (3.9 × 5.9 cm). A 0.9 × 0.4-cm osteochondral fragment was also present near the cranial aspect of the medial intercondylar eminence of the tibia (Figure 1). Therefore, the radiographic diagnosis was severe osteoarthritis of the left medial femorotibial joint with SCLs in the medial femoral condyle and medial tibial condyle. The etiology of the tibial metaphyseal cystic lesion and its relationship with the lameness were unknown, although the articular changes were presumed to be the main cause of lameness. After evaluation, the horse was discharged. Prescribed treatment consisted of stall rest and phenylbutazone (4.4 mg/kg [2 mg/lb], PO, q 24 h); however, the lameness worsened and the owners elected euthanasia 50 days after initial examination.
Radiographic and necropsy images of the left stifle joint of a 10-year-old Quarter Horse gelding (horse 1) examined because of lameness of several months' duration (exact timeframe unknown). Grade 4/5 lameness was evident on initial examination. After failing to respond to stall rest and phenylbutazone treatment, the horse was euthanized 50 days after initial examination. A—On a standing caudocranial radiographic view, periarticular osteophytes are evident on the medial articular margins of the proximal aspect of the tibia and distal aspect of the femur, with narrowing of the medial femorotibial joint, SCLs in the medial femoral condyle and medial tibial condyle (black arrows), and a large lucency in the proximal tibial metaphysis (white arrow). B—Necropsy photograph of the left medial femorotibial joint. An elongated full-thickness cartilage lesion with flattening of the condyle is apparent on the medial femoral condyle (black arrow), and a focal osteochondral defect is evident on the midcaudal aspect of the medial tibial condyle (white arrow). The medial meniscus is torn and portions of the central and caudal segments are missing. C—Necropsy photograph of a parasagittal section of the proximal aspect of the left tibia illustrating the continuity between the medial tibial condyle SCL and the medial femorotibial joint (black arrow). A large lucency is also evident in the proximal tibial metaphysis (white arrow); the proximal SCL is filled with gelatinous material, whereas the core of the metaphyseal lesion contains what appears to be trabecular bone.
Citation: Journal of the American Veterinary Medical Association 249, 11; 10.2460/javma.249.11.1313
Necropsy revealed an SCL on the weight-bearing surface of the left medial femoral condyle, a full-thickness osteochondral lesion in the center of the medial tibial condyle with an underlying SCL, and extensive tearing of the mid-to-caudal region of the medial meniscus (Figure 1). The medial tibial condyle SCL was round and lined with fibrous tissue and contained yellow gelatinous material. A cystic lesion in the proximal tibial metaphysis was also evident on a parasagittal section of the left tibia; however, the core of the lesion contained trabecular bone rather than gelatinous material only.
A 3-year-old Quarter Horse gelding (horse 2) was examined because of a 6-month history of left hind limb lameness. On radiographs of the left stifle joint obtained by the referring veterinarian, a large medial femoral condyle SCL could be seen, and the horse was referred for surgery. Initial physical examination at our hospital revealed moderate to severe effusion of the left medial femorotibial joint and grade 3/5 left hind limb lameness that was exacerbated by upper limb flexion. Radiographic examination of the left stifle joint revealed a 1.7 × 2.7-cm (width × height) SCL in the medial femoral condyle, osteophytes on the medial intercondylar eminence of the tibia and the medial articular margins of the proximal aspect of the tibia and distal aspect of the femur, and a 1.1 × 0.7-cm SCL in the medial tibial condyle (Figure 2). Radiographs of the right stifle joint were obtained and were considered unremarkable.
Radiographic images of the left stifle joint of a 3-year-old Quarter Horse gelding (horse 2) examined because of a 6-month history of left hind limb lameness. The horse had been referred for surgical treatment; grade 3/5 lameness was evident on initial examination. Caudocranial (A) and caudal 60° lateral-craniomedial oblique (B) radiographic images indicate a 1.7 × 2.7-cm (width × height) medial femoral condyle SCL (black arrow), osteophytes on the medial intercondylar eminence of the tibia and medial articular margins of the proximal aspect of the tibia and distal aspect of the femur, and a 1.1 × 0.7-cm SCL of the medial tibial condyle (white arrow). C—Caudocranial radiographic image of the left stifle joint obtained 5 months after initial examination. Notice the increased radiodensity of the medial femoral condyle SCL at the articular level (black arrow) with no change in the radiographic appearance of the medial tibial condyle SCL (white arrow; circle).
Citation: Journal of the American Veterinary Medical Association 249, 11; 10.2460/javma.249.11.1313
An IV catheter was placed in a jugular vein and the horse was premedicated with xylazine (1.1 mg/kg [0.45 mg/lb], IV). General anesthesia was induced by means of administration of midazolam (0.05 mg/kg [0.023 mg/lb], IV) and ketamine (2.2 mg/kg [1.0 mg/lb], IV), an endotracheal tube was placed, and anesthesia was maintained with isoflurane in oxygen. Tetanus toxoid was administered prophylactically. Potassium penicillin (22,000 U/kg [10,000 U/lb], IV, q 6 h) and gentamicin sulfate (6.6 mg/kg [3.0 mg/lb], IV, q 24 h) were administered for 24 hours, and phenylbutazone (4.4 mg/kg [2 mg/lb], IV, q 24 h) was administered for 2 days according to standard hospital protocol. A transcondylar screw was placed in lag fashion across the left medial femoral condyle SCL as described by Santschi et al.2 The horse recovered from general anesthesia without apparent complications and was discharged 2 days after surgery. At the time of discharge, phenylbutazone (4.4 mg/kg, PO, q 24 h) was prescribed for 7 days, with instructions for 4 months of rest and rehabilitation (an initial period of stall confinement, followed by stall rest with hand walking for 30 days, small paddock turn out for 30 days, and large paddock turn out for the remaining recovery time).
Five months after surgery, recheck examination by the referring veterinarian revealed that the lameness was unchanged (ie, grade 3/5). On repeated radiographs, the medial femoral condyle SCL was smaller at the articular level, and the medial tibial condyle SCL was unchanged (Figure 2). Because of the persistent lameness and the likely poor prognosis for return to athletic function, the horse was euthanized but a necropsy was not performed.
A 2-year-old Thoroughbred colt (horse 3) was referred for surgical treatment of bilateral medial femoral condyle SCLs by means of transcondylar lag screw placement.2 The horse had a 9-month history of left hind limb lameness. The left SCL had been treated 9 months previously by the referring veterinarian with intralesional injection of triamcinolone acetate and 5 months previously with “stem cells” (source unknown). Initial examination at our hospital revealed grade 4/5 lameness of the left hind limb, and mild (right) and severe (left) medial femorotibial joint effusion.1 Radiographic examination of both stifle joints with the horse standing indicated bilateral medial femoral condyle SCLs measuring 1.6 × 1.3 cm (width × height; right) and 1.5 × 1-cm (left; Figure 3). The patient underwent surgical treatment by means of transcondylar lag screw placement with perioperative management in a similar manner as described for horse 2.
Radiographic images of the left stifle joint of a 2-year-old Thoroughbred colt (horse 3) examined because of grade 4/5 lameness. A—On a caudocranial image, an SCL in the medial femoral condyle (black arrow) can be seen. B—On a caudocranial image obtained 3 months after initial examination, a large SCL in the medial tibial condyle (white arrow), a large osteophyte on the proximomedial aspect of the tibia, and an increase in density of the medial femoral condyle SCL (black arrow), which was treated with placement of a transcondylar lag screw 3 months previously, can be seen. C—On a caudocranial image of the left stifle joint obtained 18 months after initial examination, radiographic healing of the medial femoral condyle SCL (black arrow) and persistence of the medial tibial condyle SCL (white arrow) are apparent.
Citation: Journal of the American Veterinary Medical Association 249, 11; 10.2460/javma.249.11.1313
Three months after surgery, the lameness had improved to grade 2/5, and follow-up radiography of both stifle joints revealed that both medial femoral condyle SCLs had increased in radiodensity.1,2 However, a 1.2 × 1.5-cm SCL was now evident in the left medial tibial condyle (Figure 3). Surgical treatment of the medial tibial condyle SCL via transcondylar screw placement was offered to the owners, but they declined. After 8 additional months of pasture turnout (11 months after surgery), the horse was considered free from lameness and radiographs of the stifle joints showed increased radiodensity of all 3 SCLs. The horse began race training and again underwent stifle joint radiography 18 months after surgery. The locations of both medial femoral condyle SCLs appeared radiographically healed, but the medial tibial condyle SCL was still apparent. The horse was subsequently retired from race training because of an upper airway problem and was lost to further follow-up.
A 10-year-old American Paint Horse gelding (horse 4) used for Western performance competition was referred for treatment of chronic (7 months' duration) hind limb lameness. Bilateral medial femoral condyle SCLs and a left medial tibial condyle SCL had been previously diagnosed by the referring veterinarian. The horse had failed to respond to stall rest and several weeks of oral phenylbutazone administration. On initial examination at our hospital, the horse was lame on both hind limbs (grade 3/5), which was exacerbated by upper limb flexion. Radiographic examination of both stifle joints revealed osteophytes on the medial aspect of the proximal aspect of the tibia and distal aspect of the femur, a 1.1 × 1.7-cm (width × height) SCL in both medial femoral condyles and a 3 × 3.1-cm left medial tibial condyle SCL (Figure 4). Ultrasonographic examination of the left stifle joint revealed slight abaxial displacement of the medial meniscus. Because of the poor prognosis for soundness, as determined on the basis of the results of clinical and diagnostic imaging examinations, the owners elected euthanasia.
Radiographic and necropsy images of the left stifle joint of a 10-year-old American Paint Horse gelding (horse 4) examined because of grade 3/5 lameness of 7 months' duration. A—Caudocranial radiographic image showing osteophytes on the proximomedial aspect of the tibia and distal aspect of the femur, a medial femoral condyle SCL (black arrow), and an SCL in the medial tibial condyle (white arrow). Photographs of the left (B) and right (C) tibias obtained at necropsy revealed similar lesions in the central and caudal aspects of both medial tibial condyles (black arrows). In addition, a large SCL is evident in the left medial tibial condyle (white arrow).
Citation: Journal of the American Veterinary Medical Association 249, 11; 10.2460/javma.249.11.1313
Necropsy of the stifle joints revealed diffuse cartilage damage overlying the medial femoral condyle SCLs, a full-thickness osteochondral lesion with an underlying SCL in the center of the left medial tibial condyle, and a partial-thickness cartilage defect in the center of the right medial tibial condyle. Fibrillation of the axial aspect of both medial menisci and thickening of the abaxial aspect of the left medial meniscus were also evident. The medial tibial condyle SCL was round and lined with a fibrous layer and contained yellow and red gelatinous material (Figure 4). The articular cartilage lesions of both medial tibial condyles were at similar locations and similar in gross appearance.
Discussion
Subchondral cystic lesions can cause lameness in horses and have been identified in multiple locations in the forelimbs and hind limbs of horses.3–5 The medial femoral condyle is the most commonly affected location in the stifle joint3,6; however, tibial SCLs also occur, and 4 types have been reported previously.3–5,7–10 Subchondral cystic lesions affecting the lateral condyle of the tibia tend to occur in young horses (eg, 1 to 2 years of age) and may be a manifestation of osteochondrosis, whereas SCLs of the medial tibial condyle may affect mature horses with evidence of osteoarthritis and are reportedly associated with a poor prognosis for resolution of lameness.4,7 Other previously documented locations for tibial SCLs are the intercondylar eminence and the distal tibial epyphisis.3,4,10
For one patient of the present report (horse 1), a cyst-like lesion was identified in the proximal metaphysis of the tibia. Although histologic examination of the lesion was not performed, differential diagnoses included an aneurysmal bone cyst or an enostosis-like lesion. Because aneurysmal bone cysts result from injury to the bone marrow vasculature, they are not true cysts, but are named on the basis of their characteristic sponge-like radiographic appearance.11 We were unable to rule out an enostosis-like lesion in this patient; however, the size and location did not match the characteristics of enostosis-like lesions as recently reported12 or as for our clinical experience.
The etiology of SCLs in horses is controversial. Initial reports implicated osteochondrosis, and inflammation and trauma have also been suggested as contributing factors.6,13–17 Analysis of the tissue lining and fluid found in SCLs in horses suggests that up-regulation of inflammatory mediators may contribute to bone resorption and impaired healing of these lesions.16,17 It has also been proposed that trauma to the articular cartilage, subchondral bone, or both creates a means of communication between the subchondral bone and the joint, allowing synovial fluid to flow under pressure in the subchondral region, producing necrosis of the adjacent bone and contributing to cyst formation.13,14 In human patients, this phenomenon of bone necrosis and cyst formation in the subchondral plate can also occur after trauma without gross evidence of damage to the adjacent joint cartilage.18
A recent ex vivo study19 by our group evaluated contact pressures on the equine medial tibial condyle when the stifle joint was axially loaded to 1800 N at 130°, 145°, and 155° of flexion. Results suggested the presence of high pressures on the central aspect of the medial tibial condyle and meniscus with and without an osteochondral defect (ie, designed to simulate a medial femoral condyle SCL). This finding is in agreement with biomechanical studies20–22 of humans, in which it has been reported that 30% to 50% of the load in the medial compartment of the knee joint is transferred by the central medial tibial condyle. The high loads present on the central aspect of the medial tibial condyle are transferred by the medial femoral condyle. Therefore, we suggest that damage to the articular surface of the medial femoral condyle could cause an adjacent lesion in the opposing tibial condyle by abrasion or repetitive trauma, subsequently promoting formation of a tibial SCL. This phenomenon has been induced in an experimental study23 in ponies. After an osteochondral defect was created on the weight-bearing surface of the medial femoral condyle, subsequent damage occurred in the opposing medial tibial condyle.
When lesions are detected on joint surfaces in contact, they are considered kissing lesions and have been described in humans, dogs, and horses.3,7,23–26 In human patients, SCLs that occur simultaneously in areas of contact are believed to be the result of bone contusion or trauma and secondary subchondral bone necrosis.18 This can occur as an isolated incident of trauma or as a result of osteoarthritis. Femoral SCLs can lead to tibial cartilage thinning and subsequent formation of a tibial SCL because of trauma to the opposing surface, osteoarthritis, or both.26–28 In the present report, the location of the medial tibial condyle SCLs under the damaged area of the medial femoral condyle in all 4 horses and the development of the medial tibial condyle SCL after a diagnosis of medial femoral condyle SCL a year earlier in 1 horse (horse 3) suggested that medial tibial condyle trauma from the opposing medial femoral condyle may have had a role in the development of the cystic lesions. Additionally, similar cartilage abnormalities were detected in both medial tibial condyles in horse 4, but a medial tibial condyle SCL was only present in the left stifle joint, which suggested that the medial femoral condyle injury preceded medial tibial condyle SCL formation. It is not known why some horses with medial femoral condyle SCLs develop tibial SCLs, but we suggest that it may be related to medial femoral condyle lesion size, patient activity, the time point in the disease process when radiographs are obtained, or some combination of these factors.
Although the possible relationship between medial femoral condyle and medial tibial condyle SCLs has been briefly mentioned in a prior report,7 we are not aware of previous articles specifically describing and discussing the relationship between these 2 types of SCLs, as for the description of medial meniscal lesions associated with medial femoral condyle SCLs by Hendrix et al.29 Textor et al7 reported 6 horses with medial tibial condyle SCLs associated with osteoarthritis and described radiographic abnormalities of the medial femoral condyle in 1 horse, although 2 of 3 of the horses examined arthroscopically had medial femoral condyle cartilage fibrillation. Another report29 described 2 patients that developed medial tibial condyle SCLs after debridement of a medial femoral condyle SCL and meniscal tear, but a causal relationship was not suggested.
All 4 horses of the present report were examined over a 4-year period (2011 to 2014), with a radiographic diagnosis of medial femoral condyle SCL and concurrent or subsequent development of a medial tibial condyle SCL. During the same period, 27 additional horses were found to have medial femoral condyle SCLs without radiographic evidence of medial tibial condyle SCLs at our hospital. Because of the small number of horses with tibial SCLs, the apparent relative infrequency of medial tibial condyle SCLs in horses with medial femoral condyle SCLs (only 4 horses of 31 examined), and the heterogeneity of accompanying osteoarthritis (severe osteoarthritis, horse 1; mild to moderate osteoarthritis, horses 2 and 4; and no osteoarthritis in horse 3), conclusions cannot be drawn. We cannot definitely state whether development of medial tibial condyle SCLs occurred concurrently with or subsequent to the medial femoral condyle disease in each horse described in this report. Nonetheless, we believe that the chronicity of the lameness in all 4 horses of the present report and the severity of the medial femoral condyle damage at necropsy in 2 horses (horses 1 and 4) suggested that a preexisting severe or chronic injury to the medial femoral condyle may be necessary for development of medial tibial condyle SCLs. Furthermore, we emphasize the importance of assessing the medial tibial condyle when medial femoral condyle damage is observed radiographically or arthroscopically. Medial tibial condyle SCLs will typically be readily evident on routine standing radiographic views (particularly the caudocranial and caudal 60° lateral-craniomedial oblique views); however, when cysts are small or shallow, as in horse 2, they can be radiographically subtle.
Three of the 4 horses described in the present report were euthanized because of lack of response to treatment, suggesting a poor prognosis for horses with these lesions. However, we would note that none of the treatments were specifically directed at addressing the medial tibial condyle SCLs. Therefore, we suggest that a different outcome may have been obtained with intracyst injection of corticosteroids, cyst debridement, or placement of a screw through the lucency.2 In a previous report,7 medial tibial condyle SCLs were considered to be mostly affecting the weight-bearing surface of the proximal aspect of the tibia and inaccessible arthroscopically, a finding that was confirmed at necropsy for 2 horses in the present report. We are aware of 1 horse with medial femoral condyle and medial tibial condyle SCLs that reportedly showed improvement in lameness after lag screw placement through both lesions.a
Limitations of the present report included the retrospective nature, the small number of patients, and the lack of histologic examination of the medial tibial condyle SCLs. Furthermore, as is common in clinical practice, the severity of the radiographic changes (horses 1 and 4) and referral for medial femoral condyle transcondylar screw placement (horses 2 and 3) resulted in the omission of diagnostic local analgesia as part of the lameness examination. Therefore, it is possible that the stifle joint lesions were not the main cause of lameness in these horses. However, we believe that this was unlikely, given the clinical signs and radiographic findings.
Medial tibial condyle SCLs occur infrequently in horses and there is limited published information on them, including regarding the potential association with medial femoral condyle SCLs.3,7,29,30 The results of this small case series suggested a poor prognosis for return to athletic performance in affected horses. Further investigation is indicated.
ABBREVIATIONS
| SCL | Subchondral cystic lesion |
Footnotes
Pigott J, Cornell Ruffian Equine Specialists, Elmont, NY: Personal communication, 2015.
References
1 American Association of Equine Practitioners. Guide for veterinary service and judging of equestrian events. 4th ed. Lexington, Ky: American Association of Equine Practitioners, 1991;19.
2 Santschi EM, Williams JM, Morgan JW, et al. Preliminary investigation of the treatment of equine medial femoral condylar subchondral cystic lesions with a transcondylar screw. Vet Surg 2015; 44: 281–288.
3 Jeffcott LB, Kold SE. Clinical and radiological aspects of stifle bone cysts in the horse. Equine Vet J 1982; 14: 40–46.
4 Butler JA, Colles CM, Dyson SJ, et al. The stifle and tibia. In: Butler JA, Colles CM, Dyson SJ, et al, eds. Clinical radiology of the horse. West Sussex, England: Wiley-Blackwell, 2008;363–412.
5 von Rechenberg B, Auer JA. Subchondral bone cyst. In: Auer JA, Stick JA, eds. Equine surgery. St Louis: Elsevier Saunders, 2012;1255–1263.
6 Jeffcott LB, Kold SE, Melsen F. Aspects of the pathology of stifle bone cysts in the horse. Equine Vet J 1983; 15: 304–311.
7 Textor JA, Nixon AJ, Lumsden J, et al. Subchondral cystic lesions of the proximal extremity of the tibia in horses: 12 cases (1983–2000). J Am Vet Med Assoc 2001; 218: 408–413.
8 Ball MA, Allen D Jr, Parks A. Surgical treatment of subchondral cyst-like lesions in the tibia of an adult pony. J Am Vet Med Assoc 1996; 208: 704–706.
9 Van Duin Y, Hurtig MB. Subchondral bone cysts in the distal aspect of the tibia of three horses. Can Vet J 1996; 37: 429–431.
10 Rose PL, Graham JP, Moore I, et al. Imaging diagnosis—caudal cruciate ligament avulsion in a horse. Vet Radiol Ultrasound 2001; 42: 414–416.
11 Thomas HL, Livesey MA, Caswell JL. Multiple aneurysmal bone cysts in a foal. Can Vet J 1997; 38: 570–573.
12 Ahern BJ, Boston RC, Ross MW. Enostosis-like lesions in equids: 79 cases (1997–2009). J Am Vet Med Assoc 2014; 245: 1042–1047.
13 Ray CS, Baxter GS, McIlwraith CW, et al. Development of subchondral cystic lesions after articular cartilage and subchondral bone damage in young horses. Equine Vet J 1996; 28: 225–232.
14 Kold SE, Hickman J, Melsen F. An experimental study of the healing process of equine chondral and osteochondral defects. Equine Vet J 1986; 18: 18–24.
15 Strömberg, B. A review of the salient features of osteochondrosis in the horse. Equine Vet J 1979; 11: 211–214.
16 von Rechenberg B, Leutenegger C, Zlinsky K, et al Upregulation of mRNA of interleukin-1 and −6 in subchondral cystic lesions of four horses. Equine Vet J 2001; 33: 143–149.
17 von Rechenberg B, Guenther H, McIlwraith CW, et al. Fibrous tissue of subchondral cystic lesions in horses produce local mediators and neutral metalloproteinases and cause bone resorption in vitro. Vet Surg 2000; 29: 420–429.
18 Crema MD, Roemer FW, Zhu Y et al. Subchondral cystlike lesions develop longitudinally in areas of bone marrow edemalike lesions in patients with or at risk for knee osteoarthritis: detection with MR imaging—the MOST study. Radiology 2010; 256: 855–862.
19 Bonilla AG, Williams JM, Litsky, AS, et al. Ex-vivo equine medial tibial plateau contact pressure with an intact medial femoral condyle, with a medial femoral condylar defect, and after placement of a transcondylar screw through the condylar defect. Vet Surg 2015; 44: 289–296.
20 Lee SJ, Aadalen KJ, Malaviya P, et al. Tibiofemoral contact mechanics after serial medial meniscectomies in the human cadaveric knee. Am J Sports Med 2006; 34: 1334–1344.
21 Yang NH, Nayeb-Hashemi H, Canavan PK, et al. Effect of frontal plane angle on the stress and strain at the knee cartilage during the stance phase of gait. J Orthop Res 2010; 28: 1539–1547.
22 Paletta GA, Manning T, Snell E, et al. The effect of allograft meniscal replacement on intra-articular contact area and pressures in the human knee. A biomechanical study. Am J Sports Med 1997; 25: 692–698.
23 Convery FR, Akeson WH, Keown GH. The repair of large osteochondral defects. An experimental study in horses. Clin Orthop Relat Res 1972; 82: 253–262.
24 Fitzpatrick N, Smith TJ, Evans RB et al. Radiographic and arthroscopic findings in the elbow joints of 263 dogs with medial coronoid disease. Vet Surg 2009; 38: 213–223.
25 Johnson MR, LaPrade RF. Tibial plateau “kissing lesion” from a proud osteochondral autograft. Am J Orthop 2011; 40: 359–361.
26 Tanamas SK, Wluka AE, Pelletier JP, et al. The association between subchondral bone cysts and tibial cartilage volume and risk of joint replacement in people with knee osteoarthritis: a longitudinal study. Arthritis Res Ther 2010; 12: R58.
27 Raynauld JP, Martel-Pelletier J, Berthiaume MJ, et al. Correlation between bone lesion changes and cartilage volume loss in patients with osteoarthritis of the knee as assessed by quantitative magnetic resonance imaging over a 24-month period. Ann Rheum Dis 2008; 67: 683–688.
28 Ding C, Garnero P, Cicuttini F, et al. Knee cartilage defects: association with early radiographic osteoarthritis, decreased cartilage volume, increased joint surface area and type II collagen breakdown. Osteoarthritis Cartilage 2005; 13: 198–205.
29 Hendrix SM, Baxter GM, McIlwraith CW, et al. Concurrent or sequential development of medial meniscal and subchondral cystic lesions within the medial femoro-tibial joint in horses (1996–2006). Equine Vet J 2010; 42: 5–9.
30 Bueno AC, Kaneps AJ, Watrous BJ. What is your diagnosis? Femoral and tibial subchondral bone cysts in a horse. J Am Vet Med Assoc 1999; 215: 1097–1098.
