D. Niall, Newland Lodge, Rathbeggan, Co. Meath.

Tel. 01-8252572; Email : dniall@tinet.ie.

Increasing use of magnetic resonance imaging in the investigation of acute knee injuries in recent years has alerted clinicians to the phenonemon of "bone bruising" (1-12).This entity is recognised as focal signal abnormalities in the subchondral bone marrow of the distal femoral condyles or proximal tibial plateaus and the appearances are thought to represent trabecular fractures, haemorrhage and oedema of the marrow without disruption of the adjacent cortices or overlying articular cartilage. As these lesions cannot be detected on conventional radiographs, "bone bruises" were an unrecognised entity prior to the advent of MRI. Investigators have only recently begun to report on the prevalence and patterns of association with knee injuries, in particular anterior cruciate ligament rupture (1-3,7,8,10-12). Although some authors suspect that these lesions may account for symptoms of pain and may have substantial prognostic implications, the short term clinical implications, exact time to resolution and factors which may influence it, and the long-term significance are largely unknown.

Conventional radiographic techniques are limited in providing accurate bone marrow characterization and therefore the diagnosis of bone bruising is essentially based on MRI findings. The subcortical epiphyseal marrow cavity consists of cancellous bone that usually demonstrates fatty marrow at all ages. The normal marrow signal on MRI parallels that of subcutaneous fat, being high on conventional T1-weighted and intermediate on T2-weighted spin echo sequences. A typical bone bruise appears as an area of signal loss within the marrow on T1 images and high signal intensity on T2 images, as a result of the water content of the injured marrow. With advancing MRI techniques, further information can be gained with Short T1 Inversion Recovery ("STIR") imaging in which the signal from normal medullary fat is markedly suppressed and hence bone bruises are highlighted with increased intensity (see images 1-5).

Mink (6) was the first to identify bone bruising as a distinct entity in 1987 and several authors since then have subsequently attempted to classify the lesions (3,5,12). Some confusion exists between the distinction of bone bruises which only involve the marrow, and "occult" fractures, undetected on conventional x-rays, which are similar on MRI but breach the adjacent cortex or osteochondral surface. Vellet (12) modified Minks original classification of occult fractures about the knee, such that bone bruises represent a subgroup of true subcortical lesions. He divided bruises into three types dependent on their characteristic pattern – reticular, geographic and linear. He described reticular lesions as regions of "reticular serpiginous stranding" with variable degrees of coalescence within the marrow compartment but distant from the adjacent cortices and articular cartilage; "Geographic" lesions are characterised by their contiguity to the adjacent cortical bone and are amorphous and coalescent, with peripheral areas of reticulation of the adjacent contrasting high-signal intensity epiphyseal fat; "Linear" lesions were described as discrete and less than 2mm in width. Since Vellet’s description, the literature has paid little attention to classification and has focused on the prevalence and pattern of bone bruises in association with knee injuries. There are yet no literature reports of this phenomenon in association with other joint injuries.

The prevalence of bone bruises is still largely unknown. Lynch et al.(3) retrospectively studied the MR images of 434 consecutive patients referred for evaluation of acute kneeinjury and found an incidence of 20%, of which 77% had associated anterior cruciate rupture. No other studies to date address the prevalence of bruises in knee injuries in general. Many authors had focused their attention on populations of ACL injuries and shown a high association with bone bruises (1,2,7-11). There is a striking consistency in the findings among these retrospective and prospective studies. Speer (9) and Rosen (8) both showed retrospectively that more than 80% of acute ACL tears had bone bruising on MRI. Speer provided operative correlation at the time of ACL reconstruction and only found one chondral lesion which correlated with the imaged bone bruise. Vellet (12) in a prospective study found 83% of acute ACL tears had a bone bruise but he did not present a detailed operative correlation and did not describe any associated meniscal abnormalities. Spindler (10) provided a more detailed prospective analysis. He found 80% of patients with ACL tears subsequently proven at surgery had MR diagnosed bone bruises and of these, 69% had involvement of the lateral femoral condyle and 54% the lateral tibial plateau. The medial femoral condyle and tibial plateau were only involved in 6% and 17% respectively. Bruising of both the lateral femoral condyle and lateral tibial plateau occurred in 65%. He proposed that these "matching" lesions reflected the force of impact on the lateral compartment of the knee at the time of injury. Kaplan supported this in her review of 100 MRIs of acute ACL tears (2). While the prevalence of bruising was lower (56%), all of her patients had posterolateral tibial bruising and this was the only lesion in 43%; 48% had lesions in both the posterolateral tibia and lateral femoral condyle. An interesting finding was that, in a subsequent examination of 200 MRIs of patients without ACL tears, posterolateral tibial bruising was only found in 3 patients and in all three cases, an ACL tear was subsequently diagnosed. She concluded that posterolateral tibial bruising is a pathognomonic sign of ACL injury.

The preponderance of lesions in the lateral compartment with ACL injury would correlate with the mechanism of injury. When the ACL ruptures, the tibia subluxes anteriorly relative to the femur. The lateral tibia subluxes more than the medial side, thus causing a relative external rotation of the femur on the fixed tibia. If this traumatic "pivot shift" occurs with enough force, it is conceivable that a unique pattern of bruising may occur in the middle ( weight-bearing) portion of the lateral femoral condyle and the posterior aspect of the lateral tibial plateau as the bones are compressed against one another ( "kissing" contusions). The posterior aspect of the LTP is probably structurally weaker than the LFC and therefore is injured most often. Kaplan’s findings would support this theory.

Murphy made some interesting observations by distinguishing between complete and partial tears of the ACL (7). While he showed an incidence of bruising of the posterolateral tibia and lateral femoral condyle of 94% and 91% respectively in patients with complete tears, only 17% with partial tears had lesions. He suggested that when distinction between a partial and complete tear is uncertain, the MRI presence of bone changes in the posterior tibia and lateral femoral condyle suggests that ACL "insufficiency" exists and this observation may have prognostic value or be helpful in decisions about reconstruction.

While the literature to date has focused on the prevalence and characteristic patterns of bone bruising associated with ACL injury, little is known about its possible association with other "non-bony" knee injuries. Miller has recently reported an incidence of bone bruising of 45% associated with medial collateral ligament injuries and almost all of the lesions involved the lateral compartment (13). He also provided the only information on resolution to date. While all the lesions appeared to resolve at a year post injury, the majority had done so at 2-4 months.

The most interesting information on bone bruising to date has come from Johnson who recently provided histology on these lesions (14). Biopsied bruises in 10 patients undergoing anterior cruciate reconstruction consistently showed variable degrees of articular cartilage and subchondral bone changes. Chondrocytes in the superficial zone of the articular cartilage had different stages of degeneration including necrosis; there was loss of proteogylcan component of the matrix and variable degrees of osteocyte necrosis in the underlying subchondral bone. This data gives scientific evidence to support the suggestion by other authors that bone bruising may be a precursor of posttraumatic arthritis (12,15).

As a recently recognised entity, the natural history of bone bruising is unknown. Assuming that it represents a blunt injury to underlying articular cartilage and subchondral bone, bruising may be a predictor of future cartilage degeneration, even in the absence of a visible articular cartilage injury. Donohue has shown that indirect, blunt trauma to the adult canine articular cartilage produces profound changes in its histologic, biochemical and ultrastructural characteristics, even in the absence of surface disruption (16).Thompson subsequently used the same model to demonstrate that a single transarticular load, producing no visible articular cartilage injury, progressed to osteoarthritic-like histological changes at 6 months (17). The initial concussive blow might exceed a supraphysiologic threshold and lead to progressive chondral damage as suggested by Mankin (18). Additionally, the osseous lesion might heal into a stiffer construction than the previous normal bone. The decreased compliance might then generate greater loads in the articular cartilage, leading to a progressive degeneration of this soft tissue layer (8). The long-term significance of bone bruising demonstrated on MRI in a clinical setting remains to be determined by the presence or absence of degenerative changes in prospective follow-up studies.

The high prevalence of bone bruises in ACL injured populations has raised questions about its prognostic implications. Posttraumatic arthritis is well recognised as a complication of nonoperative treatment (19-28). Jacobsen evaluated 43 anterior cruciate insufficient knees and found that after three years 80% had sclerosis and joint space narrowing on x-ray (23). More recently, McDaniel and Dameron retrospectively reviewed 53 knees with documented anterior cruciate ligament insufficiency at a mean follow-up of 10 years (25); 74% had symptoms of arthritis and 20% had significant degenerative changes on x-ray. A more recent evaluation by the same authors revealed an incidence of 37% of profound degenerative changes at 14 years. In Sherman’s study of 127 patients, 65% of patients followed up for 10 years and 83% of those followed for 20 years had significant radiographic degeneration (28). Interestingly, there was a similar degree of x-ray changes in both those with and without meniscectomy. Noyes (26) reported 44% of patients with ACL insufficiency at a mean follow-up of 11 years had significant x-ray deterioration and again showed no statistical difference between those who had meniscectomy and those who did not. There are two possible explanations for this observation. Either initial damage to the articular cartilage is the predominant cause of degeneration, or the chronic instability provoked later injury to those menisci intact at the time of ACL rupture. Both Noyes (29) and Hirshman (30) have described the progressive injury of secondary and tertiary restraints with continuous giving-way episodes. However, the first proposal would support the theory that bone bruising may be a factor in the development of posttraumatic arthritis. Sherman’s observation that knees with ACL/ MCL injury degenerated significantly earlier than those with ACL/ meniscal tear patterns would also lend support to this theory. These patients probably have a more traumatic impact injury, particularly to the lateral compartment and it could be extrapolated that the associated bone bruising may be more extensive as a result.

The commonly held belief that a knee with a chronic ACL injury develops cartilage wear and degeneration because of instability requires further thought. The literature to date shows lack of documentation that ACL reconstruction actually prevents degenerative arthritis (20,22,31-33). Friederich and O’Brien have shown an incidence of radiographic arthritis at 5-10 years after early ACL reconstruction that does not differ from conservatively treated cohorts (22). Daniel (20) prospectively evaluated a large cohort of patients with ACL rupture and found an increased incidence of degenerative changes on x-ray and bone scan in patients with reconstructed knees compared with those treated conservatively. Associated meniscectomy did not influence the incidence of arthrosis. Both these studies would suggest that initial injury to the articular cartilage is the predominant precursor to joint degeneration. However, the cause of posttraumatic arthritis in ACL injured patients is most likely multifactorial. Chronic instability with recurrent meniscal and cartilage injuries in those treated conservatively may accelerate the process but all the above literature would suggest that an initial injury, occult or apparent is the predominant prognostic factor. Johnson’s histological findings suggest that a bone bruise will be an important variable to include in the equation for the risk of arthritis in the future.

Most of the information to date has focused on ACL associated bone bruises. While Miller has recently shown a significant prevalence in MCL tears, it may be that these lesions occur with a whole spectrum of injuries and indeed they may be found in isolation. The speculation that these lesions may occur with meniscal tears provokes interesting thought. The natural history of meniscal tears is that a significant number will develop posttraumatic arthritis. Up to 50% of patients treated with a partial or total meniscectomy show radiological signs of osteoarthrosis 5-15 years after the meniscal injury (34-36). This has always been attributed to the increased load-bearing in the affected compartment. However, the possibility exists that bone bruising occurs in the adjacent bone, in those patients who sustain an "impact" rather than a twisting type injury and the prognosis of the meniscal-injured knee may be, wholly or in part, reflective of this associated occult bony injury.

While bone bruising is being increasingly recognised, little is known about its short-term resolution, clinical symptoms and long-term prognosis. Although Miller has provided some information on resolution, larger prospective studies with serial MR imaging are necessary to determine the exact pattern, as this may alter our clinical management. If these lesions represent trabecular fractures and occult articular cartilage damage as suggested by Johnson’s histological study, should we advocate protected weight-bearing until the lesion has resolved radiologically? It is also important to identify any distinct clinical symptoms, specifically pain, which may be associated with these lesions. Selective scanning based on parameters of suspicion would be a useful adjunct and may obviate the need for arthroscopy in some situations. The long-term manifestations of bone bruising will be difficult to clarify in cohorts of ACL injuries because of the complexity of the injury. Bruising in association with medial collateral ligament injuries may be the best natural history model to examine in the future as these ligament injuries are largely treated non-operatively and tend to heal without sequelae.

Until such time as long-term follow-up studies are available, as clinicians we must assume that bone bruising as a single entity is a harbinger of posttraumatic arthritis and practice a cautious approach to management of associated knee injuries.

1. Graf BK, Cook DA, De Smet AA, Keene JS. "Bone bruises" on magnetic resonance imaging evaluation of anterior cruciate ligament injuries. Am J Sports Med 1993; 21(2):220-3.

 

2. Kaplan PA, Walker CW, Kilcoyne RF et al. Occult fracture patterns of the knee associated with anterior cruciate ligament tears: Assessment with MR imaging. Radiology 1992; 183:835-8.

 

3. Lynch TCP, Crues JV, Morgan FW, Sheehan WE, Harter LP, Ryu R. Bone Abnormalities of the knee: prevalence and significance at MR imaging. Radiology 1989; 171:761-6.

 

4. McCauley TR, Moses M, Kier R, Lynch JK, Barton JW, Jokl P. MR diagnosis of tears of anterior cruciate ligament of the knee: importance of ancillary findings. AJR 1994; 162:115-9.

 

5. Mink JH, Deutsch AL. Occult cartilage and bone injuries of the knee: Detection, classification and assessment with MR imaging. Radiology 1989; 170:823-9.

 

6. Mink JH, Reicher MA, Crues IH. (eds). Magnetic resonance imaging of the knee. New York: Raven 1987.

 

7. Murphy BJ, Smith RL, Uribe JW et al. Bone signal abnormalities in the posterolateral tibia and lateral femoral condyle in complete tears of the anterior cruciate ligament: A specific sign? Radiology 1992; 182:221-4.

 

8. Rosen MA, Jackson DW, Berger PE. Occult osseous lesions documented by magnetic resonance imaging associated with anterior cruciate ligament ruptures. Arthroscopy 1991; 7:45-51.

 

9. Speer KP, Warren RF, Wickiewicz TL, Horowitz L, Henderson L. Observations on the injury mechanism of anterior cruciate ligament tears in skiers. Am J Sports Med 1995; 23(1):77-81.

 

10. Spindler KP, Schils JP, Bergfeld JA et al. Prospective study of osseous, articular and meniscal lesions in recent anterior cruciate ligament tears by magnetic resonance imaging and arthroscopy. Am J Sports Med 1993; 21(4):551-6.

 

11. Tung GA, Davis LM, Wiggins ME, Fadale PD. Tears of the anterior cruciate ligament: Primary and secondary signs at MR imaging. Radiology 1993; 188:661-7.

 

12. Vellet AD, Marks PH, Fowler PJ, Munro TG. Occult post-traumatic osteochondral lesions: Prevalence, classification and short-term sequelae evaluated with MR imaging. Radiology 1991; 178:271-6.

 

13. Miller MD, Osborne JR, Gordon WT, Hinkin DT, Brinker MR. The Natural History of bone bruises. A prospective study of magnetic resonance imaging-detected trabecular microfractures in patients with isolated medial collateral ligament injuries. Am J Sports Med 1998; 26(1):15-19.

 

14. Johnson D, Urban WP, Caborn DNM, Vanarthos WJ, Carlson CS. Articular cartilage changes seen with magnetic resonance imaging detected bone bruises associated with acute anterior cruciate ligament rupture. Am J Sports Med 1998; 26(3):409-14.

 

15. Faber K, Dill J, Thain L. Intermediate follow-up of occult osteochondral lesions following ACL reconstruction. Arthroscopy 1996; 12:370-1.

 

16. Donohoe JM, Buss D, Oegema TR Jr,et al. The effects of indirect blunt trauma on adult canine articular cartilage. J Bone Joint Surg 1983; 65A:951-7.

 

17. Thompson RC Jr, Oegema TR Jr, Lewis JL et al. Osteoarthritic changes after acute transarticular load. J Bone Joint Surg 1991; 73A:990-1001.

 

18. Mankin HJ. The response of articular cartilage to mechanical injury. J Bone Joint Surg 1982; 64A:462-6.

 

19. Arnold JA, Coker TP, Heaton LM, Park JP, Harris WD. Natural history of anterior cruciate tears. Am J Sports Med 1979; 7(6):305.

 

20. Daniel DM, Stone ML, Dobson BE, Fithian DC, Rossman DJ, Kaufman KR. Fate of the ACL-injured patient-A prospective outcome study.Am J Sports Med 1994; 22(5):632- 44.

 

21. Fetto JF, Marshall JL. The natural history and diagnosis of anterior cruciate ligament insufficiency. Clin Orthop 1980; 147:29.

 

22. Friederich NF, O’Brien WR. Gonarthrosis after injury of the anterior cruciate ligament: A multicenter, long-term study. Z Unfallchir Versicherungsmed 1993; 86:81-9.

 

23. Jacobsen K. Osteoarthrosis following insufficiency of the cruciate ligaments in man. Acta Orthop. Scand 1977; 48:520.

 

24. Kannus P, Jarvinen M. Conservatively treated tears of the anterior cruciate ligament-long-term results. J Bone Joint Surg 1987; 69A(7):1007-12.

 

25. McDaniel WJ, Dameron TB. Untreated ruptures of the anterior cruciate ligament. J Bone Joint Surg 1980; 62A(5):696-705.

 

26. Noyes FR, Mooar PA, Matthews DS, Butler DL.The symptomatic anterior cruciate deficient knee-Part 1: The long-term functional disability in athletically active individuals. J Bone Joint Surg 1983; 65A(2):154-162.

 

27. O’Brien WR, Warren RF, Friederich NF. Degenerative arthritis of the knee following anterior cruciate ligament injury: A multi-center, long-term folow-up study. Orthop Trans 1989; 13:546.

 

28. Sherman MF, Warren RF, Marshall JL. A Clinical and radiographical analysis of 127 anterior cruciate insufficient knees. Clin Orthop 1988; 227:229-37.

 

29. Noyes FR, McGinniss GH. Controversy about the treatment of the knee with anterior cruciate laxity. Clin Orthop. 1980; 198:61-76.

 

30. Hirshman HP, Daniel DM, Miyasaka K. The fate of unoperated knee ligament injuries. Knee ligaments: structure, function,injury and repair (eds). New York. Raven Press 1990; 481-503.

 

31. Lohmander LS, Roos H. Knee ligament injury, surgery and osteoarthrosis-truth or consequences? Acta Orthop Scand 1994; 65(6):605-9.

 

32. Maletius W, Gillquist J. Long-term results of anterior cruciate ligament reconstruction with a Dacron prosthesis- the frequency of osteoarthritis after 7-11 years. Am J Sports Med 1997; 25(3):288-93.

 

33. Sommerlath K, Lysholm J, Gillquist J. The long-term course after treatment of acute anterior cruciate ligament ruptures-a9 to 16 year follow-up. Am J Sports Med 1991; 19(2):156-162.

 

34. Appel H. Late results after meniscectomy in the knee joint. A clinical and roentgenologic follow-up investigation. Acta Orthop Scand (suppl 133) 1970;41:1-111.

 

35. Hede A, Larsen E, sandberg H. Partial versus total meniscectomy. A prospective randomized study with long-term follow-up. J Bone Joint Surg 1992; 74B:118-21.

 

36. JØ rgensen U, Sonne-Holm S, Lauridsen F, Rosenklint A. Long-term follow-up of meniscectomy in athletes. J Bone Joint Sur 1987; 69B:80-3.

Short T1 inversion recovery ( STIR ) image of the right knee with a small geographic bone bruise in the weight-bearing lateral femoral condyle and an extensive bruise of the lateral tibial plateau in association with an ACL rupture.

( same knee as figure 1 )

The signal from the tibial plateau bone bruise is intensified in the extreme posterior ( non-weight bearing border while the femoral condylar bruise does not extend to its posterior margin.

Bone bruise of the medial femoral condyle and both tibial plateau of the left knee in a patient with no associated ligamentous or meniscal injury.

STIR image of the left knee in a patient with ACL rupture in association with a grade 11 medial collateral ligament injury. A reticular type bone bruise is seen in the lateral tibial plateau with a large amorphous bruise in the lateral femoral condyle.

Localised bone bruises in the medial femoral condyle and tibial plateau of a patient with an associated medial meniscal tear.