July 2012

ACL reconstruction and risk of knee OA, part 2

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This two-part series examines the link between ACL injury and the later development of osteoarthritis (OA) and how surgery may strengthen or weaken that link. This second installment explores meniscal damage, proprioception, and what MRI can add to the discussion.

By Cary Groner

Ample research has established that, after injury to the anterior cruciate ligament (ACL), concurrent or subsequent damage to the meniscus dramatically increases the risk of later osteoarthritis.1 The reason has to do with the meniscus’s role in mediating the forces that move through the knee.

“The meniscus absorbs shock, it deepens and contours the joint, and it allows the transfer of force from the femur down to the tibia across the whole surface area of the joint,” said James Murray, MD, an orthopedic knee specialist at the Avon Orthopaedic Center and Frenchay Hospital in North Bristol, UK. “It’s anchored at the front and the back, and it tries to resist displacement. So as you load it, it forms an even tension throughout and transmits the load.”

For obvious reasons, then, the most common surgical intervention for a damaged meniscus—partial or complete meni-scectomy—carries problems of its own.

“The meniscus is a critical part of the knee, and if it is torn or removed, the load pattern is no longer normal,” said Stefan Lohmander, MD, a professor in the Department of Orthopedics at Lund University in Sweden. “And because the meniscus is commonly injured at the time the ACL is torn, these factors may contribute to the development of osteoarthritis.”

“When you damage the meniscus, you get a massive increase in the transmission of forces across the joint,” explained Murray. “That’s likely to lead to chondral damage of the articular surface.”

Effects of meniscectomy

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Many studies have delineated the deleterious effects of meniscec­tomy on the knee. As early as 1986, researchers reported that partial meniscectomy led to a decrease in contact areas of about 10% and an increase in peak local contact stresses (PLCS) of 65%. Total meniscectomy decreased contact areas by 75% and increased PLCS 235%.2

In a 2009 review in the Journal of Knee Surgery, the authors reported that, in 11 studies examined, virtually all patients who underwent complete meniscectomy later had radiographic evidence of osteoarthritis, those with partial meniscectomies had a significantly greater chance of OA than those with intact menisci, and meniscal repair (as distinct from meniscectomy) led to inconsistent findings.3 Last year, researchers at Ochsner Medical Center in Baton Rouge, LA, reported that meniscectomy was associated with radiographic OA after eight to 16 years.4

Investigators are beginning to understand the biochemical and biomechanical factors associated with these dire outcomes. For example, a 2010 Stanford study of 10 patients after partial meniscectomy found significantly greater external tibial rotation (~3.2°) through stance phase in eight limbs compared with the unaffected contralateral limb; the authors noted that the altered rotational position likely resulted in alterations in tibiofemoral contact during walking that could lead to degenerative cartilage changes.5

Australian investigators reported in 2011 that partial meniscectomy was associated with adverse effects on articular cartilage and subchondral bone.6 The same year, scientists at the VA Palo Alto Health Care System in Palo Alto, CA, used a finite-element modeling approach to demonstrate that meniscectomy was associated with increased fluid pressure, fluid exudation, loss of fluid load support, and increased tensile strains centrally on the tibial condyle, patterns that correspond to clinical observations of damage to the cartilage matrix and fibrillation.7

Moreover, a study from Washington University in St. Louis, MO, published earlier this year in The American Journal of Sports Medicine (AJSM), reported that partial meniscectomy was later associated with a higher incidence of articular cartilage lesions found during revision ACL reconstruction.8 Those researchers noted that meniscal repair was not associated with the same problems, however, and lead author Robert Brophy, MD, later said meniscal repair appeared to offer a chondroprotective effect.9

Benefits, challenges of repair

Other research supports the benefits of repair over meniscectomy. For example, in a study published in The Journal of Bone and Joint Surgery in 2009, scientists reported that, in cadaver knees, repair restored peak contact pressures to normal levels after a posterior tear of the medial meniscus initially led to a 25% increase in those pressures.10 The next year, an AJSM paper found that, of patients who’d had repair following medial meniscal tear, 81% had no detectable osteoarthritic progress—versus 40% of subjects treated with meniscectomy—at long-term follow-up (~8.8 years).11

“Some orthopedists just take out the meniscus because it’s faster and more predictable, but is that doing the patients a favor?”asked Jonathan Chang, MD, a clinical associate professor of orthopedics at the University of Southern California in Los Angeles. “It appears that we’re not, and that it’s better for the patient if you can get the meniscus to heal.”

Unfortunately, repair is appropriate in only a small subset of injuries, according to Chang.

“The vast majority of meniscal injuries are nonrepairable,” he said. “I have a busy arthroscopic practice, and I haven’t done one in a year.”

The problem, he explained, lies in the nature of the meniscal tissue, which has several zones. The inner third is referred to as “white/white,” meaning that it is avascular and will not heal no matter what the surgeon does. The outer third is “red/red”—that is, fully vascularized—and generally heals quite well.

“Where controversy occurs is in the middle third, the red/white zone, because it has some vascularity,” Chang said. “But the closer you get to the inner rim, the less there is, and it becomes a judgment call. The trend is to do more of these, if possible, but what if you have a tear that goes from the inner rim into that section? That’s an issue that hasn’t been resolved.”

Nevertheless, said Chang, if he’s reconstructing a knee after ACL rupture and sees chondral damage during surgery, it affects his decision-making process vis-à-vis meniscal repair.

“Let’s say, for example, you have a chondral defect from the initial bone bruise in the lateral femoral condyle, and a small bucket-handle meniscal tear. In that circumstance I would do everything I could to repair the meniscus, because you now know you are going to have damage on that side that has a high chance of proceeding to arthritis. If you take out too much of the meniscus—fifty to eighty five percent—you’re effectively dooming the patient to future osteoarthritis, at least in that compartment, if not in the entire knee. So if it’s possible to save the meniscus, it’s more protective for the patient.”

The role of proprioception

Tim Hewett, PhD, professor and director of research at the Ohio State University Sports, Health, and Performance Institute and director of the Sports Medicine Biodynamics Center at Cincinnati Children’s Hospital, believes that another factor, not often discussed by clinicians, may be contributing to the incidence of osteoarthritis in patients who’ve had ACL reconstructions.

“Once you rupture the ACL, those mechanoreceptors are disrupted, and then in surgery the sites of the original footprints are drilled out and you put in another piece of tissue that’s not a ligament,” Hewett said. “It’s highly likely that that nervous tissue, which is the sensor of the center of the hinge of the joint, doesn’t come back. It’s possible that you get increased motion and friction because you don’t have a good sense of that joint.”

Osteoarthritis patients typically have impaired proprioception, but not everyone with proprioceptive defects will develop OA, nor is proprioceptive impairment reliably linked directly with osteo­arthritis-related pain levels.12,13

Hewett’s team is conducting a meta-analysis of the literature, and though they have not yet published results, he said existing studies make it clear that there’s a loss of proprioception and kinesthesia in the joint after ACL injury. Several investigations are referenced in an earlier paper of his, and even though that paper makes clear that the evidence can be contradictory, Hewett believes that proprioception is never fully restored.14

“Even if there was neural integration into the graft, it’s unlikely that those nerves or mechanoreceptors would be tensioned properly to sense and control the joint,” he said. “People who rupture their ACLs are playing again at six to 12 months, but we know that they still don’t sense that joint well, even at 24 months. It’s a big problem that people are ignoring.”

To Hewett, the link between ACL injury and later osteoarthritis is likely three-pronged.

“There’s the original mechanical insult and increased load,” he said. “There’s the biological cascade that those problems incite. Then there’s a lack of proprioception and kinesthesia in that joint. I think these factors lead to a vicious cycle of degradation of the cartilage over relatively short times.”

Jonathan Chang agreed, but with a caveat.

“The problem will be in proving the link between impaired proprioception and later osteoarthritis,” he said. “Measuring proprioception is difficult, but if the link can be proven, then clinicians will likely need to alter their recommendations to patients in terms of activity guidelines and the risk of OA after ACL reconstructions.”

HSS weighs in

This February, researchers at the Hospital for Special Surgery (HSS) in New York City published a paper describing their use of advanced MRI to delineate the chondral injuries associated with ACL rupture (cases with meniscal involvement were excluded).15 They found that all 40 patients sustained chondral damage at initial injury and that the damage progressed over time. Strikingly, at long-term follow up (seven to 11 years), nonsurgical patients were six times more likely to have cartilage degeneration over the medial tibial plateau and patella than patients who had early ACL reconstruction.

“The concept used to be that if you had a chondral injury, it would just remodel and wouldn’t change things,” said lead author Hollis Potter, MD, chief of the Division of Magnetic Resonance Imaging and director of research in HSS’s Department of Radiology and Imaging. “But we know that there are inflammatory cytokines upregulated in the setting of chondral injuries, some of which cause articular cartilage catabolism. Our results show a deleterious effect on surrounding cartilage that was not initially involved in the chondral fracture at the site of pivot shift, likely as a result of homeostasis imbalance.”

When Potter presented her preliminary data at orthopedic meetings, she was surprised by the contentious atmosphere.

“I’ve heard orthopedic surgeons literally yelling at each other about types of grafts and whatnot; I mean, sometimes there’s really blood on the floor about these issues,” she said, laughing. “But at the end of the day, they want to be able to tell their patients that an ACL reconstruction will slow the rate of osteoarthritis, and until now there were no solid data to support that statement. Our study did show that ACL reconstruction was chondroprotective.”

The advanced MRI technology allowed Potter and her colleagues to directly measure cartilage thickness, rather than the cruder joint-space measures provided by x-ray.

“[With x-ray] you’re looking at bone, not cartilage or synovium, so there are a lot of things you’re not evaluating,” she said.

The advanced technology, specifically quantitative T2 mapping, also allowed the researchers to assess cartilage degeneration. T1-weighted MRI pulse sequences provide data about proteoglycan, whereas T2-weighted pulse sequences reflects collagen integrity, and T2 mapping describes patterns of signal intensity within cartilage that can identify areas of degeneration. Both T1 and T2 measures are important for an accurate assessment of articular homeostasis.

“Proteoglycans afford you compressive strength, and collagen orientation affords you resistance to tensile forces,” Potter said. “You really need both to maintain your knee joint.”

Potter acknowledged that the cascade of injuries that lead from ACL tear to osteoarthritis is complex. Deeper knowledge should yield better patient outcomes, however—beginning with her new compelling evidence that ACL reconstruction likely reduces OA risk.

“So many factors affect the progression of osteoarthritis—whether the meniscus or another ligament was injured, the muscle forces and proprioception affecting the knee, how well an individual compensates for the catabolic enzymes released at the time of injury,” she said. “But this is clinically relevant, and it begs a multicenter trial using similar imaging methodology and outcome instruments. We could stratify that across types of ACL reconstruction, look at different cohorts five, seven, ten years out. Look at the rate of proteoglycan, look at changes in collagen orientation, look at changes in the subchondral bone, see which patients have synovitis—all these things that modulate the progression of osteoarthritis.”

She hopes researchers will collaborate to produce such a study and help determine which procedures produce the best outcomes.

“When we look at all that,” she said, “we’ll have the answer.”

Cary Groner is a freelance writer based in the San Francisco Bay Area.


1. Noyes FR, Barber SD, Simon R. High tibial osteotomy and ligament reconstruction in varus angulated, ACL-deficient knees: a two- to seven-year follow-up study. Am J Sports Med 1993;21(1):2-12.

2. Baratz ME, Fu FH, Mengato R. Meniscal tears: the effect of meniscectomy and of repair on intra-articular contact areas and stress in the human knee. A preliminary report. Am J Sports Med 1986;14(4):270-275.

3. Magnussen RA, Mansour AA, Carey JL, Spindler KP. Meniscus status at ACL reconstruction associated with radiographic signs of osteoarthritis at 5- to 10-year follow-up: a systematic review. J Knee Surg 2009;22(4):347-357.

4. Petty CA, Lubowitz JH. Does arthroscopic partial meniscectomy resulted in knee osteoarthritis? A systematic review with a minimum of 8 years’ follow-up. Arthroscopy 2011;27(3):419-424.

5. Netravali NA, Giori NJ, Andriacchi TP. Partial medial meniscectomy and rotational differences at the knee during walking. J Biomech 2010;16(43):2948-2953.

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7. Haemer JM, Song Y, Carter DR, Giori NJ. Changes in articular cartilage mechanics with meniscectomy: A novel image-based modeling approach and comparison to patterns of OA. J Biomech 2011;44(12):2307-2312.

8. Brophy RH, Wright RW, David TS, et al. Association between previous meniscal surgery and the incidence of chondral lesions at revision anterior cruciate ligament reconstruction. Am J Sports Med 2012;40(4):808-814.

9. Foster JB. Meniscal misadventures: Some surgeries may predict AC lesions. LER 2011;3(7):13-14.

10. Harner CD, Mauro CS, Lesniak BP, Romanowski JR. Biomechanical consequences of a tear of the posterior root of the medial meniscus. Surgical technique. J Bone Joint Surg Am 2009;91(Suppl 2):257-270.

11. Stein T, Mehling AP, Welsch F, et al. Long-term outcome after arthroscopic meniscal repair versus arthroscopic partial meniscectomy for traumatic meniscal tears. Am J Sports Med 2010;38(8):1542-1548.

12. Segal NA, Glass NA, Felson DT, et al. Effect of quadriceps strength and proprioception on risk for knee osteoarthritis. Med Sci Sports Exerc 2010;42(11):2081-2088.

13. Felson DT, Gross KD, Nevitt MC, et al. The effects of impaired joint position sense on the development of pain and structural damage in knee osteoarthritis. Arthritis Rheum 2009;61(8):1070-1076.

14. Hewett TE, Paterno MV, Myer GD. Strategies for enhancing proprioception and neuromuscular control of the knee. Clin Orthop Relat Res 2002;(402):76-94.

15. Potter HG, Jain SK, Ma Y, et al. Cartilage injury after acute, isolated anterior cruciate ligament tear: immediate and longitudinal effect with clinical/MRI follow-up. Am J Sports Med 2012;40(2):276-285.

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