This paper primarily sets out to investigate the optimum timing of reconstructive surgery after rupture of the anterior cruciate ligament (ACL) yet it also indirectly addresses the fundamental issue of whether ACL reconstruction protects the knee from secondary osteoarthritis (OA). This has been investigated at length over the past three decades and yet we appear no closer to a definitive answer.
In 1983, Frank Noyes described a ‘rule of thirds’ for the management of patients with ACL ruptures.1 He stated that one third of patients would compensate well with conservative treatment, one third would avoid symptoms of instability through ‘modification or substitution’ of activities and one third would do poorly and require reconstructive surgery. It is interesting to note that this latter group were described as non-compliant as they elected to continue active sports. Standard management of an acute ACL rupture in the 1980s and 1990s therefore consisted of a trial of conservative management followed by reconstruction if the patient developed symptoms of regular instability. Many of the early papers assessing the effect of ACL surgery on the development of OA were therefore comparing conservative ‘copers’ with late reconstructions. One notable paper by Daniel et al2 followed a cohort of acute ACL ruptures for over five years and concluded that reconstructed patients had a higher level of arthritis on radiographs and bone scans than those treated conservatively. However, over half of the reconstructed group underwent surgery more than nine months after the index injury for symptoms of recurrent instability and 63% of these patients were noted to have meniscal injuries at the time of surgery. Furthermore, there was no randomisation of patients, with those who undertook sports opting for surgery. The non-athletic patients were perhaps bound to have less degenerative change.
Numerous publications on this subject have been published over the last 20 years. Results are variable and often conflicting. This is perhaps not surprising given the number of variables involved. Not only was surgery generally carried out on patients with instability and compared with patients who had no or infrequent symptoms of instability, but it was almost impossible to match additional variables such as age, sex, obesity, muscle strength, gait, activity level, re-injury and, most importantly, associated meniscal and chondral damage. These older studies also necessarily report the results of relatively crude surgery, which often routinely included notchplasty.
A recent systematic review by Oiestad et al3 makes the point that no universal radiological classification exists, making comparison between studies difficult but points out that studies with the best methodology report lower prevalence of OA after ACL reconstruction than those with poor methodology. Another recent review by Louboutin et al4 observes that there is a difference between radiological OA and significant symptomatic OA requiring reconstruction. The authors conclude that, at 20 years follow-up, the risk of developing OA is lower after ACL reconstruction (14% to 26% with a normal medial meniscus; 37% with meniscectomy) than that after untreated ruptures (60% to 100%).
Thus, the literature is contradictory on the subject of ACL reconstruction and secondary OA yet it is unusually unanimous on the subject of secondary pathology and the subsequent development of OA. Neyret recognised the relationship between concurrent ACL and meniscal injuries and the subsequent development of OA in 1983;5 he concluded that the long term outcome of partial meniscectomy depends mainly on the state of the ACL. Numerous subsequent papers have confirmed this relationship from the opposite viewpoint ie, that the status of the meniscus is the most important predictor of developing OA after ACL reconstruction.4,6-9 In 1999, Gillquist elegantly quantified thus in a review9 by stating that patients who had undergone an isolated ACL reconstruction or meniscal repair had a 10% incidence of OA at 15 to 20 years. An isolated meniscectomy (with an intact ACL) increases this to 30% to 40% whilst an ACL reconstruction with a meniscectomy increases it to 50% to 70%.
Although there is little we can do to prevent meniscal and chondral damage at the time of ACL rupture, our evidence base would appear to support any measure which decreases the risk of secondary injuries to these structures. Although Noyes originally stated that ‘recurrent giving-way injuries, even if occurring only two or three times a year, may in time produce significant damage’, the general opinion today is that this is an understatement; even one further episode of giving way may result in further meniscal or chondral injuries which may progress to OA.
Kennedy’s paper is sympathetic to this sentiment. The large number of patients in this single surgeon study has allowed the authors to use five different time frames. Thus we can see that the incidence of high grade chondral pathology is 5% when ACL reconstruction is delayed for up to six months post-injury. For every six months delay thereafter, the incidence increases to 11%, 19% and finally to 65% if surgery is delayed by more than18 months. Similarly, the incidence of medial meniscal tears starts at 14% but increases to 25%, 52% and 71% with each 6 month’s delay. Although several authors have previously reported similar findings and concluded that ACL reconstruction is best performed within the first 12 months of injury, Kennedy’s use of these time frames has created a sense of urgency which is missing from other papers. Their finding that the incidence of lateral meniscal tears does not increase with delay to surgery would support the theory that these occur at the index injury due to the lateral compartment subluxation that leads to ACL rupture. The medial meniscus is subsequently overloaded and subject to attritional damage over time which leads to secondary tears.
Although there is general agreement that ACL reconstruction should be delayed until the knee is ‘quiet’, uncertainty remains as to the optimum timing of surgery thereafter. Most knee surgeons will anecdotally state that patients who undergo early surgery do better than those who have waited. We have come a long way from the ‘wait and see’ principle expressed by Noyes’ rule of thirds. This paper would support the sentiments of many knee surgeons that it is better to reconstruct the athlete’s ACL early than to allow the patient to experience even one further episode of instability.
1. Noyes FR, Matthews DS, Mooar PA, Grood ES. The Symptomatic anterior cruciate-deficient knee. J Bone Joint Surg [Am] 1983;65-A:163-73.
2. 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;22:632-44.
3. Oiestad BE, Engebretsen L, Storheim K, Risberg MA. Knee osteoarthritis after anterior cruciate ligament injury: a systematic review. Am J Sports Med 2009;37:1434-43.
4. Louboutin H, Debarge R, Richou J, Selmi TAS, Donell ST, Neyret P, Dubrana F. Osteoarthritis in patients with anterior cruciate ligament rupture: a review of risk factors. Knee 2009;16:239-44.
5. Neyret P, Donell ST, Dejour H. Results of partial meniscectomy related to the state of the anterior cruciate ligament: review at 20-35 years. J Bone Joint Surg [Br] 1993;75-B:36-40.
6. Meunier A, Odensten M, Good L. Long-term results after primary repair or non-surgical treatment of anterior cruciate ligament rupture: a randomized study with a 15-year follow-up. Scand J Med Sci Sports 2007;17:230-7.
7. Neuman P, Englund M, Kostogiannis I, Friden T, Roos H, Dahlburg LE. Prevalence of tibiofemoral osteoarthritis 15 years after nonoperative treatment of anterior cruciate ligament injury: a prospective cohort study. Am J Sports Med 2008;36:1717-25.
8. Ichiba A, Kishimoto I. Effects of articular cartilage and meniscus injuries at the time of surgery on osteoarthritic changes after anterior cruciate ligament reconstruction in patients under 40 years old. Arch Orthop Trauma Surg 2009;129: 409-15.
9. Gillquist J, Messner K. Anterior cruciate ligament reconstruction and the long-term incidence of gonarthrosis. Sports Med 1999;27:143-56.
Church S, Consultant Orthopaedic Surgeon
Chelsea and Westminster Hospital