Objective: 

To determine if surgical or nonsurgical treatment of anterior cruciate ligament rupture affects the prevalence of posttraumatic tibiofemoral osteoarthritis (OA).

Data Sources: 

Studies published between 1983 and April 2012 were identified via EBSCOhost and OVID. Reference lists were then screened in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement.

Study Selection: 

Studies were included if (a) treatment outcomes focused on a direct comparison of surgical versus nonsurgical treatment of anterior cruciate ligament rupture, (b) the prevalence of tibiofemoral OA was reported, and (c) they were written in English. Studies were excluded if (a) the included patients were treated with cast immobilization after surgery, (b) the mean follow-up was less than 10 years, or (c) the patients underwent anterior cruciate ligament revision surgery.

Data Extraction: 

Two independent investigators reviewed the included articles using the Newcastle-Ottawa Scale. Frequency of OA, surgical procedure, nonsurgical treatments, and participant characteristics were extracted and summarized. We calculated prevalence (%) and 95% confidence intervals for treatment groups for each individual study and overall. We developed 2 × 2 contingency tables to assess the association between treatment groups (exposed had surgery, referent was nonsurgical treatment) and the prevalence of OA.

Data Synthesis: 

Four retrospective studies were identified (140 surgical patients, 240 nonsurgical patients). The mean Newcastle-Ottawa Scale score was 5 (range = 4–6 [of 10] points). Average length of follow-up was 11.8 years (range = 10–14 years). The prevalence of OA for surgically treated patients ranged from 32.6% to 51.2% (overall = 41.4%, 95% confidence interval = 35.0%, 48.1%) and for nonsurgical patients ranged from 24.5% to 42.3% (overall = 30.9%, 95% confidence interval = 24.4%, 38.3%).

Conclusions: 

Although OA prevalence was higher in the surgical treatment group at a mean follow-up of 11.8 years, no definitive evidence supports surgical or nonsurgical treatment after anterior cruciate ligament injury to prevent posttraumatic OA. Current studies have been limited by small sample sizes, low methodologic quality, and a lack of data regarding confounding factors.

Key Points
  • This is the first systematic review to directly compare surgical and nonsurgical treatment of anterior cruciate ligament ruptures.

  • No definitive evidence supports surgical or nonsurgical treatment after anterior cruciate ligament injury to prevent posttraumatic osteoarthritis.

  • Research to date has been limited by small samples, low methodologic quality, and a lack of data on confounding factors.

Anterior cruciate ligament (ACL) reconstruction is often the treatment recommended after ACL rupture1  in a physically active individual. The intended outcome of the surgery is to restore knee anatomy and biomechanics to a functional level, thereby reducing sheer and torsional stresses on the menisci and articular surfaces29  and permitting a return to previous physical activities.7,1013  After ACL reconstruction surgery, the short-term functional results appear favorable4,1419 ; however, over the long term, at least 28% to 87%1,5,7,1517,1933  of these patients develop posttraumatic tibiofemoral osteoarthritis (OA).

Some patients opt for nonsurgical treatment of their ACL injuries.34,35  Patients recommended for this type of treatment typically have sufficient dynamic knee stability for their desired level of function3,3639  and no secondary joint injury (eg, meniscal tear, collateral ligament sprain).38  For patients treated nonsurgically, the reported rates of OA range from 11% to 73%.23,2528,32,35,4046  Although these patients are believed to have less disruption of lower extremity biomechanics after ACL rupture,47  it remains unclear if the likelihood of OA differs with surgical or nonsurgical treatment of the knee.15,35,40,44,48,49 

No systematic review has been reported to date on the prevalence of OA in patients with ACL ruptures treated surgically versus nonsurgically. Our purpose was to conduct a systematic review to determine if OA prevalence differed between the treatments. Studies used in this systematic review focused on a direct head-to-head comparison of surgical reconstruction and nonsurgical treatment. The advantage of a head-to-head approach was that the studies used the same criteria, such as the radiographic threshold for determining OA and the patient's previous level of function. Our intent was to inform evidence-based clinical care in the treatment of patients with ACL ruptures.

Inclusion and Exclusion Criteria

Studies were included if (a) treatment outcomes focused on a direct comparison of surgical versus nonsurgical treatment of ACL ruptures, (b) the prevalence of tibiofemoral OA was reported, and (c) they were written in English. Studies were excluded if (a) patients were placed in casts after surgery, (b) the mean follow-up was less than 10 years,50  or (c) patients underwent ACL revision surgery. Before 1983, the standard postsurgical care was straight-leg casting for 8 to 12 weeks.51  More contemporary postsurgical treatment calls for mobilization and rehabilitation beginning immediately after surgery.52  Because the long-term outcomes may differ between these postsurgical treatment protocols, we excluded articles published before 1983. Randomized control trials were initially considered for inclusion; however, none met the eligibility criteria for inclusion. If the reviewer (K.P.H.) was unsure that a study met all the necessary criteria, the study was reviewed by the other authors, and a consensus was reached.

Search Strategy

We conducted a comprehensive literature search from 1983 through April 2012 with the assistance of an experienced reference librarian. Databases searched with EBSCOhost were Academic Search Premier, CAB abstracts, CINAHL, Education Research Complete, Education Resources Information Center, MEDLINE, SPORTDiscus with full text, and Research Starters-Education. Databases searched with OVID were Cochrane Database of Systematic Reviews, ACP Journal Club (1991 to April 2012), Database of Abstracts of Reviews of Effects (second quarter of 2012), Cochrane Library Central Register of Controlled Trials (second quarter of 2012), Cochrane Library Methodology Register, Cochrane Library Health Technology Assessment, Cochrane Library Economic Evaluation Database, Journals@Ovid, Global Health, and Ovid MEDLINE. Key words used in the database searches were ACL OR anterior cruciate ligament AND osteoarthritis OR osteoarthrosis OR degenerative joint disease OR arthritis OR coxarthritis OR gonarthrosis AND reconstructi* OR repair OR surgery OR replacement AND meniscus OR menisci OR tear OR torn OR injury OR injuries OR injured. Although we focused on tibiofemoral OA, we did not specify the type of OA for the literature search to avoid eliminating studies of both tibiofemoral and patellofemoral OA.

Study Selection

The primary search yielded 799 studies, and the lead author (K.P.H.) screened the titles, key words, dates of publication, and abstracts. A total of 759 articles were eliminated because their titles or abstracts indicated that the studies either did not meet the inclusion criteria or they met the exclusion criteria. We then obtained the full text of the 40 remaining articles and further screened them for all inclusion and exclusion criteria. The reference lists of all 40 full-text articles were searched manually to identify any additional articles not located through the electronic database search process; no additional articles were cited. A total of 11 articles were provisionally identified as meeting the inclusion criteria. For 2 studies,26,53  it was unclear if patients were placed in casts after surgery. Therefore, we contacted the first author of each and confirmed that patients were treated with casts, so the studies were excluded. Three additional studies5456  were later excluded during the data-extraction process because prevalence data were not reported. Another study28  was excluded due to a mixed study design (cohort and cross-sectional study design) and the inclusion of patients who did not improve with nonsurgical treatment. One additional study27  was later eliminated for not meeting the inclusion criteria for an adequate length of follow-up. The study-elimination process is shown in the Figure. The final 4 studies are presented in Table 1.

Figure. 

Study-elimination sequence according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement.57

Figure. 

Study-elimination sequence according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement.57

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Table 1. 

Study Design, Participant Characteristics, Exposures, and Outcomes for Studies (n = 4) Included in the Systematic Review Extended on Next Page

Study Design, Participant Characteristics, Exposures, and Outcomes for Studies (n = 4) Included in the Systematic Review Extended on Next Page
Study Design, Participant Characteristics, Exposures, and Outcomes for Studies (n = 4) Included in the Systematic Review Extended on Next Page
Table 1. 

Extended From Previous Page

Extended From Previous Page
Extended From Previous Page

Assessment of Study Quality

Two independent reviewers (K.P.H., N.M.C.) assessed the quality of all included studies using the Newcastle-Ottawa Scale (NOS), which we modified for use in this systematic review (Appendix).58  Although not developed specifically for OA research, the NOS has been recommended for the qualitative evaluation of observational studies58  because it is easy to use and includes specific items based on study design (eg, case control, cohort).58  A recent analysis59  of several quality-assessment tools also deemed the NOS appropriate for its intended use in this study. We transferred the NOS to an electronic form for more efficient assessment and operationally defined the NOS criteria to make them applicable to the study population. Specifically, questions that assessed the representativeness of the cohorts (items 1 and 2) were modified to meet the objective of our systematic review. The question regarding the representativeness of the ACL population (item 1) was changed from “representativeness of the community of selection” to “representativeness of the general ACL-deficient population.” The question assessing the selection of the nonexposed cohort (item 2) was changed from “drawn from the same community as the exposed cohort” to “drawn from the general ACL-deficient population.” The question assessing the ascertainment of exposure of the exposed cohort (item 3) defined as the surgical cohort. To assess the exposure of the nonsurgical cohort, a fifth item was added. Items used to assess the comparability of cohorts were defined as follows: (a) Did the study control for secondary injuries (ie, meniscal, ligamentous injuries other than ACL injury)? and (b) Did the study control for the body mass index (BMI) of participants at either baseline or follow-up? This indicated that the authors attempted to control for important, known influences on the development of OA. Of the 3 items designated to assess the outcomes of each study, 2 items were further defined. The adequate follow-up time for the outcome (prevalence of OA) to occur (item 2) was defined as 10 or more years, and the adequacy of follow-up cohorts (item 3) was defined as greater than 80%. The modified total possible score was 10 points, as opposed to 9 in the original instrument.

To standardize the way in which items were scored by the reviewers, we established criteria for specific questions on the NOS. To score the representativeness of the surgical group (item 1), the following criteria were assessed: (a) Were patients randomly or consecutively chosen (reduced risk of selection bias)? (b) Were patients between 15 and 55 years of age at the time of injury60–62? (c) Was the cohort mean BMI61  less than 30? and (d) Was surgery performed within 8 weeks of injury? Studies that fulfilled all 4 criteria were considered representative of the general population with ACL ruptures. Studies adhering to 3 of the 4 criteria were considered to be somewhat representative. Investigations adhering to 2 or fewer of the 4 criteria were not considered representative of the general population with ACL ruptures. To score the representativeness of the nonsurgical group (item 2), we used 3 criteria: (a) Were patients randomly or consecutively chosen? (b) Were patients between 15 and 55 years of age at the time of injury? and (c) Was the cohort mean BMI less than 30? Studies that fulfilled all 3 criteria were considered representative of the general population with ACL ruptures. Those adhering to 2 or fewer of the 3 criteria were not considered representative of the general population with ACL ruptures.

Before rating the quality of the 4 included studies, we pilot tested the rating procedures using 3 sample articles that were not included in the analysis. Studies were randomized by a blinded, independent investigator (M.R.S.). Each article was then read and scored independently by 2 raters. Consensus scores were determined for each article. If the scores of rater 1 (K.P.H.) and rater 2 (N.M.C.) agreed, then that score was used as the consensus score. If the scores of raters 1 and 2 differed by 1 point, the raters discussed and agreed on a consensus score. If the scores of raters 1 and 2 differed by 2 or more points, a third rater (J.B.D.) reviewed the article, and a final consensus score was agreed on by all 3 raters.

We created a spreadsheet for data extraction. The following information was extracted from each of the studies by the primary investigator (K.P.H): (a) publication information: first author's name, journal, and year of publication; (b) study methods: study design, report of meniscal injury, and NOS score; (c) OA outcomes: definition of OA and time of follow-up; (d) patient descriptors: source of exposed (surgical) and nonexposed (nonsurgical) cohorts, matching variables (eg, age, sex, Tegner Activity Scale score), sport, level of participation, percentage lost to follow-up, sample size, age, weight, height, BMI; and (e) outcomes measures: frequency of OA, prevalence of OA ([No. yes surgical / total surgical] · 100), and adjustment variables (eg, meniscal injury, age, BMI).

For each study, the number of patients with OA at follow-up, stratified by treatment group (surgical, nonsurgical), was populated in a 2 × 2 contingency table. Prevalence (%) of OA was calculated using the following formula: number with OA in a treatment group/total in the treatment group at baseline. Prevalence ratios (PRs) were calculated using the formula (No. surgical and OA / all surgical) / (No. nonsurgical and OA / all nonsurgical). The nonsurgical treatment group was considered the referent group. We calculated 95% confidence intervals (CIs) for proportions and PRs using standard methods63  and prevalence proportions and PRs for each individual study and for all studies combined (overall prevalence).

All 4 reviewed studies23,25,32,41  used a retrospective cohort design. A total of 380 patients (260 men, 120 women), 140 (37%) of whom were treated surgically, were included in the 4 studies.23,25,32,41  The mean patient ages reported at follow-up25,32  and time of trauma23,41  were 37.9 and 24.9 years, respectively. In all 4 studies,23,25,32,41  bone–patellar tendon–bone autograft was the primary surgical method. The reported postsurgical follow-up for each study ranged from 10 to 14 years (mean = 11.8 years).

Methodologic Quality

No study fulfilled all of the NOS criteria. The highest score recorded was 6 (of 10 possible points), and the lowest was 4. The mean score for all studies was 5 points. All studies23,25,32,41  included patients with meniscal injury; authors of only 1 study23  adjusted statistically for this using a logistic regression model. Two groups25,41  used matching variables (age, sex, and Tegner Activity Scale score) in allocating the exposed and nonexposed cohorts. No authors reported inclusion and exclusion criteria for patients treated nonsurgically or fulfilled the requirement of “representative of the general ACL-deficient population” for either the exposed or nonexposed cohort. All studies23,25,32,41  ascertained exposure of the surgically treated cohort through surgical records or a structured interview. No group reported the absence of OA (eg, on radiographs) at the start of the study, mitigating the ability to determine the incidence of OA.

Prevalence of Tibiofemoral OA

Overall, OA prevalence for the 4 studies23,25,32,41  ranged from 24.5% to 51.2%. The OA prevalence for surgically treated patients ranged from 32.6% to 51.2% (overall = 41.4%, 95% CI = 35.0%, 48.1%) and for nonsurgical patients ranged from 24.5% to 42.3% (overall = 30.9%, 95% CI = 24.4%, 38.3%). Because all studies included patients with compromised menisci, we did not report prevalence data comparing isolated ACL ruptures with nonisolated ACL ruptures.

Prevalence Ratios of Tibiofemoral OA

Across the 4 studies, the PRs of tibiofemoral OA among surgical patients compared with nonsurgical controls ranged from 1.01 to 1.84. The surgical group had a 34% higher prevalence of tibiofemoral OA (PR = 1.34; 95% CI = 1.01, 1.77) compared with the nonsurgical group (Table 2).

Table 2. 

Frequency, Prevalence (%), and Unadjusted Prevalence Ratios of Tibiofemoral Osteorarthritis by Treatment (Surgical or Nonsurgical) Among Athletes with Anterior Cruciate Ligament Ruptures

Frequency, Prevalence (%), and Unadjusted Prevalence Ratios of Tibiofemoral Osteorarthritis by Treatment (Surgical or Nonsurgical) Among Athletes with Anterior Cruciate Ligament Ruptures
Frequency, Prevalence (%), and Unadjusted Prevalence Ratios of Tibiofemoral Osteorarthritis by Treatment (Surgical or Nonsurgical) Among Athletes with Anterior Cruciate Ligament Ruptures

Radiologic Classification System

To quantify radiographic OA, authors of all 4 included studies23,25,32,41  used the Kellgren-Lawrence Scale score.64  Two studies25,41  defined the presence of OA as greater than or equal to Kellgren-Lawrence grade 1. Combined, these studies demonstrated an OA prevalence of 45.9% (95% CI = 35.7%, 56.4%) for surgically treated patients and 25.7% (95% CI = 17.1%, 36.6%) for nonsurgically treated patients. The surgical group had a higher prevalence of tibiofemoral OA than did the nonsurgically treated patients (PR = 1.79, 95% CI = 1.14, 2.81). Two studies23,32  defined OA as a Kellgren-Lawrence score of greater than or equal to grade 2. Use of this scale resulted in a reported OA prevalence of 38.5% (95% CI = 30.5%, 47.0%) for surgically treated patients and 35.1% (95% CI = 26.1%, 45.3%) for nonsurgically treated patients. Based on these 2 studies, the prevalence of tibiofemoral OA was similar among both treatment groups (PR = 1.09, 95% CI = 0.77, 1.56). Furthermore, radiographic OA was determined using at least 2 patient positions. Two studies25,41  used full–weight-bearing anteroposterior radiographs with the knee at 0° of extension, and the other 2 studies23,32  used full–weight-bearing anteroposterior radiographs with the knee in 15° of flexion.

This is the first systematic review to report on the prevalence of OA in patients with ACL ruptures treated surgically or nonsurgically based on studies directly comparing these treatments.23,25,27,28,32,41,5456  This approach allowed us to use the PR to compare OA prevalence between the treatments. Unfortunately, because the included studies did not rule out the presence of OA at baseline, the incidence of tibiofemoral OA could not be determined. This limited our systematic review to the evaluation of OA prevalence and the association (ie, the PR) between the treatments. Based on these results, the prevalence of tibiofemoral OA may be greater among surgically treated ACL-deficient patients than among nonsurgically treated ACL-deficient patients. Unfortunately, the lack of methodologic quality and insufficient data in these studies prohibit a conclusive statement. Regardless, the tibiofemoral OA prevalence rates for both treatments were higher than for the general population,65,66  which may suggest that an optimal long-term treatment strategy for preventing tibiofemoral OA after ACL injury is yet to be determined.

Surgical ACL treatments focus on reconstructing the damaged ligament to restore normal knee biomechanics. In contrast, nonsurgical ACL treatment consists of joint mobility training to regain full range of motion, muscle strengthening, and neuromuscular training to promote the restoration of knee function.67  Shortly after injury, both surgical4,1419  and nonsurgical35,46  treatment options appear favorable for the athlete who wants to return to activity. Although the short-term results are promising, the long-term results (10 years or more) of either treatment are less clear. Initial return-to-activity rates for nonsurgical patients appear encouraging, but only 10% to 14% of patients actually returned to their preinjury activity level without limitations.35,45  Furthermore, the rates of ACL-deficient patients who are unable to adequately cope with knee instability and later opt for surgery range from 12% to 39%.35,42,47,68 

One explanation for the increased long-term prevalence of OA after ACL injury is the disruption of joint biochemistry. Immediately after injury, the joint undergoes a cascade of changes (eg, increase in inflammatory mediators and cartilage turnover markers)10,49,69,70  that disrupt the equilibrium between synthesis and catabolism of articular cartilage,71  influencing how articular cartilage and subchondral bone respond to new loading patterns.3,10,49,72  Elevated levels of C-telopeptide fragments in synovial fluid (a biomarker of cartilage degeneration) and matrix metalloproteinases (catabolic enzymes involved in the degradation of the extracellular matrix72,73) occur within hours of ACL rupture; they gradually decrease over the next year but never return to preinjury levels.52,73  In the nonsurgically treated ACL-deficient knee, type II collagen cleavage begins to return to normal at 12 months after injury, whereas type II collagen synthesis remains elevated at 12 and 24 months postinjury.10  At the time of ACL reconstruction surgery, biochemical synthesis and degeneration of type II collagen were elevated in the injured knee compared with the normal knee.52  At 12 months postsurgery, although cleavage of type II collagen has returned to normal limits, synthesis of type II collagen is elevated and remains so through 24 months. At 24 months, aggrecan turnover begins to approach normal levels but is still elevated. Unfortunately, current treatment strategies do not address these biochemical changes to the joint and, therefore, both surgically and nonsurgically treated patients may be susceptible to tibiofemoral OA.

Although ACL reconstruction does not address the aforementioned biochemical concerns, it may correct the disrupted joint kinematics. However, the long-term outcomes are yet to be determined.13,7476  Tashman et al13  used a 3-dimensional radiographic stereophotogrammetric motion-analysis system to determine joint kinematics in 6 ACL-reconstructed patients during downhill running. In all reconstructed knees, the femur was more externally rotated and adducted relative to the tibia than in the uninjured contralateral knee. Vertical loading during heel strike and loading rate directed in line with the tibia were less in patients with reconstructed ACLs than in healthy control participants.75  Collectively, these findings demonstrate persistent altered kinematics and biochemical changes not only postinjury but also postsurgery.

The findings of all studies included in this systematic review were limited by the fact that the type and incidence of meniscal injury were not controlled. Patients who have undergone a meniscal repair or meniscectomy have a higher prevalence of OA than those with no meniscal injury.* In an ACL-deficient knee, which is already experiencing biomechanical and biochemical joint changes, meniscal injuries compound the risk of developing OA by further altering the mechanical loading and contact points on the articular cartilage.12,14,45,75  Meniscal status is important to the long-term OA outcomes of patients with ACL ruptures. In addition, although partial meniscectomies resulted in a greater risk of radiographic changes, the risk was still lower than with total meniscectomies, and substantial function may remain in the residual meniscus.84  However, the potential effect of this remaining tissue on OA risk remains unknown.

The large age range in this systematic review indicates that these results are generalizable to the population with ACL ruptures, but it limits our ability to make inferences about specific groups of patients (eg, high school or college athletes). Although the authors of 2 studies25,41  matched patients according to their Tegner Activity Scale scores, authors of the other studies included patients ranging from high-level European soccer players to more sedentary patients injured in motor vehicle accidents or falls. Patients with various activity levels may react differently to treatment options and may have different risks of OA based on their activity levels (eg, sedentary lifestyle, high-level competition).84,85  Another limitation introduced by the large age range is that some patients may have already had joint degeneration at the time of surgery. Therefore, we could not assess whether incidence rates were different between nonsurgical and surgical treatments for ACL injuries.

It is also important to note that we identified only studies of patients with bone–patellar tendon–bone grafts. Other surgical techniques or grafts, such as the hamstrings tendon graft, were not investigated. Future researchers should evaluate the long-term effectiveness of new surgical approaches and graft selections because evidence suggests that patients reconstructed with hamstrings tendon grafts have lower rates of knee OA than those receiving bone–patellar tendon–bone grafts.8688  Unfortunately, a critical challenge to performing long-term follow-up studies is that new treatment strategies may be adopted as the standard of care before high-quality, long-term follow-up studies can assess their long-term efficacy. This was evident during the study-selection process: a number of groups compared surgical and nonsurgical treatments yet included patients who were immobilized in casts after surgery. This practice is no longer the standard of care, but it was discarded recently enough that an insufficient amount of time has passed to allow degenerative changes to become detectable.

Both the number and quality of studies identified as eligible for inclusion in the systematic review were low. The small number of articles may reflect a publication bias (eg, papers without significant findings were not published). Among the 4 studies, the mean NOS score was 5 of 10 possible points, which was attributed to methodologic weakness and inadequate reporting. Although we redefined certain NOS criteria in an effort to standardize the scoring, this could have resulted in lower study scores because some groups reported details concerning the item being assessed but did not provide enough information to meet the necessary number of criteria to qualify for credit on the NOS.

Although the Kellgren-Lawrence score is the most common method for detecting OA, disagreement exists as to the threshold for determining OA, which has been shown to affect the overall classification of OA.8991  One strength of this systematic review was that we included only articles with direct comparisons: both treatment groups were evaluated using the same diagnostic criteria.23,25,32,41  A limitation to the radiographic OA classification system is the possibility of false-negatives, especially in mild cases, when the diseased compartment or joint is compared with internal controls (ie, opposite compartment [medial versus lateral], contralateral knee). No authors of studies included in this systematic review used diagnostic magnetic resonance imaging, which is more costly than radiographic analysis but also more sensitive to degenerative changes.92 

Furthermore, if we do not know whether tibiofemoral OA was present at baseline, we cannot truly determine the risk of tibiofemoral OA. This is also problematic with respect to previous or subsequent knee injuries and is especially limiting when assessing OA in a strictly athletic population. Future researchers must not only include patients with no signs of radiographic OA at baseline but also be diligent in collecting and reporting both this information and a comprehensive history of previously sustained injuries.

Although the systematic review is designed to present the body of literature concerning a specific topic, our systematic review was limited by insufficient reporting on a number of factors, which greatly limits the results from being generalized to the population of those with ACL ruptures. Authors of the included studies did not report on many factors associated with the development of OA (eg, osteochondral lesions, previous injury). Higher-quality study designs would aid our understanding of how OA develops after surgical or nonsurgical ACL treatment. A randomized controlled trial93  comparing these 2 treatment options is thus far limited to a 2-year follow-up. We need more randomized clinical trials with sufficient posttreatment follow-up and effective control of confounding factors to increase our understanding of surgical versus nonsurgical management of ACL and the incidence of knee OA.

It is also important for future investigators to consider as subcohorts patients who do not undergo reconstruction but instead modify their level of activity (copers, noncopers, and adapters). Assessing the difference between surgical and nonsurgical treatment of ACL ruptures in copers and noncopers can lead to an improved understanding of the true effectiveness of the 2 treatment options by helping us to identify which treatment effectively decreases the episodes of instability and the occurrence of OA. Although some research has been completed to date,93  lengthier follow-up is needed to better assess the development of OA.

To date, no definitive evidence supports surgical or nonsurgical treatment after ACL injury to prevent posttraumatic OA. The prevalence of OA in the included studies was slightly higher in surgically treated than in nonsurgically treated ACL patients at follow-up of approximately 12 years. However, large, overlapping confidence intervals indicate that there is no clear difference. This finding may have clinical importance, but the available studies were methodologically weak. Therefore, a significant relationship cannot be determined between having or not having ACL reconstruction surgery and developing tibiofemoral OA. The current studies were limited by small numbers, low methodologic quality, and a lack of data on confounding factors. Future authors should account for the presence of OA at baseline and focus on directly comparing the surgical and nonsurgical treatment of ACL ruptures while controlling for confounding factors (eg, age, meniscal status, BMI, physical activity).

1
Jarvela
T,
Kannus
P,
Jarvinen
M.
Anterior cruciate ligament reconstruction in patients with or without accompanying injuries: a re-examination of subjects 5 to 9 years after reconstruction
.
Arthroscopy
.
2001
;
17
(
8
):
818
825
.
2
Allen
CR,
Livesay
GA,
Wong
EK,
Woo
SL.
Injury and reconstruction of the anterior cruciate ligament and knee osteoarthritis
.
Osteoarthritis Cartilage
.
1999
;
7
(
1
):
110
121
.
3
Barrance
PJ,
Williams
GN,
Snyder-Mackler
L,
Buchanan
TS.
Do ACL-injured copers exhibit differences in knee kinematics? An MRI study
.
Clin Orthop Relat Res
.
2007
;
454
:
74
80
.
4
Andriacchi
TP,
Dyrby
CO.
Interactions between kinematics and loading during walking for the normal and ACL deficient knee
.
J Biomech
.
2005
;
38
(
2
):
293
298
.
5
Howe
JG,
Johnson
RJ,
Kaplan
MJ,
Fleming
B,
Jarvinen
M.
Anterior cruciate ligament reconstruction using quadriceps patellar tendon graft, part 1: long-term followup
.
Am J Sports Med
.
1991
;
19
(
5
):
447
457
.
6
Kaplan
MJ,
Howe
JG,
Fleming
B,
Johnson
RJ,
Jarvinen
M.
Anterior cruciate ligament reconstruction using quadriceps patellar tendon graft, part 2: a specific sport review
.
Am J Sports Med
.
1991
;
19
(
5
):
458
462
.
7
Lebel
B,
Hulet
C,
Galaud
B,
Burdin
G,
Locker
B,
Vielpeau
C.
Arthroscopic reconstruction of the anterior cruciate ligament using bone–patellar tendon–bone autograft: a minimum 10-year follow-up
.
Am J Sports Med
.
2008
;
36
(
7
):
1275
1282
.
8
Frost-Christensen
LN,
Mastbergen
SC,
Vianen
ME,
et al.
Degeneration, inflammation, regeneration, and pain/disability in dogs following destabilization or articular cartilage grooving of the stifle joint
.
Osteoarthritis Cartilage
.
2008
;
16
(
11
):
1327
1335
.
9
Glasson
SS,
Blanchet
TJ,
Morris
EA.
The surgical destabilization of the medial meniscus (DMM) model of osteoarthritis in the 129/SvEv mouse
.
Osteoarthritis Cartilage
.
2007
;
15
(
9
):
1061
1069
.
10
Nelson
F,
Billinghurst
RC,
Pidoux
I,
et al.
Early post-traumatic osteoarthritis-like changes in human articular cartilage following rupture of the anterior cruciate ligament
.
Osteoarthritis Cartilage
.
2006
;
14
(
2
):
114
119
.
11
Buckland-Wright
JC,
Lynch
JA,
Dave
B.
Early radiographic features in patients with anterior cruciate ligament rupture
.
Ann Rheum Dis
.
2000
;
59
(
8
):
641
646
.
12
Andriacchi
TP,
Briant
PL,
Bevill
SL,
Koo
S.
Rotational changes at the knee after ACL injury cause cartilage thinning
.
Clin Orthop Relat Res
.
2006
;
442
:
39
44
.
13
Tashman
S,
Collon
D,
Anderson
L,
Kolowich
P,
Anderst
W.
Abnormal rotational knee motion during running after anterior cruciate ligament reconstruction
.
Am J Sports Med
.
2004
;
32
(
4
):
975
983
.
14
Andreisek
G,
White
LM,
Sussman
MS,
et al.
Quantitative MR imaging evaluation of the cartilage thickness and subchondral bone area in patients with ACL-reconstructions 7 years after surgery
.
Osteoarthritis Cartilage
.
2009
;
17
(
7
):
871
878
.
15
Ferretti
A,
Conteduca
F,
De Carli
A,
Fontana
M,
Mariani
PP.
Osteoarthritis of the knee after ACL reconstruction
.
Int Orthop
.
1991
;
15
(
4
):
367
371
.
16
Hertel
P,
Behrend
H,
Cierpinski
T,
Musahl
V,
Widjaja
G.
ACL reconstruction using bone-patellar tendon-bone press-fit fixation: 10-year clinical results
.
Knee Surg Sports Traumatol Arthrosc
.
2005
;
13
(
4
):
248
255
.
17
Jomha
NM,
Borton
DC,
Clingeleffer
AJ,
Pinczewski
LA.
Long-term osteoarthritic changes in anterior cruciate ligament reconstructed knees
.
Clin Orthop Relat Res
.
1999
;
358
:
188
193
.
18
Arendt
EA,
Agel
J,
Dick
R.
Anterior cruciate ligament injury patterns among collegiate men and women
.
J Athl Train
.
1999
;
34
(
2
):
86
92
.
19
Sommerlath
K,
Lysholm
J,
Gillquist
J.
The long-term course after treatment of acute anterior cruciate ligament ruptures: a 9 to 16 year follow-up
.
Am J Sports Med
.
1991
;
19
(
2
):
156
162
.
20
Hart
AJ,
Buscombe
J,
Malone
A,
Dowd
GS.
Assessment of osteoarthritis after reconstruction of the anterior cruciate ligament: a study using single-photon emission computed tomography at ten years
.
J Bone Joint Surg Br
.
2005
;
87
(
11
):
1483
1487
.
21
Jonsson
H,
Riklund-Ahlstrom
K,
Lind
J.
Positive pivot shift after ACL reconstruction predicts later osteoarthrosis: 63 patients followed 5–9 years after surgery
.
Acta Orthop Scand
.
2004
;
75
(
5
):
594
599
.
22
Keays
SL,
Newcombe
PA,
Bullock-Saxton
JE,
Bullock
MI,
Keays
AC.
Factors involved in the development of osteoarthritis after anterior cruciate ligament surgery
.
Am J Sports Med
.
2010
;
38
(
3
):
455
463
.
23
Lohmander
LS,
Ostenberg
A,
Englund
M,
Roos
H.
High prevalence of knee osteoarthritis, pain, and functional limitations in female soccer players twelve years after anterior cruciate ligament injury
.
Arthritis Rheum
.
2004
;
50
(
10
):
3145
3152
.
24
Maletius
W,
Messner
K.
Eighteen- to twenty-four-year follow-up after complete rupture of the anterior cruciate ligament
.
Am J Sports Med
.
1999
;
27
(
6
):
711
717
.
25
Meuffels
DE,
Favejee
MM,
Vissers
MM,
Heijboer
MP,
Reijman
M,
Verhaar
JA.
Ten year follow-up study comparing conservative versus operative treatment of anterior cruciate ligament ruptures: a matched-pair analysis of high level athletes
.
Br J Sports Med
.
2009
;
43
(
5
):
347
351
.
26
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
(
3
):
230
237
.
27
Myklebust
G,
Maehlum
S,
Engebretsen
L,
Bahr
R.
Clinical, functional, and radiologic outcome in team handball players 6 to 11 years after anterior cruciate ligament injury: a follow-up study
.
Am J Sports Med
.
2003
;
31
(
6
):
981
989
.
28
Neuman
P,
Englund
M,
Kostogiannis
I,
Friden
T,
Roos
H,
Dahlberg
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
(
9
):
1717
1725
.
29
Pinczewski
LA,
Lyman
J,
Salmon
LJ,
Russell
VJ,
Roe
J,
Linklater
J. A
10-year comparison of anterior cruciate ligament reconstructions with hamstring tendon and patellar tendon autograft: a controlled, prospective trial
.
Am J Sports Med
.
2007
;
35
(
4
):
564
574
.
30
Ruiz
AL,
Kelly
M,
Nutton
RW.
Arthroscopic ACL reconstruction: a 5–9 year follow-up
.
Knee
.
2002
;
9
(
3
):
197
200
.
31
Ait Si Selmi T, Fithian D, Neyret P
.
The evolution of osteoarthritis in 103 patients with ACL reconstruction at 17 years follow-up
.
Knee
.
2006
;
13
(
5
):
353
358
.
32
von Porat
A,
Roos
EM,
Roos
H.
High prevalence of osteoarthritis 14 years after an anterior cruciate ligament tear in male soccer players: a study of radiographic and patient relevant outcomes
.
Ann Rheum Dis
.
2004
;
63
(
3
):
269
273
.
33
Seon
JK,
Song
EK,
Park
SJ.
Osteoarthritis after anterior cruciate ligament reconstruction using a patellar tendon autograft
.
Int Orthop
.
2006
;
30
(
2
):
94
98
.
34
McDaniel
WJ,
Dameron
TB.
Untreated ruptures of the anterior cruciate ligament: a follow-up study
.
J Bone Joint Surg Am
.
1980
;
62
(
5
):
696
705
.
35
Hawkins
RJ,
Misamore
GW,
Merritt
TR.
Follow-up of the acute nonoperated isolated anterior cruciate ligament tear
.
Am J Sports Med
.
1986
;
14
(
3
):
205
210
.
36
Chmielewski
TL,
Hurd
WJ,
Rudolph
KS,
Axe
MJ,
Snyder-Mackler
L.
Perturbation training improves knee kinematics and reduces muscle co-contraction after complete unilateral anterior cruciate ligament rupture
.
Phys Ther
.
2005
;
85
(
8
):
740
749
.
37
Eastlack
ME,
Axe
MJ,
Snyder-Mackler
L.
Laxity, instability, and functional outcome after ACL injury: copers versus noncopers
.
Med Sci Sports Exerc
.
1999
;
31
(
2
):
210
215
.
38
Moksnes
H,
Snyder-Mackler
L,
Risberg
MA.
Individuals with an anterior cruciate ligament-deficient knee classified as noncopers may be candidates for nonsurgical rehabilitation
.
J Orthop Sports Phys Ther
.
2008
;
38
(
10
):
586
595
.
39
Powell
B,
Hurd
W,
Snyder-Mackler
L.
Nonoperative patient management after acute, isolated anterior cruciate ligament injury
.
Athl Ther Today
.
2006
;
11
(
2
):
24
27
.
40
Kannus
P,
Jarvinen
M.
Conservatively treated tears of the anterior cruciate ligament. Long-term results
.
J Bone Joint Surg Am
.
1987
;
69
(
7
):
1007
1012
.
41
Kessler
MA,
Behrend
H,
Henz
S,
Stutz
G,
Rukavina
A,
Kuster
MS.
Function, osteoarthritis and activity after ACL-rupture: 11 years follow-up results of conservative versus reconstructive treatment
.
Knee Surg Sports Traumatol Arthrosc
.
2008
;
16
(
5
):
442
448
.
42
McDaniel
WJ,
Dameron
TB.
The untreated anterior cruciate ligament rupture
.
Clin Orthop Relat Res
.
1983
;
172
:
158
163
.
43
Pattee
GA,
Fox
JM,
Del Pizzo
W,
Friedman
MJ.
Four to ten year follow-up of unreconstructed anterior cruciate ligament tears
.
Am J Sports Med
.
1989
;
17
(
3
):
430
435
.
44
Noyes
FR,
Mooar
PA,
Matthews
DS,
Butler
DL.
The symptomatic anterior cruciate-deficient knee, part I: the long-term functional disability in athletically active individuals
.
J Bone Joint Surg Am
.
1983
;
65
(
2
):
154
162
.
45
Fowler
PJ,
Regan
WD.
The patient with symptomatic chronic anterior cruciate ligament insufficiency: results of minimal arthroscopic surgery and rehabilitation
.
Am J Sports Med
.
1987
;
15
(
4
):
321
325
.
46
Giove
TP,
Miller
SJ,
Kent
BE,
Sanford
TL,
Garrick
JG.
Nonoperative treatment of the torn anterior cruciate ligament
.
J Bone Joint Surg Am
.
1983
;
65
(
2
):
184
192
.
47
Noyes
FR,
Matthews
DS,
Mooar
PA,
Grood
ES.
The symptomatic anterior cruciate-deficient knee. Part II: the results of rehabilitation, activity modification, and counseling on functional disability
.
J Bone Joint Surg Am
.
1983
;
65
(
2
):
163
174
.
48
Kostogiannis
I,
Ageberg
E,
Neuman
P,
Dahlberg
L,
Friden
T,
Roos
H.
Activity level and subjective knee function 15 years after anterior cruciate ligament injury: a prospective, longitudinal study of nonreconstructed patients
.
Am J Sports Med
.
2007
;
35
(
7
):
1135
1143
.
49
Marks
PH,
Donaldson
ML.
Inflammatory cytokine profiles associated with chondral damage in the anterior cruciate ligament-deficient knee
.
Arthroscopy
.
2005
;
21
(
11
):
1342
1347
.
50
Roos
H,
Adalberth
T,
Dahlberg
L,
Lohmander
LS.
Osteoarthritis of the knee after injury to the anterior cruciate ligament or meniscus: the influence of time and age
.
Osteoarthritis Cartilage
.
1995
;
3
(
4
):
261
267
.
51
Noyes
FR,
Mangine
RE,
Barber
S.
Early knee motion after open and arthroscopic anterior cruciate ligament reconstruction
.
Am J Sports Med
.
1987
;
15
(
2
):
149
160
.
52
Beynnon
BD,
Uh
BS,
Johnson
RJ,
et al.
Rehabilitation after anterior cruciate ligament reconstruction: a prospective, randomized, double-blind comparison of programs administered over 2 different time intervals
.
Am J Sports Med
.
2005
;
33
(
3
):
347
359
.
53
Andersson
C,
Odensten
M,
Good
L,
Gillquist
J.
Surgical or non-surgical treatment of acute rupture of the anterior cruciate ligament: a randomized study with long-term follow-up
.
J Bone Joint Surg Am
.
1989
;
71
(
7
):
965
974
.
54
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
644
.
55
O'Brien
WR.
Degenerative arthritis of the knee following anterior cruciate ligament injury: role of the meniscus
.
Sports Med Arthrosc Rev
.
1993
;
1
(
2
):
114
118
.
56
Zysk
SP,
Refior
HJ.
Operative or conservative treatment of the acutely torn anterior cruciate ligament in middle-aged patients: a follow-up study of 133 patients between the ages of 40 and 59 years
.
Arch Orthop Trauma Surg
.
2000
;
120
(
1–2
):
59
64
.
57
Moher
D,
Liberati
A,
Tetzlaff
J,
Altman
DG,
PRISMA Group. Preferred reporting items for systematic reviews and meta-analyses: the PRISMA statement
.
J Clin Epidemiol
.
2009
;
62
(
10
):
1006
1012
.
58
The Cochrane Collaboration Review Group on HIV Infection and AIDS
.
Editorial policy: inclusion and appraisal of experimental and non-experimental (observational) studies
.
June
2014
.
59
Hootman
JM,
Driban
JB,
Sitler
MR,
Harris
KP,
Cattano
NM.
Reliability and validity of three quality rating instruments for systematic reviews of observational studies
.
Res Synth Methods
.
2011
;
2
(
2
):
110
118
.
60
Beynnon
BD,
Johnson
RJ,
Naud
S,
et al.
Accelerated versus nonaccelerated rehabilitation after anterior cruciate ligament reconstruction: a prospective, randomized, double-blind investigation evaluating knee joint laxity using roentgen stereophotogrammetric analysis
.
Am J Sports Med
.
2011
;
39
(
12
):
2536
2548
.
61
Bowers
AL,
Spindler
KP,
McCarty
EC,
Arrigain
S.
Height, weight, and BMI predict intra-articular injuries observed during ACL reconstruction: evaluation of 456 cases from a prospective ACL database
.
Clin J Sport Med
.
2005
;
15
(
1
):
9
13
.
62
Li
RT,
Lorenz
S,
Xu
Y,
Harner
CD,
Fu
FH,
Irrgang
JJ.
Predictors of radiographic knee osteoarthritis after anterior cruciate ligament reconstruction
.
Am J Sports Med
.
2011
;
39
(
12
):
2595
2603
.
63
Portney
LG,
Watkins
MP.
Foundations of Clinical Research: Applications to Practice
.
Norwalk, CT
:
Appleton & Lange;
1993
.
64
Kellgren
JH,
Lawrence
JS.
Radiological assessment of osteoarthrosis
.
Ann Rheum Dis
.
1957
;
16
(
4
):
494
502
.
65
Jordan
JM,
Helmick
CG,
Renner
JB,
et al.
Prevalence of knee symptoms and radiographic and symptomatic knee osteoarthritis in African Americans and Caucasians: the Johnston County Osteoarthritis Project
.
J Rheumatol
.
2007
;
34
(
1
):
172
180
.
66
Felson
DT,
Naimark
A,
Anderson
J,
Kazis
L,
Castelli
W,
Meenan
RF.
The prevalence of knee osteoarthritis in the elderly: the Framingham Osteoarthritis Study
.
Arthritis Rheum
.
1987
;
30
(
8
):
914
918
.
67
von Porat
A,
Henriksson
M,
Holmström
E,
Roos
EM.
Knee kinematics and kinetics in former soccer players with a 16-year-old ACL injury: the effects of twelve weeks of knee-specific training
.
BMC Musculoskelet Disord
.
2007
;
8
:
35
.
68
McErlain
DD,
Appleton
CT,
Litchfield
RB,
et al.
Study of subchondral bone adaptations in a rodent surgical model of OA using in vivo micro-computed tomography
.
Osteoarthritis Cartilage
.
2008
;
16
(
4
):
458
469
.
69
Lohmander
LS,
Atley
LM,
Pietka
TA,
Eyre
DR.
The release of crosslinked peptides from type II collagen into human synovial fluid is increased soon after joint injury and in osteoarthritis
.
Arthritis Rheum
.
2003
;
48
(
11
):
3130
3139
.
70
Cameron
ML,
Fu
FH,
Paessler
HH,
Schneider
M,
Evans
CH.
Synovial fluid cytokine concentrations as possible prognostic indicators in the ACL-deficient knee
.
Knee Surg Sports Traumatol Arthrosc
.
1994
;
2
(
1
):
38
44
.
71
Andriacchi
TP,
Mundermann
A,
Smith
RL,
Alexander
EJ,
Dyrby
CO,
Koo
S.
A framework for the in vivo pathomechanics of osteoarthritis at the knee
.
Ann Biomed Eng
.
2004
;
32
(
3
):
447
457
.
72
Jarvela
T,
Paakkala
T,
Kannus
P,
Jarvinen
M.
The incidence of patellofemoral osteoarthritis and associated findings 7 years after anterior cruciate ligament reconstruction with a bone-patellar tendon-bone autograft
.
Am J Sports Med
.
2001
;
29
(
1
):
18
24
.
73
Pearle
AD,
Warren
RF,
Rodeo
SA.
Basic science of articular cartilage and osteoarthritis
.
Clin Sports Med
.
2005
;
24
(
1
):
1
12
.
74
Shefelbine
SJ,
Ma
CB,
Lee
KY,
et al.
MRI analysis of in vivo meniscal and tibiofemoral kinematics in ACL-deficient and normal knees
.
J Orthop Res
.
2006
;
24
(
6
):
1208
1217
.
75
Timoney
JM,
Inman
WS,
Quesada
PM,
et al.
Return of normal gait patterns after anterior cruciate ligament reconstruction
.
Am J Sports Med
.
1993
;
21
(
6
):
887
889
.
76
Kinds
MB,
Vincken
KL,
Hoppinga
TN,
et al.
Influence of variation in semiflexed knee positioning during image acquisition on separate quantitative radiographic parameters of osteoarthritis, measured by Knee Images Digital Analysis
.
Osteoarthritis Cartilage
.
2012
;
20
(
9
):
997
1003
.
77
Marcacci
M,
Zaffagnini
S,
Giordano
G,
Iacono
F,
Presti
ML.
Anterior cruciate ligament reconstruction associated with extra-articular tenodesis: a prospective clinical and radiographic evaluation with 10- to 13-year follow-up
.
Am J Sports Med
.
2009
;
37
(
4
):
707
714
.
78
Shelbourne
KD,
Gray
T.
Anterior cruciate ligament reconstruction with autogenous patellar tendon graft followed by accelerated rehabilitation: a two- to nine-year follow-up
.
Am J Sports Med
.
1997
;
25
(
6
):
786
795
.
79
Hunter
DJ.
Imaging insights on the epidemiology and pathophysiology of osteoarthritis
.
Rheum Dis Clin North Am
.
2009
;
35
(
3
):
447
463
.
80
Kessler
MA,
Stutz
G,
Behrend
H,
Rukavina
A,
Kuster
M.
Is ACL reconstruction necessary to prevent osteoarthritis? 12 year follow up results after non-operative treatment of ACL rupture [abstract]
.
Br J Sports Med
.
2005
;
39
(
6
):
393
.
81
Lynch
MA,
Henning
CE,
Glick
KR.
Knee joint surface changes: long-term follow-up meniscus tear treatment in stable anterior cruciate ligament reconstructions
.
Clin Orthop Relat Res
.
1983
;
172
:
148
153
.
82
Walla
DJ,
Albright
JP,
McAuley
E,
Martin
RK,
Eldridge
V,
El-Khoury
G.
Hamstring control and the unstable anterior cruciate ligament-deficient knee
.
Am J Sports Med
.
1985
;
13
(
1
):
34
39
.
83
Englund
M,
Guermazi
A,
Lohmander
LS.
The meniscus in knee osteoarthritis
.
Rheum Dis Clin North Am
.
2009
;
35
(
3
):
579
590
.
84
Scarvell
JM,
Smith
PN,
Refshauge
KM,
Galloway
H,
Woods
K.
Comparison of kinematics in the healthy and ACL injured knee using MRI
.
J Biomech
.
2005
;
38
(
2
):
255
262
.
85
Snyder-Mackler
L,
Fitzgerald
GK,
Bartolozzi
AR,
Ciccotti
MG.
The relationship between passive joint laxity and functional outcome after anterior cruciate ligament injury
.
Am J Sports Med
.
1997
;
25
(
2
):
191
195
.
86
Rudolph
KS,
Eastlack
ME,
Axe
MJ,
Snyder-Mackler
L.
1998 Basmajian Student Award Paper: Movement patterns after anterior cruciate ligament injury: a comparison of patients who compensate well for the injury and those who require operative stabilization
.
J Electromyogr Kinesiol
.
1998
;
8
(
6
):
349
362
.
87
Leys
T,
Salmon
L,
Waller
A,
Linklater
J,
Pinczewski
L.
Clinical results and risk factors for reinjury 15 years after anterior cruciate ligament reconstruction: a prospective study of hamstring and patellar tendon grafts
.
Am J Sports Med
.
2012
;
40
(
3
):
595
605
.
88
Sajovic
M,
Strahovnik
A,
Dernovsek
MZ,
Skaza
K.
Quality of life and clinical outcome comparison of semitendinosus and gracilis tendon versus patellar tendon autografts for anterior cruciate ligament reconstruction: an 11-year follow-up of a randomized controlled trial
.
Am J Sports Med
.
2011
;
39
(
10
):
2161
2169
.
89
Spector
TD,
Cooper
C.
Radiographic assessment of osteoarthritis in population studies: whither Kellgren and Lawrence?
Osteoarthritis Cartilage
.
1993
;
1
(
4
):
203
206
.
90
Altman
R,
Asch
E,
Bloch
D,
et al.
Development of criteria for the classification and reporting of osteoarthritis: classification of osteoarthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association
.
Arthritis Rheum
.
1986
;
29
(
8
):
1039
1049
.
91
Schiphof
D,
de Klerk
BM,
Kerkhof
HJ,
et al.
Impact of different descriptions of the Kellgren and Lawrence classification criteria on the diagnosis of knee osteoarthritis
.
Ann Rheum Dis
.
2011
;
70
(
8
):
1422
1427
.
92
Frobell
RB,
Le Graverand
MP,
Buck
R,
et al.
The acutely ACL injured knee assessed by MRI: changes in joint fluid, bone marrow lesions, and cartilage during the first year
.
Osteoarthritis Cartilage
.
2009
;
17
(
2
):
161
167
.
93
Frobell
RB,
Roos
EM,
Roos
HP,
Ranstam
J,
Lohmander
LS.
A randomized trial of treatment for acute anterior cruciate ligament tears
.
N Engl J Med
.
2010
;
363
(
4
):
331
342
.
*

References 2,19,22,24,26,31,33,34,45,7681 .

References 2,15,1922,24,26,31,33,34,41,77,8183 .

Appendix. 

Newcastle-Ottawa Scale Scores

Newcastle-Ottawa Scale Scores
Newcastle-Ottawa Scale Scores