scholarly journals High genetic contribution to anterior cruciate ligament rupture: Heritability ~69%

2020 ◽  
pp. bjsports-2020-102392
Author(s):  
Karin Magnusson ◽  
Aleksandra Turkiewicz ◽  
Velocity Hughes ◽  
Richard Frobell ◽  
Martin Englund
Keyword(s):  
Anterior Cruciate Ligament ◽  
Genetic Risk ◽  
Cruciate Ligament ◽  
Familial Risk ◽  
Acl Rupture ◽  
Genetic Contribution ◽  
Study Approach ◽  
Healthcare Data ◽  
High Genetic Risk ◽  
Anterior Cruciate

ObjectivesWe aimed to determine the lifetime genetic risk for anterior cruciate ligament (ACL) rupture.MethodsWe used a twin study approach, linking the Swedish Twin Register with national healthcare data to form a 30 year, population wide, longitudinal twin cohort. We studied ACL rupture in this cohort of 88 414 identical and fraternal twins, aged ≥17 years, to determine the familial risk and heritability of ACL rupture.ResultsThe incidence rate of ACL rupture was 70 (95% CI 66 to 74) per 100 000 person years. The familial risk, which is the excess risk ratio (RR) of the second twin having ACL rupture given that the first twin has had such a rupture, was higher in identical twin pairs (RR=8.6, 95% CI 6.2 to 11.0) than in fraternal twin pairs (RR=1.9, 95% CI 0.9 to 3.0). The overall heritability of ACL rupture was high, 69% (95% CI 47 to 91), increasing from 60% at age 17 years to 80% at age 60 years. Women and men had similar familial risk and heritability of ACL rupture.ConclusionThe genetic contribution to ACL rupture of ~69% is high and suggests strong familial clustering. If clinicians recognise the high genetic risk of such injury, they may be better able to counsel athletes whose near relatives have had ACL rupture.

Anterior Cruciate Ligament Rupture Associated with Cardiomyopathy in Three Cats

1991 ◽  
Vol 4 (01) ◽  
pp. 35-37 ◽  
Author(s):  
G. O. Janssens ◽  
D. L. Janssens ◽  
L. A. A. Janssens
Keyword(s):  
Anterior Cruciate Ligament ◽  
Cruciate Ligament ◽  
Anterior Cruciate Ligament Rupture ◽  
Acl Rupture ◽  
Thoracic Radiography ◽  
Ligament Rupture ◽  
Cruciate Ligament Rupture ◽  
Previous Trauma ◽  
History Of ◽  
Anterior Cruciate

SummaryOver a period of 14 years, three cats with anterior cruciate ligament (ACL) rupture were seen in our practice. In all, the rupture had occurred without a history of previous trauma. All were treated surgically. All died within a period of 14 days. The reason of death was in all cases cardiomyopathy. We now suggest that cats with rupture of the anterior cruciate ligament undergo an electrocardiographic recording and eventually an thoracic radiography before surgery is considered. We also suggest that cats with ACL rupture should preferably be treated conservatively.

The Femoral Footprint Position of the Anterior Cruciate Ligament Might Be a Predisposing Factor to a Noncontact Anterior Cruciate Ligament Rupture

2019 ◽  
Vol 47 (14) ◽  
pp. 3365-3372 ◽  
Author(s):  
Dimitris Dimitriou ◽  
Zhongzheng Wang ◽  
Diyang Zou ◽  
Tsung-Yuan Tsai ◽  
Naeder Helmy
Keyword(s):  
Anterior Cruciate Ligament ◽  
Matched Control ◽  
Cruciate Ligament ◽  
Magnetic Resonance Images ◽  
Small Sample ◽  
Transverse Plane ◽  
Acl Rupture ◽  
Coronal Plane ◽  
Predisposing Factor ◽  
Anterior Cruciate

Background: Although the femoral tunnel position is crucial to anatomic single-bundle anterior cruciate ligament (ACL) reconstruction, the recommendations for the ideal femoral footprint position are mostly based on cadaveric studies with small sample sizes, elderly patients with unknown ACL status, and 2-dimensional techniques. Furthermore, a potential difference in the femoral ACL footprint position and ACL orientation between ACL-ruptured and ACL-intact knees has not been reported in the literature. Hypothesis: The femoral ACL footprint position and ACL orientation vary significantly between ACL-ruptured and matched control ACL-intact knees. Study Design: Cross-sectional study; Level of evidence, 3. Methods: Magnetic resonance images of the knees of 90 patients with an ACL rupture and 90 matched control participants who had a noncontact knee injury without an ACL rupture were used to create 3-dimensional models of the femur and tibia. The ACL footprints were outlined on each model, and their positions (normalized to the lateral condyle width) as well as ACL orientations were measured with an anatomic coordinate system. Results: The femoral ACL footprint in patients with an ACL rupture was located at 36.6% posterior and 11.2% distal to the flexion-extension axis (FEA). The ACL orientation was 46.9° in the sagittal plane, 70.3° in the coronal plane, and 20.8° in the transverse plane. The ACL-ruptured group demonstrated a femoral ACL footprint position that was 11.0% more posterior and 7.7% more proximal than that of the control group (all P < .01). The same patients also exhibited 5.7° lower sagittal elevation, 3.1° higher coronal plane elevation, and 7.9° lower transverse plane deviation (all P < .01). The optimal cutoff value of the femoral ACL footprint position to prevent an ACL rupture was at 30% posterior and 12% distal to the FEA. Conclusion: The ACL femoral footprint position might be a predisposing factor to an ACL rupture. Patients with a >30% posterior and <12% distal position of the femoral ACL footprint from the FEA might have a 51.2-times increased risk of an ACL rupture.

scholarly journals No Association Between Risk of Anterior Cruciate Ligament Rupture and Selected Candidate Collagen Gene Variants in Female Elite Athletes From High-Risk Team Sports

2018 ◽  
Vol 47 (1) ◽  
pp. 52-58 ◽  
Author(s):  
Einar Andreas Sivertsen ◽  
Kari Bente Foss Haug ◽  
Eirik Klami Kristianslund ◽  
Anne-Marie Siebke Trøseid ◽  
Jari Parkkari ◽  
...  
Keyword(s):  
Anterior Cruciate Ligament ◽  
High Risk ◽  
Elite Athletes ◽  
Cruciate Ligament ◽  
Team Sports ◽  
Acl Injury ◽  
Acl Rupture ◽  
Acl Injuries ◽  
Genes Encoding ◽  
Anterior Cruciate

Background: Several single-nucleotide variants (SNVs) in collagen genes have been reported as predisposing factors for anterior cruciate ligament (ACL) tears. However, the evidence is conflicting and does not support a clear association between genetic variants and risk of ACL ruptures. Purpose: To assess the association of previously identified candidate SNVs in genes encoding for collagen and the risk of ACL injury in a population of elite female athletes from high-risk team sports. Study Design: Cohort study; Level of evidence, 2. Methods: A total of 851 female Norwegian and Finnish elite athletes from team sports were included from 2007 to 2011. ACL injuries acquired before inclusion in the cohort were registered by interview. The participants were followed prospectively through 2015 to record new complete ACL injuries. Six selected SNVs were genotyped ( COL1A1: rs1800012, rs1107946; COL3A1: rs1800255; COL5A1: rs12722, rs13946; COL12A1: rs970547). Results: No associations were found between ACL rupture and the SNVs tested. Conclusion: The study does not support a role of the 6 selected SNVs in genes encoding for collagen proteins as risk factors for ACL injury. Clinical Relevance: Genetic profiling to identify athletes at high risk for ACL rupture is not yet feasible.

scholarly journals Anterior Cruciate Ligament Rupture and Osteoarthritis Progression

2012 ◽  
Vol 6 (1) ◽  
pp. 295-300 ◽  
Author(s):  
James Min-Leong Wong ◽  
Tanvir Khan ◽  
Chethan S Jayadev ◽  
Wasim Khan ◽  
David Johnstone
Keyword(s):  
Anterior Cruciate Ligament ◽  
Acl Reconstruction ◽  
Cruciate Ligament ◽  
Degenerative Change ◽  
Acl Rupture ◽  
Osteoarthritis Progression ◽  
Anterior Cruciate ◽  
The Relationship ◽  
Meniscal Damage ◽  
Acl Deficient

Anterior Cruciate Ligament (ACL) rupture is a common sporting injury that frequently affects young, athletic patients. Apart from the functional problems of instability, patients with ACL deficient knees also develop osteoarthritis. Although this is frequently cited as an indication for ACL reconstruction, the relationship between ACL rupture, reconstruction and the instigation and progression of articular cartilage degenerative change is controversial. The purpose of this paper is to review the published literature with regards ACL rupture and the multifactorial causes for osteoarthritis progression, and whether or not this is slowed or stopped by ACL reconstruction. There is no evidence in the published literature to support the view that ACL reconstruction prevents osteoarthritis, although it may prevent further meniscal damage. It must be recognised that this conclusion is based on the current literature which has substantial methodological limitations.

Genetic risk factors for anterior cruciate ligament ruptures: COL1A1 gene variant

2009 ◽  
Vol 43 (5) ◽  
pp. 352-356 ◽  
Author(s):  
M Posthumus ◽  
A V September ◽  
M Keegan ◽  
D O'Cuinneagain ◽  
W Van der Merwe ◽  
...  
Keyword(s):  
Risk Factors ◽  
Anterior Cruciate Ligament ◽  
Genetic Risk ◽  
Cruciate Ligament ◽  
Genetic Risk Factors ◽  
Gene Variant ◽  
Col1a1 Gene ◽  
Anterior Cruciate

Matrix Metalloproteinase Inhibition With Doxycycline Affects the Progression of Posttraumatic Osteoarthritis After Anterior Cruciate Ligament Rupture: Evaluation in a New Nonsurgical Murine ACL Rupture Model

2019 ◽  
Vol 48 (1) ◽  
pp. 143-152 ◽  
Author(s):  
Xueying Zhang ◽  
Xiang-Hua Deng ◽  
Zhe Song ◽  
Brett Croen ◽  
Camila B. Carballo ◽  
...  
Keyword(s):  
Anterior Cruciate Ligament ◽  
Matrix Metalloproteinase ◽  
Untreated Control ◽  
Cruciate Ligament ◽  
Cartilage Damage ◽  
Acl Rupture ◽  
Male Mice ◽  
Posttraumatic Osteoarthritis ◽  
Rupture Model ◽  
Anterior Cruciate

Background: Doxycycline has broad-spectrum activity as a matrix metalloproteinase (MMP) inhibitor and thus could reduce the progression of posttraumatic osteoarthritis (PTOA) after anterior cruciate ligament (ACL) rupture. Hypothesis: Doxycycline would inhibit progression of PTOA in a murine ACL rupture model. Study Design: Controlled laboratory study. Methods: For the in vitro study, cadaveric C57BL/6 male mice knees (N = 108) were used for the development of a nonsurgical ACL rupture model. For the in vivo study, 24 C57BL/6 male mice then underwent ACL rupture with our manual procedure and were divided into 4 groups: untreated control; doxycycline, 10 mg/kg/d; doxycycline, 50 mg/kg/d; and doxycycline, 100 mg/kg/d. Doxycycline was administered in drinking water beginning immediately after ACL rupture. Radiographic imaging and paw prints were evaluated at 3, 7, 14, and 28 days. The foot length and toe spread were analyzed as measures of function. Histology and MMP-13 immunohistochemistry were done at 4 weeks. Results: Radiographs demonstrated anterior tibial subluxation and meniscal extrusion after ACL rupture, confirming knee joint instability without fractures. Statistically significant differences in gait were found between the intact and experimental groups. Histologic examination demonstrated cartilage damage, meniscal tears, and mild osteoarthritis after ACL rupture, similar to what occurs in human patients. Hypertrophy of the posterior horn of the medial and lateral meniscus was found, and tears of the posterior horn of the menisci were common. All doxycycline groups had a lower score than the untreated control group, indicating less cartilage damage. The posterior tibia of the untreated group had the most cartilage damage as compared with the 3 doxycycline groups, with a significant difference between the untreated and 50-mg/kg/d doxycycline groups, suggesting that the latter dose may protect against proteoglycan loss and decrease the progression of osteoarthritis. The nondoxycycline group had the highest synovial inflammation score among all groups, indicating that doxycycline has an inhibitory effect on synovitis. There was significantly lower MMP-13 expression on the tibia in the doxycycline-treated groups, with a positive correlation between doxycycline concentration and MMP-13 inhibition. Conclusion: Modulation of MMP-13 activity by doxycycline treatment may offer a novel biological pathway to decrease the progression of PTOA after ACL rupture. Clinical Relevance: Doxycycline is an approved, readily available drug with infrequent side effects of photosensitivity and gastrointestinal symptoms. Future clinical trials could evaluate doxycycline to reduce or prevent progressive cartilage damage after ACL rupture.

scholarly journals Generation of stem cell-based bioartificial anterior cruciate ligament (ACL) grafts for effective ACL rupture repair

2016 ◽  
Vol 17 (2) ◽  
pp. 448-457 ◽  
Author(s):  
Dimitrios Kouroupis ◽  
Athena Kyrkou ◽  
Eleni Triantafyllidi ◽  
Michalis Katsimpoulas ◽  
George Chalepakis ◽  
...  
Keyword(s):  
Anterior Cruciate Ligament ◽  
Stem Cell ◽  
Cruciate Ligament ◽  
Acl Rupture ◽  
Anterior Cruciate

Evaluating Different Criteria to Diagnose ACL Rupture Using a Knee Arthrometer

2009 ◽  
Author(s):  
Damoon Soudbakhsh ◽  
Mohammad-Naghi Tahmasebi ◽  
Mohamad Parnianpour
Keyword(s):  
Anterior Cruciate Ligament ◽  
Cruciate Ligament ◽  
Knee Injuries ◽  
Acl Rupture ◽  
Ligament Injuries ◽  
Acl Injuries ◽  
Anterior Laxity ◽  
Anterior Cruciate

Every year many people suffer from knee injuries. Previous studies on patients with knee injuries has shown that about 40% percent of knee injuries are ligament injuries, and about 50% of the ligament injuries are the Anterior Cruciate Ligament (ACL) injuries [1–2]. Knee arthrometers are widely used to diagnose ACL injuries, along with other methods [3–4]. In the current research, a knee arthrometer which was developed to provide an accurate measurement of AP displacement of the knee [5] was used to measure anterior laxity of the knees of 20 subjects, and the results were analyzed to find better criteria to diagnose ACL rupture using knee arthrometers.

scholarly journals Early Patellofemoral Cartilage and Bone Degeneration in a Rat Model of Noninvasive Anterior Cruciate Ligament Rupture

2021 ◽  
Author(s):  
Samantha E. Hartner ◽  
Michael D. Newton ◽  
Mackenzie M. Fleischer ◽  
Kevin C. Baker ◽  
Tristan Maerz
Keyword(s):  
Anterior Cruciate Ligament ◽  
Articular Cartilage ◽  
Rat Model ◽  
Patellofemoral Joint ◽  
Cruciate Ligament ◽  
Acl Rupture ◽  
Post Injury ◽  
Ligament Rupture ◽  
Contrast Enhanced ◽  
Anterior Cruciate

ABSTRACTBackgroundAnterior cruciate ligament rupture (ACLR) is a well-known risk factor for the development of post-traumatic osteoarthritis (PTOA). While clinical and pre-clinical studies have characterized the onset and progression of PTOA in the tibiofemoral joint compartment, very little is known about degenerative changes in the patellofemoral compartment after ACL injury.Hypothesis/PurposeTo evaluate the extent to which ACL rupture induces acute patellofemoral joint degeneration by quantifying articular cartilage morphology and remodeling of subchondral and trabecular bone microarchitecture in the patellofemoral compartment.Study DesignDescriptive laboratory study.MethodsAdult female Lewis rats were randomized to undergo either a non-surgical ACL rupture or a Sham procedure (n = 6 per group). Ex vivo contrast-enhanced micro-computed tomography (µCT) and histological evaluation of the patellofemoral compartment were performed at 2-weeks post-injury, representing a timepoint of documented early PTOA in the tibiofemoral compartment in this model.ResultsACL rupture causes osteophyte formation in the patella and mild degeneration in the superficial zone of articular cartilage (AC), including surface fibrillation, fissures, increased cellularity, and abnormal chondrocyte clustering at two weeks post-injury. Contrast-enhanced µCT analysis demonstrates significant increases in AC thickness of patellar and trochlear cartilage. Loss of subchondral bone thickness, bone volume fraction, and tissue mineral density, as well as changes to trabecular microarchitecture in both the patella and trochlea, were indicative of catabolic bone remodeling.ConclusionThese results demonstrate that the patellofemoral joint develops mild but evident degenerative changes in the acute time period following ACL rupture, extending the utility of this rat model to the study of degenerative patellofemoral changes following joint trauma.Clinical RelevanceACL rupture causes mild degeneration and swelling of articular cartilage, coupled with catabolic bone remodeling in the patellofemoral compartment. Characterizing the pathophysiology of patellofemoral PTOA in its early stages may provide a better understanding of disease progression and provide opportunities for preventative therapeutic intervention.

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