Evidence map›Paper›PMID 26792705›Full record

ArticleThe American journal of sports medicine2016

Abnormal Mechanical Loading Induces Cartilage Degeneration by Accelerating Meniscus Hypertrophy and Mineralization After ACL Injuries In Vivo.

Guoqing Du, Hongsheng Zhan, Daofang Ding, Shaowei Wang, Xiaochun Wei, Fangyuan Wei, Jianzhong Zhang, Bahar Bilgen, Anthony M Reginato, Braden C Fleming and 2 more

Abstract read
In one paragraph

Article in The American journal of sports medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.8field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 47 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 8 institutions in 2 countries.

Guoqing DuShi's Center of Orthopedics and Traumatology, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China Institute of Traumatology & Orthopedics, Shanghai Academy of Traditional Chinese Medicine, Shanghai, China Department of Orthopaedics, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, Rhode Island, USA.
Hongsheng ZhanShi's Center of Orthopedics and Traumatology, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China Institute of Traumatology & Orthopedics, Shanghai Academy of Traditional Chinese Medicine, Shanghai, China.
Daofang DingShi's Center of Orthopedics and Traumatology, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China Institute of Traumatology & Orthopedics, Shanghai Academy of Traditional Chinese Medicine, Shanghai, China.
Shaowei WangDepartment of Orthopaedics, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, Rhode Island, USA Department of Orthopaedics, The Second Hospital, Shanxi Medical University, Taiyuan, China.
Xiaochun WeiDepartment of Orthopaedics, The Second Hospital, Shanxi Medical University, Taiyuan, China.
Fangyuan WeiFoot and Ankle Orthopaedic Surgery Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Jianzhong ZhangFoot and Ankle Orthopaedic Surgery Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Bahar BilgenDepartment of Orthopaedics, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, Rhode Island, USA Providence VA Medical Center, Providence, Rhode Island, USA.
Anthony M ReginatoDivision of Rheumatology, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, Rhode Island, USA.
Braden C FlemingDepartment of Orthopaedics, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, Rhode Island, USA.
Jin DengDepartment of Orthopaedics, Affiliated Hospital of Guiyang Medical University, Guiyang, China.
Lei WeiDepartment of Orthopaedics, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, Rhode Island, USA Department of Orthopaedics, The Second Hospital, Shanxi Medical University, Taiyuan, China lei_wei@brown.edu.
Beijing Tongren Hospital · CNBrown University · USRhode Island Hospital · USShanghai University of Traditional Chinese Medicine · CNGuiyang Medical University · CNSecond Hospital of Shanxi Medical University · CNShanxi Medical University · CNShuguang Hospital · CN

Funding

COBRE for Skeletal Health and RepairP20GM104937 · NIGMS · RHODE ISLAND HOSPITAL · PI CHEN, QIAN · 2012 to 2016
$10.8M
Histone Deacetylation Regulates Growth Plate DevelopmentR01AR059142 · NIAMS · RHODE ISLAND HOSPITAL · PI WEI, LEI · 2011 to 2015
$1.5M
Design of an Engineered Cartilage Biocomposite for Joint RehabilitationIK2RX000760 · VA · PROVIDENCE VA MEDICAL CENTER · PI BILGEN, BAHAR · 2012 to 2017
–
NIAMS NIH HHS R01 AR059142NIAMS NIH HHS R01AR059142NIGMS NIH HHS P20 GM104937NIGMS NIH HHS P20GM104937RRD VA IK2 RX000760
6 · The paper itself

Abstract

backgroundAlthough patients with an anterior cruciate ligament (ACL) injury have a high risk of developing posttraumatic osteoarthritis (PTOA), the role of meniscus hypertrophy and mineralization in PTOA after an ACL injury remains unknown. PURPOSE/HYPOTHESIS: The purpose of this study was to determine if menisci respond to abnormal loading and if an ACL injury results in meniscus hypertrophy and calcification. The hypotheses were that (1) abnormal mechanical loading after an ACL injury induces meniscus hypertrophy and mineralization, which correlates to articular cartilage damage in vivo, and (2) abnormal mechanical loading on bovine meniscus explants induces the overexpression of hypertrophic and mineralization markers in vitro. STUDY

designControlled laboratory study.

methodsIn vivo guinea pig study (hypothesis 1): Three-month-old male Hartley guinea pigs (n = 9) underwent ACL transection (ACLT) on the right knee; the left knee served as the control. Calcification in the menisci was evaluated by calcein labeling 1 and 5 days before knee harvesting at 5.5 months. Cartilage and meniscus damage and mineralization were quantified by the Osteoarthritis Research Society International score and meniscus grade, respectively. Indian hedgehog (Ihh), matrix metalloproteinase-13 (MMP-13), collagen type X (Col X), progressive ankylosis homolog (ANKH), ectonucleotide pyrophosphatase/phosphodiesterase-1 (ENPP1), alkaline phosphatase (ALP), inorganic pyrophosphate (PPi), and inorganic phosphate (Pi) concentrations were evaluated by immunohistochemistry and enzyme-linked immunosorbent assay. In vitro bovine meniscus explant study (hypothesis 2): Bovine meniscus explants were subjected to 25% strain at 0.3 Hz for 1, 2, and 3 hours. Cell viability was determined using live/dead staining. The levels of mRNA expression and protein levels were measured using real-time quantitative reverse transcription polymerase chain reaction and Western blot after 24, 48, and 72 hours in culture. The conditioned medium was collected for sulfated glycosaminoglycan (GAG) release and Pi/PPi assay.

resultsIn vivo guinea pig study: Meniscus size and area as well as intensity of meniscus calcification were significantly increased in the ACLT group compared with the control group. Both calcified area and intensity were correlated with cartilage damage in the ACLT group (meniscus calcified area: r = 0.925, P < .0001; meniscus calcified intensity: r = 0.944, P < .0001). Ihh, MMP-13, Col X, ANKH, ENPP1, and ALP expression were increased in the ACLT group compared with the control group. The Pi level and Pi/PPi ratio increased by 63% and 42%, respectively, in the ACLT group compared with the control group. In vitro bovine meniscus explant study: Cell death was found in the superficial zone of the bovine meniscus explants after loading for 3 hours. The mRNA expression and protein levels of MMP-13, ANKH, ENPP1, and ALP were up-regulated in all 3-hour loaded samples. The Pi/PPi ratio and sulfated GAG content in the culture medium were increased in the 3-hour loaded group.

conclusionMeniscus hypertrophy and mineralization correlated to cartilage degeneration after ACL injuries. CLINICAL RELEVANCE: The study data suggest that the suppression of meniscus hypertrophy and calcification may decrease the risk of PTOA after ACL injuries.

Indexed as

AnimalsAnterior Cruciate LigamentAnterior Cruciate Ligament InjuriesCalcinosisCartilage, ArticularFemaleGuinea PigsHypertrophyKnee InjuriesMaleMatrix Metalloproteinase 13Menisci, TibialTibial Meniscus InjuriesMatrix Metalloproteinase 13abnormal mechanical loadingACL injurycartilage degenerationmeniscus hypertrophy and mineralization

Identifiers

PMID26792705
PMCPMC4775287
OpenAlexW2252368007

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.