Evidence map›Paper›PMID 29843672›Full record

ArticleBMC musculoskeletal disorders2018

Effects of controlled abnormal joint movement on the molecular biological response in intra-articular tissues during the acute phase of anterior cruciate ligament injury in a rat model.

Yuichi Nishikawa, Takanori Kokubun, Naohiko Kanemura, Tetsuya Takahashi, Masayasu Matsumoto, Hirofumi Maruyama, Kiyomi Takayanagi

Open access · goldAbstract read
In one paragraph

Article in BMC musculoskeletal disorders, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

6 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
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

7 authors at 4 institutions in 1 country.

Yuichi NishikawaDepartment of Neuroscience and Therapeutics, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan.
Takanori KokubunDepartment of Physical Therapy, School of Health and Social Services, Saitama Prefectural University, 820 Sannomiya, Koshigaya-shi, Saitama, 343-8540, Japan.
Naohiko KanemuraDepartment of Physical Therapy, School of Health and Social Services, Saitama Prefectural University, 820 Sannomiya, Koshigaya-shi, Saitama, 343-8540, Japan.
Tetsuya TakahashiDepartment of Neuroscience and Therapeutics, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan.
Masayasu MatsumotoSakai City Medical Center, Osaka, Japan.
Hirofumi MaruyamaDepartment of Neuroscience and Therapeutics, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan.
Kiyomi TakayanagiDepartment of Physical Therapy, School of Health and Social Services, Saitama Prefectural University, 820 Sannomiya, Koshigaya-shi, Saitama, 343-8540, Japan. takayanagi-kiyomi@spu.ac.jp.
Saitama Prefectural University · JPHiroshima University · JPHiroshima University Hospital · JPSakai Municipal Hospital · JP

Funding

Japan Society for the Promotion of Science 21500484
6 · The paper itself

Abstract

backgroundThe anterior cruciate ligament (ACL) is responsible for braking forward movement of the tibia relative to the femur and for tibial rotation. After ACL injury, this braking performance deteriorates, inducing abnormal joint movement. The purpose of this study was to clarify the effects of controlled abnormal joint movement on the molecular biological response in intra-articular tissues during the acute phase of ACL injury.

methodsEighty-four mature Wistar male rats were randomly assigned to a controlled abnormal movement (CAM) group, an ACL-transection (ACL-T) group, a sham-operated group, or an intact group. The ACL was completely transected at its midportion in the ACL-T and CAM groups, and a nylon suture was used to control abnormal tibial translation in the CAM group. The sham-operated group underwent skin and joint capsule incisions and tibial drilling without ACL transection. Animals were not restricted activity until sacrifice 1, 3, or 5 days after surgery for histological and gene expression assessments. Acute-phase inflammation requires an important balance between degenerative and biosynthetic processes and is controlled by the activities of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). Both types of gene were analyzed in this study.

resultsThe ACL-T and CAM groups exhibited cleavage of the ACL at all time points. However, for the CAM group, the gap in the ligament stump was extremely small, and fibroblast proliferation was observed around the stump. Relative to the ACL-T group, the CAM group demonstrated significantly lower expression of MMP-13 mRNA and a lower MMP-13/TIMP-1 ratio on days 1 and 5 in the ACL, the medial meniscus and the lateral meniscus. The expression of TIMP-1 mRNA was not significantly different between the ACL-T and CAM groups.

conclusionsThe study results suggested that controlling abnormal movement inhibited the inflammatory reaction in intra-articular tissues after ACL injury. This reaction was down-regulated in intra-articular tissues in the CAM group. Abnormal joint control caused prolonged inflammation and inhibited remodeling during the acute phase of ACL rupture.

Indexed as

Disease Models, AnimalAcute DiseaseAnimalsAnterior Cruciate Ligament InjuriesBiomechanical PhenomenaCartilage, ArticularKnee JointLigaments, ArticularMaleMatrix Metalloproteinase 13RatsRats, WistarTissue Inhibitor of Metalloproteinase-1Matrix Metalloproteinase 13Mmp13 protein, ratTIMP1 protein, ratTissue Inhibitor of Metalloproteinase-1Anterior cruciate ligament, Matrix metalloproteinase-13, Conservative therapy, Acute phase injury

Identifiers

PMID29843672
PMCPMC5975588
OpenAlexW2807657410

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.