Early impairment of cartilage poroelastic properties in an animal model of ACL tear.


Journal

Orthopaedics & traumatology, surgery & research : OTSR
ISSN: 1877-0568
Titre abrégé: Orthop Traumatol Surg Res
Pays: France
ID NLM: 101494830

Informations de publication

Date de publication:
05 2022
Historique:
received: 26 01 2021
revised: 16 04 2021
accepted: 23 04 2021
pubmed: 20 10 2021
medline: 20 5 2022
entrez: 19 10 2021
Statut: ppublish

Résumé

In more than 50% of cases, anterior cruciate ligament (ACL) lesions lead to post-traumatic osteoarthritis. Ligament reconstruction stabilizes the joint, but the tear seems to impair the poroelasticity of the cartilage: synovial membrane fluid inflammation is observed 3 weeks after tearing. There have been some descriptions of visible cartilage changes, but poroelasticity has never been analyzed at this early stage. The present animal study aimed to determine (1) whether cartilage showed early poroelastic deterioration after ACL tear; (2) whether an impairment correlated with macroscopic changes; and (3) whether cartilage poroelasticity deteriorated over time. In the days following trauma, cartilage poroelasticity is greatly impaired, without macroscopically visible change. ACL tear was surgically induced in 18 New-Zealand rabbits. Cartilage poroelasticity was assessed on indentation-relaxation test in 3 groups: "early", at 2 weeks postoperatively (n=6), "mid-early" at 6 weeks (n=6) and in a non-operated control group ("non-op"). Macroscopic changes were scored in the same groups. Poroelastic impairment was greatest at the early time-point (2 weeks). Permeability ranged from a mean 0.08±0.05×10 The severe rapid deterioration in poroelasticity following ACL tear in an animal model, as notably seen in increased permeability, corresponds to changes in cartilage microstructure, with easier outflows of interstitial fluid. This mechanical degradation may underlie onset of microcracks within the cartilage, leading to physiological loading that the cartilage by its nature is unable to repair. Further investigations are needed to correlate these experimental data with clinical findings. III; comparative study with control group.

Sections du résumé

BACKGROUND
In more than 50% of cases, anterior cruciate ligament (ACL) lesions lead to post-traumatic osteoarthritis. Ligament reconstruction stabilizes the joint, but the tear seems to impair the poroelasticity of the cartilage: synovial membrane fluid inflammation is observed 3 weeks after tearing. There have been some descriptions of visible cartilage changes, but poroelasticity has never been analyzed at this early stage. The present animal study aimed to determine (1) whether cartilage showed early poroelastic deterioration after ACL tear; (2) whether an impairment correlated with macroscopic changes; and (3) whether cartilage poroelasticity deteriorated over time.
HYPOTHESIS
In the days following trauma, cartilage poroelasticity is greatly impaired, without macroscopically visible change.
MATERIAL AND METHODS
ACL tear was surgically induced in 18 New-Zealand rabbits. Cartilage poroelasticity was assessed on indentation-relaxation test in 3 groups: "early", at 2 weeks postoperatively (n=6), "mid-early" at 6 weeks (n=6) and in a non-operated control group ("non-op"). Macroscopic changes were scored in the same groups.
RESULTS
Poroelastic impairment was greatest at the early time-point (2 weeks). Permeability ranged from a mean 0.08±0.05×10
DISCUSSION
The severe rapid deterioration in poroelasticity following ACL tear in an animal model, as notably seen in increased permeability, corresponds to changes in cartilage microstructure, with easier outflows of interstitial fluid. This mechanical degradation may underlie onset of microcracks within the cartilage, leading to physiological loading that the cartilage by its nature is unable to repair. Further investigations are needed to correlate these experimental data with clinical findings.
LEVEL OF EVIDENCE
III; comparative study with control group.

Identifiants

pubmed: 34666200
pii: S1877-0568(21)00369-8
doi: 10.1016/j.otsr.2021.103116
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

103116

Informations de copyright

Copyright © 2021. Published by Elsevier Masson SAS.

Auteurs

Cartherine Bosser (C)

HealthDataSciences, 45, chemin du Barthélémy, 69260 Charbonnières-les-Bains, France.

Jean Charles Auregan (JC)

Université de Paris, B3OA, UMR CNRS 7052, Inserm U1271, 10, avenue de Verdun, 75010 Paris, France; Service d'orthopédie, université Paris-Saclay, AP-HP, Antoine Béclère, 157, rue de la Porte-de-Trivaux, 92140 Clamart, France.

Morad Bensidhoum (M)

Université de Paris, B3OA, UMR CNRS 7052, Inserm U1271, 10, avenue de Verdun, 75010 Paris, France.

Thierry Hoc (T)

Université de Paris, B3OA, UMR CNRS 7052, Inserm U1271, 10, avenue de Verdun, 75010 Paris, France; École centrale de Lyon, département de mécanique, MSGMGC, 36, avenue Guy-de-Collongue, 69134 Ecully cedex, France.

Thierry Bégué (T)

Service d'orthopédie, université Paris-Saclay, AP-HP, Antoine Béclère, 157, rue de la Porte-de-Trivaux, 92140 Clamart, France.

Raphaël Vialle (R)

Service de chirurgie orthopédique et réparatrice de l'enfant, AP-HP-Sorbonne université, hôpital Trousseau, 26, avenue du Docteur-Arnold-Netter, 75012 Paris, France.

Cécile Nouguier-Lehon (C)

Université de Lyon, LTDS UMR CNRS 5513, école centrale de Lyon, 36, avenue Guy-de-Collongue, 69134 Ecully cedex, France.

Manon Bachy (M)

Université de Paris, B3OA, UMR CNRS 7052, Inserm U1271, 10, avenue de Verdun, 75010 Paris, France; Service de chirurgie orthopédique et réparatrice de l'enfant, AP-HP-Sorbonne université, hôpital Trousseau, 26, avenue du Docteur-Arnold-Netter, 75012 Paris, France. Electronic address: manon.bachy@aphp.fr.

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