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Case Report: Anterior Cruciate Ligament Calcification in a Patient With Chondrocalcinosis: Micro-Computed Tomography Presentation.

ABSTRACT: In this case report, an incidental postoperative diagnosis of anterior cruciate ligament (ACL) calcification, associated with calcification of posterior cruciate ligament (PCL) and lateral meniscus insertions, was made using micro-computed tomography (μCT) technology in a knee specimen obtained during a total knee replacement (TKR) surgery due to painful tri-compartmental osteoarthritis (OA) with chondrocalcinosis signs at preoperative X-ray. Anterior cruciate ligament calcification is an uncommon finding, and conventional X-ray and MRI are not so helpful in its identification. μCT scan, in contrast, is of interest because it provides highly spatial three-dimensional information with excellent visualization of bones and calcifications. The μCT technology used in this case report allowed us to perform a detailed analysis and a 3-D reconstruction of the calcium pyrophosphate dihydrate (CPPD) crystal deposition about the knee without the need to section the specimens into slice as performed in previous studies. The 3-D model obtained with μCT scan permits to gain more insight into the shape of the calcification within the fibers of the ligamentous structures of the joint.

SUBMITTER: Grassi A

PROVIDER: S-EPMC8358067 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundNearly three-quarters of anterior cruciate ligament (ACL) injuries occur as "noncontact" failures from routine athletic maneuvers. Recent in vitro studies revealed that repetitive strenuous submaximal knee loading known to especially strain the ACL can lead to its fatigue failure, often at the ACL femoral enthesis.HypothesisACL failure can be caused by accumulated tissue fatigue damage: specifically, chemical and structural evidence of this fatigue process will be found at the femoral enthesis of ACLs from tested cadaveric knees, as well as in ACL explants removed from patients undergoing ACL reconstruction.Study designControlled laboratory study.MethodsOne knee from each of 7 pairs of adult cadaveric knees were repetitively loaded under 4 times-body weight simulated pivot landings known to strain the ACL submaximally while the contralateral, unloaded knee was used as a comparison. The chemical and structural changes associated with this repetitive loading were characterized at the ACL femoral enthesis at multiple hierarchical collagen levels by employing atomic force microscopy (AFM), AFM-infrared spectroscopy, molecular targeting with a fluorescently labeled collagen hybridizing peptide, and second harmonic imaging microscopy. Explants from ACL femoral entheses from the injured knee of 5 patients with noncontact ACL failure were also characterized via similar methods.ResultsAFM-infrared spectroscopy and collagen hybridizing peptide binding indicate that the characteristic molecular damage was an unraveling of the collagen molecular triple helix. AFM detected disruption of collagen fibrils in the forms of reduced topographical surface thickness and the induction of ~30- to 100-nm voids in the collagen fibril matrix for mechanically tested samples. Second harmonic imaging microscopy detected the induction of ~10- to 100-µm regions where the noncentrosymmetric structure of collagen had been disrupted. These mechanically induced changes, ranging from molecular to microscale disruption of normal collagen structure, represent a previously unreported aspect of tissue fatigue damage in noncontact ACL failure. Confirmatory evidence came from the explants of 5 patients undergoing ACL reconstruction, which exhibited the same pattern of molecular, nanoscale, and microscale structural damage detected in the mechanically tested cadaveric samples.ConclusionThe authors found evidence of accumulated damage to collagen fibrils and fibers at the ACL femoral enthesis at the time of surgery for noncontact ACL failure. This tissue damage was similar to that found in donor knees subjected in vitro to repetitive 4 times-body weight impulsive 3-dimensional loading known to cause a fatigue failure of the ACL.Clinical relevanceThese findings suggest that some ACL injuries may be due to an exacerbation of preexisting hierarchical tissue damage from activities known to place larger-than-normal loads on the ACL. Too rapid an increase in these activities could cause ACL tissue damage to accumulate across length scales, thereby affecting ACL structural integrity before it has time to repair. Prevention necessitates an understanding of how ACL loading magnitude and frequency are anabolic, neutral, or catabolic to the ligament.

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Case Report: Anterior Cruciate Ligament Calcification in a Patient With Chondrocalcinosis: Micro-Computed Tomography Presentation.

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