The anterolateral ligament (ALL) is considered a secondary stabilizer of internal rotation and, due to proximity to the lateral collateral ligament (LCL), it may contribute to anterolateral rotatory stability. This study characterized the anatomy of the ALL and associated tissues of the anterolateral complex (ALC) to determine if structural and histological compensatory adaptations exist in patients without an ALL. Forty-nine cadaveric knees were dissected from distal-to-proximal using established landmarks with the aid of internal rotation stress to localize the ALL (if present), LCL, iliotibial band (ITB), and anterolateral capsule. The width and thickness of ALL and LCL were measured with digital calipers at the origin, middle, and insertion, and cross-sectional areas were calculated. ALL and LCL length and ITB thickness were also obtained. Samples of each tissue were stained with hematoxylin and eosin and picrosirius red, and histological images were evaluated with ImageJ to quantify collagen density (mean gray value [mgv]) and quantity (percent coverage). Size measurements and collagen characteristics were compared between ALL-present and ALL-deficient knees. The ALL was identified in 63% of knees with mean cross-sectional areas of 8.9, 5.8, and 9.7 mm at the origin, middle, and insertion, respectively. Mean collagen density of the ALL was 106.9 mgv on a scale of 0 (black) to 255 (white), and overall collagen quantity was 40.3%. Proximal LCL width ( = 0.04), distal LCL thickness ( = 0.03), and cross-sectional area ( = 0.01), and ITB thickness ( = 0.02) were significantly greater in ALL-deficient knees. A significantly higher collagen density was found within the LCL ( = 0.04), and higher overall quantity of collagen within the LCL ( < 0.01) and ITB ( < 0.01), of ALL-deficient knees. Gross anatomical and histological alterations exist in knees without an ALL compared with those with an ALL. These may reflect adaptations in the ALC and LCL that are present to compensate for the absence of the anterolateral rotatory stability afforded by the ALL.
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http://dx.doi.org/10.1055/s-0044-1801749 | DOI Listing |
Laryngoscope Investig Otolaryngol
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J Orthop Surg Res
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Medical Physiology Department, Faculty of Medicine, Menoufia University, Menoufia, Egypt.
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Dental School, The University of Western Australia, 17 Monash Avenue, Nedlands, WA, 6009, Australia.
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View Article and Find Full Text PDFCalcif Tissue Int
January 2025
Division of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Aeschenvorstadt 57, 4051, Basel, Switzerland.
Pentosidine (PEN), a surrogate marker of advanced glycation end-product formation, reflects increased non-enzymatic cross-linking in bone collagen, which is thought to be an important determinant of bone fragility in type 2 diabetes mellitus (T2DM). We aimed to investigate serum concentrations of PEN in patients with T2DM and controls without T2DM and to examine its relationship with bone parameters and metabolic state such as glycaemic control, insulin resistance and body weight. In a cross-sectional study-design, data from postmenopausal women and men with T2DM (n = 110) and controls without T2DM (n = 111) were evaluated.
View Article and Find Full Text PDFOsteoporos Int
January 2025
Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark.
Unlabelled: In patients receiving long-term treatment with denosumab, denosumab discontinuation via sequential treatment with zoledronate, resulted in a minor decrease in bone mass density (BMD) of 0-2.5% within the first year and stabile BMD in the second year, thus showing that repeated treatments with zoledronate limit the loss of BMD, when discontinuing denosumab.
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