Characterization of primary chondrocytes harvested from hips with femoroacetabular impingement

Bretschneider, Henriette; Stiehler, Maik; Hartmann, A.; Boger, Erich T.; Oßwald, C.; Mollenhauer, J.; Gaissmaier, Christoph; Günther, Klaus Peter

doi:10.1016/j.joca.2016.04.011

Cited by 11 publications

(15 citation statements)

References 36 publications

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“…These findings suggest that the pattern of expression of selected inflammatory and catabolic markers was not related to a loss of cell viability but to the state of cellular activity, that is, whether cells are producing these proteins. Similarly, previous studies have shown that high chondrocyte viability (87%-95%) was confirmed in delaminated acetabular cartilage 4,23,38 and more than 95% viability in damaged femoral head-neck cartilage in patients with FAI. 4…”

Section: Discussionsupporting

confidence: 75%

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Distinct Pattern of Inflammation of Articular Cartilage and the Synovium in Early and Late Hip Femoroacetabular Impingement

et al. 2020

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Background: The molecular mechanism of how femoroacetabular impingement (FAI) morphology leads to hip osteoarthritis (OA) is yet to be determined. The expression and location of inflammation-related molecules during early- and late-stage FAI have not been previously described. Moreover, the characterization of intra-articular inflammation away from the cam deformity as well as the nature of adjacent synovial tissue have also not been extensively reported. Hypothesis: Early-stage FAI has a similar expression of inflammation-related markers in the head-neck and acetabular cartilage but less synovitis than late-stage FAI. Study Design: Controlled laboratory study. Methods: Head-neck cartilage, acetabular cartilage, and synovial samples were obtained from patients undergoing hip preservation surgery for the treatment of symptomatic cam FAI (early FAI group; n = 15) and advanced OA secondary to cam FAI (late FAI group; n = 15). Samples procured from healthy young adult donors served as the control group (n = 7). Cartilage degeneration was assessed by histology, and the expression of inflammation-related proteins (interleukin–1 beta [IL-1β], matrix metalloproteinase–13 [MMP-13], a disintegrin and metalloproteinase with thrombospondin motifs–4 [ADAMTS-4], type II collagen [COL2], and aggrecan neoepitope [NITEGE]) was measured by immunostaining. Synovial samples in the early and late FAI groups were examined for synovitis and the expression of IL-1β. Results: Head-neck cartilage in the early FAI group showed significantly more degeneration than the control group and an increased expression of inflammation-related proteins (IL-1β: 69.7% ± 18.1% vs 20.2% ± 4.9%, respectively; MMP-13: 79.6% ± 12.6% vs 25.3% ± 9.5%; ADAMTS-4: 83.9% ± 12.2% vs 24.3% ± 11.1%; NITEGE: 89.7% ± 7.7% vs 39.8% ± 20.5%) ( P < .001). Head-neck and acetabular cartilage in the early and late FAI groups showed a similar degree of degeneration. Moreover, a similar expression of inflammation-related proteins was observed between the early and late FAI groups for head-neck cartilage (IL-1β: 69.7% ± 18.1% vs 72.5% ± 13.2%; MMP-13: 79.6% ± 12.6% vs 71.4% ± 18.8%; ADAMTS-4: 83.9% ± 12.2% vs 82.6% ± 12.5%; COL2: 93.6% ± 3.9% vs 92.5% ± 5.8%; NITEGE: 89.7% ± 7.7% vs 95.7% ± 4.7%) and acetabular cartilage (IL-1β: 83.3% ± 24.8% vs 80.7% ± 15.6%; MMP-13: 94.3% ± 9.7% vs 85.2% ± 12.3%; ADAMTS-4: 98.5% ± 2.3% vs 98.4% ± 3.4%; COL2: 99.8% ± 0.7% vs 99.7% ± 1.1%; NITEGE: 96.7% ± 6.7% vs 99.2% ± 2.2%). In contrast, synovitis was minimal with a low expression of IL-1β in the early FAI group compared with the late FAI group. Conclusion: Hip cartilage exhibited an OA phenotype in patients with early-stage FAI, similar to what was observed in hip OA secondary to FAI. Severe synovitis was only evident with late-stage FAI. Clinical Relevance: This study supports the concept that early hip impingement is associated with cartilage degeneration and catabolism.

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Section: Discussionsupporting

confidence: 75%

“…Similarly, previous studies have shown that high chondrocyte viability (87%-95%) was confirmed in delaminated acetabular cartilage 4,23,38 and more than 95% viability in damaged femoral head-neck cartilage in patients with FAI. 4…”

Section: Discussionsupporting

confidence: 75%

Distinct Pattern of Inflammation of Articular Cartilage and the Synovium in Early and Late Hip Femoroacetabular Impingement

et al. 2020

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“…33,42,43 Since FAI was established by Ganz et al 16 as an important etiologic factor for hip OA, various studies on the pathogenesis and pathologic process of hip OA have been conducted. 9,20,36,39 Prevalence of cartilage damage in patients with symptomatic FAI is high, with delamination cartilage lesions observed commonly in the superolateral aspect of the acetabulum (impingement zone) and early degenerative malacia lesions observed in the posterior peripheral rim. 6,27,30 However, the molecular mechanisms by which hip FAI leads to progression of disease resulting in hip OA are not well-understood.…”

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confidence: 99%

Inflammatory Response of Articular Cartilage to Femoroacetabular Impingement in the Hip

et al. 2020

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Background: Femoroacetabular impingement (FAI) has been proposed as an etiologic factor in up to 50% of hips with osteoarthritis (OA). Inflammation is thought to be one of the main initiators of OA, yet little is known about the origin of intra-articular inflammation in FAI hips. Hypothesis: Articular cartilage from the impingement zone of patients with FAI has high levels of inflammation, reflecting initial inflammatory process in the hip. Study Design: Controlled laboratory study. Methods: Head-neck cartilage samples were obtained from patients with cam FAI (cam FAI, early FAI; n = 15), advanced OA secondary to cam FAI (FAI OA, late FAI; n = 15), and advanced OA secondary to developmental dysplasia of the hip (DDH OA, no impingement; n = 15). Cartilage procured from young adult donors (n = 7) served as control. Safranin O–stained sections were assessed for cartilage abnormality. Tissue viability was detected by TUNEL assay. Immunostaining of interleukin 1β (IL-1β), catabolic markers (matrix metalloproteinase 13 [MMP-13], a disintegrin and metalloproteinase with thrombospondin motif 4 [ADAMTS-4], aggrecan antibody to C-terminal neoepitope [NITEGE]), and an anabolic marker (type II collagen [COL2]) was performed to evaluate molecular inflammation and metabolic activity. The average percentage of immunopositive cells from the total cell count was calculated. Kruskal-Wallis test followed by Steel-Dwass post hoc test was used for multiple comparisons. Results: Microscopic osteoarthritic changes were more prevalent in cartilage of cam FAI and FAI OA groups compared with DDH OA and control groups. Cartilage in cam FAI and FAI OA groups, versus the DDH group, had higher expression of inflammatory molecules IL-1β (69.7% ± 18.1% and 72.5% ± 13.2% vs 32.7% ± 14.4%, respectively), MMP-13 (79.6% ± 12.6% and 71.4% ± 18.8% vs 38. 5% ± 13.3%), ADAMTS-4 (83.9% ± 12.2% and 82.6% ± 12.5% vs 45.7% ± 15.5%), and COL2 (93.6% ± 3.9% and 92.5% ± 5.8% vs 53.3% ± 21.0%) ( P < .001). Expression of NITEGE was similar among groups (cam FAI, 89.7% ± 7.7%; FAI OA, 95.7% ± 4.7%; DDH OA, 93.9% ± 5.2%; P = .0742). The control group had minimal expression of inflammatory markers. Inflammatory markers were expressed in all cartilage zones of early and late FAI but only in the superficial zone of the no impingement group. Conclusion: Cartilage from the impingement zone in FAI is associated with a high expression of inflammatory markers, extending throughout all cartilage zones. Clinical Relevance: Inflammation associated with FAI likely has a deleterious effect on joint homeostasis. Further clinical and translational studies are warranted to assess whether and how surgical treatment of FAI reduces molecular inflammation.

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“… 5 , 39 But, encouragingly, the chondrocytes were able to be redifferentiated and maintained differentiation when seeded in tri-dimensional hyaluronan-based hydrogel cultivation, showing high expression levels of Col II and aggrecan, as well as decreased production of IL-1β. 6 Clearly, as shown by these studies and ours, there are varying results for percentage viability in chondral flaps and surrounding tissue. However, the data suggest that these chondrocytes may not be suitable for efficient cartilage regeneration given the tissue quality and microenvironment where they are found.…”

Section: Discussionmentioning

confidence: 60%

“…The authors suggested that the varying amounts of fibrocartilage represented anabolic repairing attempts of a metabolically active tissue due to inflammation. 32 Interestingly, a study by Bretschneider et al, 6 which included 6 patients with cam-type FAI, tested the proliferation and differentiation potential of chondrocytes found in samples retrieved from the anterosuperior acetabulum and the anterolateral head-neck region. The chondrocytes were found to be viable in monolayer expansion after 19 days, reaching viability above 90%.…”

Section: Discussionmentioning

confidence: 99%

Viability and Tissue Quality of Cartilage Flaps From Patients With Femoroacetabular Hip Impingement: A Matched-Control Comparison

Rodríguez-Fontán

Payne

Chahla

et al. 2017

Orthopaedic Journal of Sports Medicine

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Background:Chondrolabral damage is commonly observed in patients with cam-type femoroacetabular impingement (FAI). Chondral flap reattachment has recently been proposed as a possible preservation technique.Purpose/Hypothesis:The purpose of this study was to determine the viability and tissue quality of chondral flaps from patients with FAI at the time of arthroscopy. It was hypothesized that chondral flaps from patients with cam lesions of the hip would exhibit less viability and greater tissue degeneration than would those of a matched control group.Study Design:Cohort study; Level of evidence, 2.Methods:Patients with cam-type FAI who were treated with hip arthroscopy between 2014 and 2016 were asked to participate in this study. The cartilage lesions were localized and classified intraoperatively according to Beck classification. A chondral flap (study group) and a cartilage sample (control group) were obtained from each patient for histologic evaluation. Cellular viability and tissue quality were examined and compared in both groups. Cellular viability was determined with live/dead staining, and tissue quality was evaluated using safranin O/fast green, hematoxylin and eosin (H&E) staining, and immunohistochemistry for collagen II. Osteoarthritis Research Society International (OARSI) grading was used for quality assessment, and Image J software was used to calculate the percentage of tissue viability and Col II stain.Results:A total of 10 male patients with a mean age of 38.4 years (range, 30-55 years) were enrolled. All chondral flaps were classified as Beck grade 4. The mean cellular viability of the chondral flaps was reduced (54.6% ± 25.6%), and they were found to be degenerated (OARSI grade, 4 ± 1.27). Control samples also had reduced viability (38.8% ± 30.3%) and were degenerative (OARSI grade, 3.5 ± 1.38). There was no statistically significant intergroup difference for viability (P = .203) or OARSI grade (P = .645), nor was there an intragroup correlation between viability and OARSI grade (P > .05). A significant negative correlation (r = −0.9, P = .035) was found between OARSI grade and collagen II percentage scale in 5 selected samples.Conclusion:Despite appearing normal macroscopically, the chondral flaps from patients with cam-type FAI displayed loss of viability and tissue degeneration. In addition, control samples obtained away from the injury area also displayed cartilage damage and degeneration. Careful consideration should be taken when attempting to reattach the chondral flap.

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Characterization of primary chondrocytes harvested from hips with femoroacetabular impingement

Abstract: hC derived from damaged acetabular and femoral site are qualified for autologous matrix-assisted cartilage transplantation paving the way for cell-based cartilage regeneration in FAI patients.

Cited by 11 publications

References 36 publications

Distinct Pattern of Inflammation of Articular Cartilage and the Synovium in Early and Late Hip Femoroacetabular Impingement

Distinct Pattern of Inflammation of Articular Cartilage and the Synovium in Early and Late Hip Femoroacetabular Impingement

Inflammatory Response of Articular Cartilage to Femoroacetabular Impingement in the Hip

Viability and Tissue Quality of Cartilage Flaps From Patients With Femoroacetabular Hip Impingement: A Matched-Control Comparison

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