To test the hypothesis that physical disruption of an intervertebral disc disturbs cell-matrix binding, leading to cell clustering and increased expression of matrix degrading enzymes that contribute towards degenerative disc cell phenotype. Lumbar disc tissue was removed at surgery from 21 patients with disc herniation, 11 with disc degeneration, and 8 with adolescent scoliosis. 5 μm sections were examined with histology, and 30-µm sections by confocal microscopy. Antibodies were used against integrin α5beta1, matrix metalloproteinases (MMP) 1, MMP-3, caspase 3, and denatured collagen types I and II. Spatial associations were sought between cell clustering and various degenerative features. An additional, 11 non-herniated human discs were used to examine causality: half of each specimen was cultured in a manner that allowed free ‘unconstrained’ swelling (similar to a herniated disc in vivo), while the other half was cultured within a perspex ring that allowed ‘constrained’ swelling. Changes were monitored over 36 h using live-cell imaging. 1,9-Di-methyl methylene blue (DMMB) assay for glycosaminoglycan loss was carried out from tissue medium. Partially constrained specimens showed little swelling or cell movement in vitro. In contrast, unconstrained swelling significantly increased matrix distortion, glycosaminoglycan loss, exposure of integrin binding sites, expression of MMPs 1 and 3, and collagen denaturation. In the association studies, herniated disc specimens showed changes that resembled unconstrained swelling in vitro. In addition, they exhibited increased cell clustering, apoptosis, MMP expression, and collagen denaturation compared to ‘control’ discs. Results support our hypothesis. Further confirmation will require longitudinal animal experiments.
BackgroundRecently introduced total knee arthroplasty (TKA) implants have been linked with the early development of periprosthetic radiolucency (PPRL). The aim of this study was to carry out a retrospective clinical and radiographical analysis of a consecutive series of a new TKA, and to assess the incidence and distribution of PPRL.MethodsA retrospective review of all new TKA implants performed by a single surgeon at a single hospital between March 2013 and October 2017 was performed. The minimum follow‐up period was 3 months, with ongoing patient review at 6, 12 and 36 months. Sequential post‐operative radiographs were performed to determine the presence of PPRL.ResultsA total of 122 TKAs were identified in 112 patients over the 4.5‐year study period. The average follow‐up time was 21 months (range 3–51 months). PPRL was noted in 29 TKAs (23.8%). When comparing the PPRL group to those without PPRL, there was a difference in body mass index, with body mass index associated with an increased likelihood of PPRL (P = 0.003). There was no difference in constraint of implant (P = 0.818), cement type (P = 0.340), patella resurfacing (P = 0.286), age (P = 0.984) gender (P = 0.376) or initial mechanical axis deviation (P = 0.054) between groups. PPRL were most commonly seen in tibial anterior‐posterior (AP) zone 1 and zone 2 (96.6%), followed by femoral lateral zone 5 (58.6%), tibia lateral zone 1 (55.2%) and tibial lateral zone 2 (53.2%). No patients have required revision surgery.ConclusionA high incidence of early PPRL is seen in patients undergoing primary TKA using a new implant system, mainly involving the tibial component. Ongoing clinical and radiological assessment for patients seems warranted based on these findings.
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