Periprosthetic osteolysis remains a leading complication of total hip and knee arthroplasty, often resulting in aseptic loosening of the implant and necessitating revision surgery. Wear-induced particulate debris is the main cause initiating this destructive process. The purpose of this article is to review recent advances in understanding of how wear debris causes osteolysis, and emergent strategies for the avoidance and treatment of this disease. A strong activator of the peri-implant innate immune this debris-induced inflammatory cascade is dictated by macrophage secretion of TNF-α, IL-1, IL-6, and IL-8, and PGE2, leading to peri-implant bone resorption through activation of osteoclasts and inhibition of osteoblasts through several mechanisms, including the RANK/RANKL/OPG pathway. Therapeutic agents against proinflammatory mediators, such as those targeting tumor necrosis factor (TNF), osteoclasts, and sclerostin, have shown promise in reducing peri-implant osteolysis in vitro and in vivo; however, radiographic changes and clinical diagnosis often lag considerably behind the initiation of osteolysis, making timely treatment difficult. Considerable efforts are underway to develop such diagnostic tools, therapies, and identify novel targets for therapeutic intervention.

Previous studies have demonstrated that online patient educational materials are written at reading levels too advanced for the average patient. The average American reads at the eighth-grade reading level. To date, the readability of online educational material of academic centers for shoulder arthroplasty has not been analyzed. Online patient educational materials from the top 25 orthopedic institutions, as ranked by U.S. News & World Report, were assessed utilizing the following readability assessments: Flesch-Kincaid (FK), Flesch Reading Ease, Gunning Fog Index, Coleman-Liau Index, Simple Measure of the Gobbledygook Index, Automated Readability Index, FORCAST, and the New Dale and Chall Readability. All of these scores, with the exception of the Flesch Reading Ease, provide an output indicating reading difficulty based on grade level. Correlations between academic institutional ranking and FK scores were evaluated using a Spearman regression. Lastly, additional factors including geographical location, private versus public institution, and use of concomitant multi-media modalities that may impact institutional readability scores (as determined by FK) were evaluated. Only 16.0% of the top 25 institutions included online material at or below the eighth-grade reading level. Moreover, half of the online resources evaluated (those with FK score ≥9.3) were not at a suitable reading level for more than two-thirds of the general United States population (∼70%). Overall, the composite mean scores were 9.5 ± 2.1 for FK, 52.8 ± 9. for 4 Flesch Reading Ease, 12.2 ± 2.4 for Gunning Fog, 11.6 ± 1.8 for Coleman-Liau, 12.3 ± 1.7 for Simple Measure of the Gobbledygook Index, 9.6 ± 2.6 for Automated Readability, 11.1 ± 0.6 for FORCAST, and 5.9 ± 0.6 for New Dale and Chall. There was no correlation between institutional ranking and FK scores (ρ = −0.15; P = .946). Geographical location, private versus public institution, and use of concomitant multi-media modalities were not significantly associated with readability. Shoulder arthroplasty online patient educational material at top-ranked orthopedic institutions have poor readability and are likely not suitable for the majority of patients in the United States.

Despite advances in techniques for acetabular labral repair, strategies for mitigating or reversing damage to the chondrolabral junction do not yet exist. Cartilage repair techniques such as autologous chondrocyte implantation, matrix‐induced autologous chondrocyte implantation, osteochondral autograft transfer, microfracture, and bone marrow aspirate concentrate (BMAC) have all been suggested to restore joint congruity and minimize further chondral deterioration. However, chondrocyte implantation techniques and osteochondral grafts are technically challenging in the hip because of its constrained nature, and many cell‐based therapies have shown suboptimal results near the chondrolabral junction because of the increased shear forces at the peripheral acetabulum and increased stress at the weight‐bearing region of the joint. By using BMAC to augment labral repairs and coat chondrolabral junction breakdown, we are able to introduce mesenchymal stem cells to peripheral acetabular tissue with little to no drawbacks, while avoiding donor‐site morbidity, open procedures, and multiple surgeries. The purpose of this Technical Note is to describe a reproducible method for harvesting, processing, and applying BMAC to the chondrolabral surface of the hip during hip arthroscopy without the need for donor‐site morbidity or increased labral repair time. Technique Video: video See video under supplementary data.

Introduction . Klippel–Feil syndrome (KFS) is a congenital anomaly resulting from fusion of cervical vertebral bodies secondary to the dysregulation of signaling pathways during somite development. It is commonly associated with scoliosis and Sprengel deformity. We present a case of KFS with commonly associated abnormalities as well as deformities that have not yet been reported in the literature. Case Presentation . A 3‐year‐old girl presented for further evaluation of a left upper extremity deformity following a negative genetic workup. Upon physical exam and radiographic imaging, the patient was diagnosed with KFS and associated abnormalities including cervical scoliosis, Sprengel deformity, and congenital deformity of the left upper extremity. Deformities of the left upper extremity include radioulnar synostosis, a four‐rayed hand, and absent thenar musculature. The Sprengel deformity was corrected surgically with a Woodward procedure. Discussion . Congenital musculoskeletal deformities can be differentiated based upon spinal and limb embryology. The presence of extraspinal abnormalities not originating from somite differentiation may suggest a severe form of KFS. Important considerations in the workup of the KFS patient include looking for deformities of the shoulder girdle and upper extremities to identify abnormalities for intervention at a young age.

Case: We describe 2 patients with no historical, examination, or imaging evidence of ischiofemoral impingement; they both developed hip abductor insufficiency and subsequent ischiofemoral impingement with progression that was confirmed by examination and advanced imaging. Conclusion: Hip abductor insufficiency may lead to dynamic progressive ischiofemoral impingement. Hemipelvic instability from hip abductor weakness results in a Trendelenburg gait, narrowing the ischiofemoral space and impinging the quadratus femoris muscle. Treatment options for dynamic ischiofemoral impingement potentially can focus on treatment of the underlying cause of the hemipelvic instability, preventing additional ischiofemoral-space narrowing and quadratus femoris damage by minimizing the Trendelenburg gait.