Jae-Hyuk Yang

Background: Although patellofemoral arthritis is a common and debilitating orthopedic disorder, its treatment varies and remains controversial. This review aims to provide an overview of the current understanding of the pathophysiology of patellofemoral arthritis, as well as its various diagnostic and treatment options.Current Concepts: The pathophysiology of patellofemoral arthritis includes lower limb malalignment, trochlear and/or patellar dysplasia, patellar instability, trauma, and obesity. The disorder is characterized by chronic anterior knee pain aggravated by flexion of the knee joint. A critical imaging study of the Merchant and lateral knee radiographs may show the progression of patellofemoral arthritis and dysplasia of the patellofemoral joints. Non-pharmacologic treatment options for patellofemoral arthritis include patient education, self-management, exercise, weight loss, taping, bracing, and orthotics. Pharmacologic agents (non-steroidal anti-inflammatory drugs, acetaminophen, oral narcotics, and duloxetine) and intra-articular injection therapies (glucocorticoids, hyaluronic acid, platelet-rich plasma, and other regenerative therapies) can be helpful for symptom relief in patients with patellofemoral arthritis. The surgical treatment can begin with lateral retinacular release to realign and decompress the patellofemoral joint. If failure in the improvement of symptoms is noted, a tibial tubercle osteotomy can be considered in young and active patients. While the early design and technique of patellofemoral arthroplasty were less than encouraging, more recent implant design and surgical techniques have demonstrated robust results.Discussion and Conclusion: Patellofemoral arthritis is a unique entity compared with tibiofemoral arthritis marked by distinct epidemiology, biomechanics, and risk factors and treatment options. It is essential to understand its pathophysiology and ensure proper treatment options.

Kim DH, et al. Clin Orthop Surg. 2022 Nov;14:e92. https://doi.org/10.4055/cios21214

Yang JH, et al. Clin Orthop Surg. 2022 Aug;14:e76. https://doi.org/10.4055/cios21246

김상균, et al. J Korean Orthop Assoc. 2022 Apr;57(2):106-114. https://doi.org/10.4055/jkoa.2022.57.2.106

최대현, et al. J Korean Orthop Assoc. 2022 Feb;57(1):73-77. https://doi.org/10.4055/jkoa.2022.57.1.73

LBSA0103 is a recently developed high-molecular-weight, cross-linked, non-animal hyaluronic acid (HA). The safety of LBSA0103 has been investigated only in a limited number of patients, therefore this prospective study was designed. This study sought to assess the safety including injection-site reactions and adverse drug reactions after a single intra-articular injection of LBSA0103 in patients with osteoarthritis (OA) of the knee joint. This study was a multicenter, single-arm, prospective cohort study. After screening, eligible patients with OA of the knee joint (Kellgren–Lawrence grades I–III) were enrolled, received a single intra-articular HA (LBSA0103) injection, and were followed up for two weeks. Any adverse events including injection-site reactions and adverse drug reactions were evaluated by the investigators. A total of 1949 subjects (2976 knee joints) was enrolled, all of whom received a single intra-articular injection of LBSA0103. Injection-site reactions occurred in 5.59% of enrolled subjects (109/1949), and the most frequently reported injection-site reaction was pain (4.87%), followed by swelling (1.03%). Most of the injection-site reactions were transient and resolved within 14 days without additional treatment. The incidence of adverse drug reactions other than injection-site reactions was 0.67% (13/1949). Most adverse events were of mild severity. No serious adverse events related to the study drug were reported. A single intra-articular injection of LBSA0103 in patients with OA of the knee joint was safe, and no significant safety concerns were observed. As such, LBSA0103 could be safely applied as an intra-articular injection for management of knee OA. The study was registered at ClinicalTrials.gov (identifier: NCT04369261).

Transforming growth factor β1 (TGFβ1) is a major mediator in the modulation of osteoblast differentiation. However, the underlying molecular mechanism is still not fully understood. Here, we show that TGFβ1 has a dual stage-dependent role in osteoblast differentiation; TGFβ1 induced matrix maturation but inhibited matrix mineralization. We discovered the underlying mechanism of the TGFβ1 inhibitory role in mineralization using human osteoprogenitors. In particular, the matrix mineralization-related genes of osteoblasts such as osteocalcin (OCN), Dickkopf 1 (DKK1), and CCAAT/enhancer-binding protein beta (C/EBPβ) were dramatically suppressed by TGFβ1 treatment. The suppressive effects of TGFβ1 were reversed with anti-TGFβ1 treatment. Mechanically, TGFβ1 decreased protein levels of C/EBPβ without changing mRNA levels and reduced both mRNA and protein levels of DKK1. The degradation of the C/EBPβ protein by TGFβ1 was dependent on the ubiquitin–proteasome pathway. TGFβ1 degraded the C/EBPβ protein by inducing the expression of the E3 ubiquitin ligase Smad ubiquitin regulatory factor 1 (SMURF1) at the transcript level, thereby reducing the C/EBPβ-DKK1 regulatory mechanism. Collectively, our findings suggest that TGFβ1 suppressed the matrix mineralization of osteoblast differentiation by regulating the SMURF1-C/EBPβ-DKK1 axis.