Coronal plane alignment of the knee (CPAK) has recently been proposed as a simple and universal classification system to determine the suitability of a particular phenotype of the knee to a specific alignment strategy for knee replacement surgery. Although racial differences may affect knee alignment, there are no reports on the racial distribution of this classification system. We aimed to clarify the distribution of CPAK classification in patients with osteoarthritis who underwent total knee arthroplasty (TKA) in Japan. Consecutive patients who underwent primary TKA were analyzed retrospectively. The knees were categorized according to the CPAK classification system which comprised of two independent variables (arithmetic hip–knee–ankle [aHKA] angle and joint-line obliquity [JLO]) with three respective subgroups to create the following nine phenotypes of the knee: type I (varus aHKA and apex distal JLO), type II (neutral aHKA and apex distal JLO), type III (valgus aHKA and apex distal JLO), type IV (varus aHKA and neutral JLO), type V (neutral aHKA and neutral JLO), and type VI (valgus aHKA and neutral JLO), type VII (varus aHKA and apex proximal), type VIII (neutral aHKA and apex proximal), and type IX (valgus aHKA and apex proximal). The distribution of the phenotypes in the Japanese population was investigated as a primary outcome. To accurately compare the results with previous studies conducted on non-Japanese patients, a sex-matched distribution was investigated as a secondary outcome. A total of 570 knees were investigated of which 500 knees were examined after exclusions. The most common distribution was type I (53.8%), followed by type II (25.4%), type III (8.2%), type IV (7.2%), type V (4.4%), and type VI (1.0%). Types VII, VIII, and IX were not distributed. The sex-matched distribution was nearly identical to the overall distribution in Japan. The majority of patients with knee osteoarthritis in Japan had medially tilted joints with constitutional varus alignment.

Background: Individual skeletal elements of the vertebrate limbs arise through a segmentation process introducing joints in specific locations. However, the molecular pathways controlling joint formation and subsequent joint maintenance are largely unknown. In this study, we focused on SOX11, and its contribution to the regulation of GDF5, a secreted signal necessary for proper joint formation and postnatal joint homeostasis. Results: Sox11 is initially expressed broadly in the murine cartilage condensations at early stages of skeletal development, but its expression is specifically increased in the forming joint interzone as is forms. SOX11 overexpression can directly activate GDF5 expression both in vitro and in micromass cell cultures prepared from chick limb buds. Conserved SOX family binding sites are present in the 5’ UTR region of the GDF5 gene and we show SOX11 can specifically bind to one of them. While misexpression of Sox11 in developing chick limbs through RCAS virus infection does not induce Gdf5 expression in ectopic locations, it does enhance its expression. To explore the roles of Sox11 in joint homeostasis, we analyzed adult knee joints in an osteoarthritis mouse model where the medial meniscus and the medial collateral ligament were removed. We also analyzed knee joints from human subjects who underwent total knee replacement surgery. We find that SOX11 is mainly expressed in the weight-bearing areas of knee joints, and its expression is decreased in degraded cartilage during progression of knee osteoarthritis in both mice and humans. Conclusions: This work implicates SOX11 as a potential regulator of GDF5 expression in joint maintenance and suggests a possible role in the pathogenesis of osteoarthritis.

Traumatic injury and surgical meniscectomy of a medial meniscus are known to cause subsequent knee osteoarthritis. However, the difference in the prevalence of osteoarthritis caused by the individual type of the medial meniscal tear has not been elucidated. The aim of this study was to investigate what type of tear is predominantly responsible for the degradation of articular cartilage in the medial compartment of knee joints.