Medial Ankle Stability Evaluation With Dynamic Ultrasound: Establishing Natural Variations in the Healthy Cohort.

INTRODUCTION: Destabilizing injuries to the deltoid ligament have relied on radiographic stress examination for diagnosis, with a focus on medial clear space (MCS) widening. Recently, studies have demonstrated the use of ultrasonography to assess deltoid ligament injury, but not the medial ankle stability. The purpose of this study was to assess the MCS via ultrasonography while weight-bearing and with a gravity stress test (GST) in the uninjured ankle as a means of establishing normative values for future comparison. METHODS: Twenty-six participants with no reported ankle injury in their premedical history were included. The MCS was examined using ultrasonography with the patient lying in a lateral decubitus position to replicate a GST with the ankle held in a neutral and plantarflexed position as well as while weight-bearing. The MCS was assessed in mm at the anteromedial and inferomedial aspect of the ankle joint. RESULTS: With weight-bearing, the average anterior MCS and inferior MCS were 3.6 and 3.3 mm, respectively. During the GST in neutral ankle position, the average anterior MCS was 4.1 mm, whereas the average inferior MCS was 4.0 mm. When measured during the GST in plantarflexed ankle position, the averages anterior MCS and inferior MCS increased to 4.4 mm. MCS values were notably higher with GST than with weight-bearing measurements (P < 0.001). MCS values were notably higher with the foot in a plantarflexed compared with a neutral position when doing GST (P < 0.001). No notable differences in MCS distance were found when comparing laterality (P > 0.05). Height had a notable effect on all MCS values (P < 0.05). Inter- and intra-rater reliabilities for ultrasonographic MCS measurements were all excellent (interclass correlation coefficient >0.75). DISCUSSION: Ultrasound can reliably measure the MCS of the ankle while doing dynamic stress manoeuvres. With the deltoid ligament intact, a GST increases MCS widening more than weight-bearing, and holding the ankle in plantarflexion while doing a gravity stress view, further increases this difference. LEVELS OF EVIDENCE: Diagnostic studies-investigating a diagnostic test: Level III.

Regulation of Chondrocyte Survival in Mouse Articular Cartilage by p63.

OBJECTIVE: Transcription factor p63, of the p53 family, regulates cell proliferation, survival, and apoptosis in various cells and tissues. This study was undertaken to examine the expression and roles of p63 transcript variants in the mouse growth plate and articular chondrocytes. METHODS: For in vivo analyses, we generated Cre-mediated TAp63α-transgenic and TAp63γ-transgenic mice. To induce tissue-specific overexpression or deletion in chondrocytes, chondroprogenitor cells, or early limb bud mesenchymal cells, we used Col2a1-Cre, Sox9-Cre, and Prx1-Cre mice, respectively. We analyzed osteoarthritis (OA) development with aging or surgically induced instability in Prx1-Cre;p63fl/fl (P-conditional knockout) mice. RESULTS: Among major variants, TAp63α and TAp63γ are highly expressed in mouse primary costal and articular chondrocytes. The p63 protein was predominantly localized in the hypertrophic zone of the embryonic limb cartilage, and in the middle zone of articular cartilage. No obvious change was observed in skeletal growth of TAp63α-transgenic mice, Sox9-Cre;p63fl/fl , or P-conditional knockout mice, while that of TAp63γ-transgenic mice was impaired due to ectopic apoptosis and the resulting decreased number of chondrocytes. Expression of proapoptotic genes including bax, noxa, puma, and fas was increased in TAp63γ-transgenic mouse chondrocytes, and their transcription was probably sustained by p53 in p63-conditional knockout mouse chondrocytes because both proteins were coexpressed in the growth plate. In contrast, p53 was expressed in the superficial zone of articular cartilage, differently from p63. Notably, P-conditional knockout mice showed significant resistance to OA development, with suppression of chondrocyte apoptosis in the aging and surgical models. CONCLUSION: We demonstrated regulation of chondrocyte survival in articular cartilage by p63.