Suito Hirai, Minamizono Wataru, Yashima Nao, Matsunaga Hiroya, Fujikawa Kaoru, Ohsako Masafumi
Life Innovation Institute, Toyo University, Tokyo, Japan.
Department of Anatomy, Teikyo University of School of Medicine, Tokyo, Japan.
J Anat. 2025 Jan;246(1):148-159. doi: 10.1111/joa.14128. Epub 2024 Sep 5.
The tibial tuberosity has a superficial patellar tendon-embedded portion and a deep uncalcified cartilage portion. Suppressed calcification of the tibial tuberosity leads to Osgood-Schlatter disease. The tibial tuberosity calcifies with age; load reduction degrades the cartilage matrix and promotes calcification, suggesting that reduced mechanical stimulation of the tibial tuberosity promotes calcification. However, this is yet to be clarified. Therefore, in this study, we aimed to investigate the effects of mechanical stimulation reduction on the tibial tuberosity tissue structure and calcification mechanism. Specifically, we examined the effect of load reduction on tibial tuberosity calcification in 20 male 7-week-old Wistar rats classified into two groups: hind-limb suspension (HS, n = 10) and control (CO, n = 10). We observed superficial and deep tibial tuberosities in both groups. The tibial tuberosity in the HS group had narrower areas of deep portions than did those in the CO group (p = 0.000539), and immature bone tissue and cartilage tissue were observed in the HS group. Enpp1 expression did not significantly differ between the groups (p = 0.804). In contrast, Alpl (p = 0.001) and Mmp3 (p = 0.006) expression increased whereas Timp3 expression decreased (p = 0.002) in the HS group. Thus, these results showed a maturing of bone ossification, and this gene expression trend was similar to that observed in a murine join instability model of osteoarthritis with articular cartilage calcification and ossification. The HS tibial tuberosity also showed immature bone tissue. In conclusion, reduced mechanical stimulation caused tibial tuberosity calcification and pathological changes. These findings highlight the importance of optimal exercise to avoid premature pathological structural changes in bones and joints.
胫骨结节有一个浅层的髌腱嵌入部分和一个深层的未钙化软骨部分。胫骨结节钙化抑制会导致奥斯古德-施拉特病。胫骨结节会随着年龄增长而钙化；负荷降低会使软骨基质退化并促进钙化，这表明对胫骨结节的机械刺激减少会促进钙化。然而，这一点尚未得到明确证实。因此，在本研究中，我们旨在探究机械刺激减少对胫骨结节组织结构和钙化机制的影响。具体而言，我们将20只7周龄雄性Wistar大鼠分为两组：后肢悬吊组（HS，n = 10）和对照组（CO，n = 10），研究负荷降低对胫骨结节钙化的影响。我们观察了两组大鼠的胫骨结节浅层和深层。HS组胫骨结节深层区域比CO组窄（p = 0.000539），且在HS组观察到不成熟的骨组织和软骨组织。两组间Enpp1表达无显著差异（p = 0.804）。相比之下，HS组中Alpl（p = 0.001）和Mmp3（p = 0.006）表达增加，而Timp3表达降低（p = 0.002）。因此，这些结果显示了骨矿化的成熟，且这种基因表达趋势与在伴有关节软骨钙化和骨化的骨关节炎小鼠关节不稳定模型中观察到的相似。HS组的胫骨结节也显示出不成熟的骨组织。总之，机械刺激减少会导致胫骨结节钙化和病理变化。这些发现凸显了适度运动对于避免骨骼和关节过早出现病理结构变化的重要性。
