The dysplastic trochlear sulcus due to the insufficient patellar stress in growing rats

Abstract

Background Developmental factors were assumed to be the key factors that influenced the morphology of femoral trochlea. This study investigated the effects of insufficient patellar stress after birth on the morphological development of the femoral trochlea. Effects of insufficient patellar stress on femoral trochlea were investigated using surgical induced patellectomy and patellar dislocation in growing rat model. Methods In this study, two experimental groups and one sham group (SG) were established. Thirty-six Wistar rats (female, 28 days of age) were randomly assigned to three groups. The patellectomy group (PG), rats underwent the patellectomy in this group. The dislocation group (DG), rats underwent the surgery-induced patellar dislocation. Histological staining (Safranin-O and fast green), Micro-computed tomographic (Micro-CT) analysis in two experimental endpoints (3, 12 weeks postoperatively) were selected to evaluate morphological changes of the femoral trochlea. Results Articular cartilage on the trochlear sulcus was remodeled at 3 weeks after the surgery, and degenerated at 12 weeks through the histological staining. The femoral trochlear angle (FTA) did not show a significant difference at 3 week between the experimental groups and the sham group (PG vs SG P = 0.38, DG vs SG p = 0.05), but the FTA was significantly increased in experimental groups at 12 weeks(PG vs SG P = 0.001, DG vs SG p = 0.005). The Bone volume density (BV/TV), Trabecular number (Tb.N) under the trochlea groove were significantly reduced at 3 weeks postoperatively in the experimental groups (PG vs SG p = 0.001, DG vs SG p = 0.002). No significant difference was found in BV/TV and Tb. N among the three groups at 12 weeks postoperatively. Conclusion Surgical induced patellectomy and patellar dislocation leads to the dysplastic trochlear sulcus in growing rats. Besides the bone morphology of trochlear sulcus, the articular cartilage and subchondral trabecula under the trochlear sulcus were remodeled early stage after the surgery.

Cartilage degeneration is associated with activation of the PI3K/AKT signaling pathway in a growing rat experimental model of developmental trochlear dysplasia

“…Notably, our previous study con rmed that TD can lead to cartilage degeneration [24,25]. In the present study, we found that, with increasing age, cartilage morphology changed in the rat TD model: its surface became rough, vertical cracks appeared, and articular chondrocytes aggregated.…”

“…An incision was then made along the midline of the skin; the skin and subcutaneous tissue were separated, exposing the joint capsule through the medial approach to the knee. The procedure to induce patellar instability was performed as described in our previous studies [24,25]. Speci cally, a 0.5-cm longitudinal incision was made along the patella at the medial capsule and retinaculum.…”

“…Transforming growth factor β1 (TGFβ1) is known to be an important contributor to chondrocyte development; it can regulate extracellular matrix biosynthesis and has been extensively studied as a regulator of cartilage metabolic activity [23]. Previous studies have shown that TD can cause articular cartilage degeneration [24,25]. However, the molecular mechanism of TD-induced cartilage degeneration has been uncertain thus far.…”

The cartilage degeneration in a growing rat experimental model of developmental trochlear dysplasia is associated with activation of PI3K/AKT signal pathway

“…Incising along the midline of the skin, separating the skin and subcutaneous tissue subsequently, exposing the joint capsule via the medial approach of the knee. Similar surgeries of patellar instability have been informed in our earlier researches [24,25]. In this research, along the patellar, making a 0.5 cm longitudinal incision at the medial capsule and retinaculum.…”

“…We all know that transforming growth factor β1 (TGFβ1) plays an significant part in the development of chondrocytes, it has a good ability to regulate the extracellular matrix (ECM) biosynthesis, and it is one of the regulators of cartilage metabolic activity that we have extensively studied [23]. Previous studies have shown that TD can cause degeneration of articular cartilage [24,25]. However, the molecular mechanism of TD induced cartilage degeneration is uncertain until now.…”