Histological evaluation of the possible role of Na+/ H+ entiporter and anion exchanger in endochondral ossification activities of secondary bone healing in rats

• Main Authors: Sahar Ibrahim, Thana’a M Ibrahim, Kareem Handool, Abubakar Abdul, jalila abu, Sabri Yusof, Mehdi Ibrahimmi, Loqman Yusof
• Format: Article
• Language: Arabic
• Published: University of Mosul, College of Veterinary Medicine 2020-04-01
• Series: Iraqi Journal of Veterinary Sciences
• Subjects: histology; nhe-1; ae-2; secondary bone healing
• Online Access: https://vetmedmosul.com/article_164492_3d9460adb3691a78c4b61152db219b58.pdf
• ISSN: 1607-3894; 2071-1255

In secondary fracture healing, callus proliferate, undergo hypertrophy and the extracellular matrix becomes calcified. This step to some extent, recapitulates the embryological bone development with a combination of cellular proliferation and differentiation, increasing cellular volume and matrix deposition. The causes of the chondrocytes volume increase in secondary bone healing are poorly known, but cell membrane transporters perhaps could be implicated. We hypothesize that NHE-1 and AE-2 are among plasma membrane transporters that have a role in cellular differentiation and regulation of endochondral ossification for secondary bone fracture healing. Study of closed tibia fracture healing in 2 groups of 25 of 8-weeks-old Sprague-Dawley rats were undertaken and histological evaluation were made at 5 different time points at 1, 2, 3, 4, and 6 weeks after induction of the fracture. Histological evaluation of proliferative and hypertrophic chondrocyte zone area showed a significant difference in week 1 compared to other weeks. Immunohistochemistry study revealed a significant high level of labeling intensity of NHE-1 at the first four weeks. While labeling intensity of AE-2 showed moderate reaction at 1 and 2 weeks, that increased and reached the highest level at 3 and 4 weeks. These results suggested that NHE-1 and AE-2 had role in the endochondral ossification of secondary bone healing.