Abstract
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.
Highlights
Large bone defects and nonunion present the most challenging therapeutic issue to the surgeon that is often associated with significant morbidity
Diisothiocyanatostilbene-2,2’-disulfonic acid disodium salt hydrate (DIDS) and EIPA reduced the size of the hypertrophic chondrocytes zone in growth plate chondrocyte hypertrophy and bone lengthening in bone rudiments of Sprague-Dawley seven days old rats through inhibition Anion exchanger-2 (AE-2) and NHE-1 respectively [6]
Proliferative chondrocyte zone at secondary fracture healing site Histological sections showed proliferative chondrocyte zone (PCZ) percentage area was at a high level in week one 63.64 ± 9.31% after the fracture
Summary
Large bone defects and nonunion present the most challenging therapeutic issue to the surgeon that is often associated with significant morbidity. In order for bone renewal in progress, the initial soft cartilaginous callus that formed needs to be absorbed and replaced via a hardbony callus This phase of bone fracture healing, to some extent, runs through the embryonic bone development with a mixture of chondrocytes differentiation and proliferation, swelling chondrocytes volume, increasing matrix deposition [10]. The joining between bone development and bone regeneration has been further strengthened through a topical understanding of the role of transport proteins in the chondrocyte plasma membrane, especially the NHE-1 and AE-2 in endochondral ossification of secondary bone healing. The expression, regulation and activity of transporters in the plasma cell membrane must be implicated in coordinating the complex procedure of bone growth linear throughout driving and supporting chondrocyte proliferation, hypertrophy and apoptosis that are vital phases in lengthening of bone [5]. Diisothiocyanatostilbene-2,2’-disulfonic acid disodium salt hydrate (DIDS) and EIPA reduced the size of the hypertrophic chondrocytes zone in growth plate chondrocyte hypertrophy and bone lengthening in bone rudiments of Sprague-Dawley seven days old rats through inhibition AE-2 and NHE-1 respectively [6]
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