In the 7-day cellular proliferation assay, hTMSCs from the hypertrophied inferior Tubeimoside-I turbinate exhibited less proliferation than those from the normal-sized inferior turbinate from days 1 to 3, while hTMSCs from the hypertrophied inferior turbinate expanded more rapidly than those from the normal-sized inferior turbinate from days 5 to day 7. There was a significant difference in proliferation between the two groups from days 5 to 7. However, the proliferation pattern of hTMSCs was similar between the hypertrophic and normal turbinate groups. These findings suggest that turbinate size did not significantly affect the proliferation of hTMSCs. The three distinct phases of MSC differentiation and bone formation comprise proliferation, extracellular matrix maturation and matrix mineralization. The first stage of cell proliferation occurs within the first 4 days. Early cell differentiation occurs during the second stage, which spans days 5 to 14, and is characterized by 
the transcription and protein expression of Col1 and alkaline phosphatase. Terminal differentiation and matrix maturation occurs during the third stage, from day 15 to day 28, which results in high expression of OP, BSP, and OC, followed by calcium and phosphate deposition. Runx2 and Osx are primary osteoblast-specific transcription factors for osteoblastic differentiation, which positively regulate OC and BSP expression. BMP-2 is known to regulate the mechanism Anemarsaponin-BIII upstream of Runx2 in osteogenic differentiation. After culturing in osteogenic media, the expression levels of osteoblast-related genes were determined by RT-PCR. The expression levels of the other osteoblast-associated genes were not different between the two groups. These findings suggest that turbinate size does not significantly affect the osteogenic capacity of hTMSCs. This study was the first to analyze the etiology of ITH secondary to septal deviation based on MSCs rather than histological and radiological findings. In particular, the cause of turbinate bone hypertrophy had not been evaluated. Based on the previous findings that MSCs reside in virtually all post-natal organs and contribute to their maintenance and regeneration, and because turbinate size does not affect the characteristics, proliferation, and osteogenic differentiation potential of hTMSCs, the hypertrophic turbinate and normal turbinate would possess the similar hTMSCs distribution with parallel potency, which meant that there would be the same bony hypertrophy in both turbinatesdespite NSD only in view of MSCs. However, the expected in-vivo phenomenon contradicts with the known radiologic and histologic findings. Therefore, we assumed that bony turbinate hypertrophy might not result from the characteristics of hTMSCs. However, because this was an in vitro study, the possibility of a genetic difference of MSCs stimulating signals in hypertrophic and contralateral turbinates in vivo could not be excluded. In addition, further studies at the cellular, biochemical and molecular levels should be performed to permit effective control of hTMSC proliferation and differentiation. Through this study, because hTMSCs express MSC-specific surface proteins, are highly proliferative, and differentiate into cells with an osteogenic phenotype irrespective of turbinate size, the turbinate size would not be a deciding factor in the clinical use of autologous or allogenic hTMSCs.