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Published on: July 21, 2023
Age-related changes in biological characteristics of human alveolar osteoblasts
1Department of Periodontology, College of Stomatology, Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Objectives:
Age-related changes are common in many tissues and organs. However, cell-related causes in human alveolar bone remain unclear. This study has been carried out to explore the possibility that advancing age might change the biological characteristics of alveolar osteoblasts (AOBs) in women.
Materials And Methods:
Alveolar osteoblasts from women donors (five women aged 33-38 years and five women aged 62-68 years) were cultured in vitro. The cells were serially passaged and maximal lifespan evaluated. Cell viability, ultramicrostructure and osteogenic differentiation ability were determined respectively, using MTT assay, transmission electron microscopy, alkaline phosphatase (ALP) activity assay and von Kossa staining assay. These parameters of the two groups of AOBs were evaluated.
Results:
When compared with cells from young adult donors, AOBs from elderly women exhibited lower maximal lifespan (P < 0.05). Mean rate of population doubling was lower in elderly donor cells compared to those from young adult cells (P < 0.05). Organelles from AOBs of elderly donors were much fewer than those from young donors. MTT value of elderly donor cells was significantly lower than those of young adult donors from day 2 (P < 0.05). Relative ratio of ALP activity in elderly donor cells was significantly lower than those of the young womens' cells at 8, 12, 16 and 20 days (P < 0.05). Calcium nodules of young adult donors' specimens were significantly more numerous and larger than those from elderly donors.
Conclusions:
Comparison of biological characteristics of AOBs from young adult women with those from elderly women in vitro revealed differences in proliferative capacity and bone formation functions, which decreased with aging. These data indicate that aging may play an important role in pathogenesis of human AOBs loss.
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