Number and proliferative capacity of osteogenic stem cells are maintained during aging and in patients with osteoporosis

Decreased bone formation is an important pathophysiological mechanism respo nsible for bone loss associated with aging and osteoporosis. Osteoblasts (O Bs), originate from mesenchymal stem cells (MSCs) that are present in the b one marrow and form colonies (termed colony-forming units-fibroblastic [CFU -Fs]) when cultured in vitro. To examine the effect of aging and osteoporos is on the MSC population, we quantified the number of MSCs and their prolif erative capacity in vitro. Fifty-one individuals were studied: 38 normal vo lunteers (23 young individuals [age, 22-44 years] and 15 old individuals [a ge, 66-74 years]) and 13 patients with osteoporosis (age, 58-83 years). Bon e marrow was aspirated from iliac crest; mononuclear cells were enriched in MSCs by magnetic activated cell sorting (MACS) using STRO-1 antibody. Tota l CFU-F number, size distribution, cell density per CFU-F, number of alkali ne phosphatase positive (ALP(+)) CFU-Fs, and the total ALP(+) cells were de termined. In addition, matrix mineralization as Estimated by alizarin red S (AR-S) staining was quantified. No significant difference in colony-formin g efficiency between young individuals (mean a SEM; 87 +/- 12 CFU-Fs/cultur e), old individuals (99 +/- 19 CFU-Fs/culture), and patients with osteoporo sis (129 +/- 13 CFU-Fs/culture; p = 0.20) was found. Average CFU-F size and cell density per colony were similar in the three groups. Neither the perc entage of ALP(+) CFU-Fs (66 +/- 6%, 65 +/- 7%, and 72 +/- 4% for young indi viduals, old individuals, and patients with osteoporosis, respectively) nor the percentage of ALP(+) cells per culture (34 +/- 5%, 40 +/- 6%, and 41 /- 4%) differed between groups. Finally, mineralized matrix formation was s imilar in young individuals, old individuals, and patients with osteoporosi s. Our study shows that the number and proliferative capacity of osteoproge nitor cells are maintained during aging and in patients with osteoporosis a nd that other mechanisms must be responsible for the defective osteoblast ( OB) functions observed in these conditions.