Association between pelvic organ prolapse and bone mineral density in postmenopausal women.

Both pelvic organ prolapse (POP) and osteoporosis are age-related diseases in older aged women. Both POP and bone metabolism may be associated with collagen metabolism. Our study determined the relationship between POP and bone mineral density (BMD) of the lumbar spine and femur neck in postmenopausal women. We selected 554 postmenopausal women (aged 50-79 years) and divided them into two groups (moderate to severe POP and absent to mild POP). We compared the BMDs of the lumbar spine and femur neck between the moderate to severe POP and absent to mild POP groups. Lumbar spine BMD was inversely correlated with POP severity (p = 0.001). However, after adjusting for age, time since menopause, height, weight, body mass index (BMI), and vaginal delivery, the BMDs of both the lumbar spine and femur neck were not significantly different between the moderate to severe POP and absent to mild POP groups (p = 0.583 and p = 0.305, respectively). A lower BMD is associated with increased fracture risk and we postulated that women with severe POP would have an increased risk of osteoporotic fracture.

Association between metabolic syndrome and serum leptin levels in postmenopausal women.

Menopausal status is associated with weight gain, increased central fat mass, abnormal lipid metabolism, insulin resistance and susceptibility to metabolic syndrome (MetS). Leptin is synthesised and secreted by adipocytes. Serum leptin levels are highly correlated with fat mass. We determined the association between MetS and serum leptin levels in 153 postmenopausal women. The difference in serum leptin level between MetS and non-MetS groups showed a statistical significance after adjusting for body mass index (BMI; 19.9 ± 9.5 vs 12.1 ± 5.9 ng/ml, p = 0.013). The indicator of abdominal obesity, waist-to-hip ratio (WHR) and visceral fat area (VFA), had a positive correlation with serum leptin level in non-obese subjects after adjusting for BMI (p = 0.017, p < 0.001, respectively). Of the components of MetS, abdominal obesity and the number of MetS components had a positive correlation with serum leptin level (p < 0.05, p < 0.001, respectively).

Concurrence of replicative senescence and elevated expression of p16(INK4A) with subculture-induced but not calcium-induced differentiation in normal human oral keratinocytes.

Primary normal human oral keratinocytes (NHOKs) undergo differentiation in the presence of calcium concentrations higher than 0.15 mM in vitro, which is useful in investigating the mechanisms involved in the differentiation of epithelial cells. Serial subculture of NHOKs to the postmitotic stage also induces terminal differentiation. However, the detailed mechanisms of both differentiation processes remain substantially unknown. To investigate the molecular differences in these processes, NHOKs were induced to differentiate by exposure to 1.2 mM of calcium and by serial subculture to the postmitotic stage. To study whether the cells were induced to differentiate and to undergo replicative senescence, the amount of cellular involucrin and the expression of senescence-associated beta-galactosidase (SA-beta-gal) were measured respectively. The expression of replicative senescence-associated genes and the activity of telomerase from the differentiated cells were also determined. Both calcium treatment and serial subculture to the postmitotic stage notably elevated the cellular involucrin. The percentage of SA-beta-gal-positive cells was significantly elevated by the continued subculture, but such changes were not observed in keratinocytes exposed to calcium. The concentration of cellular p16(INK4A) protein was progressively increased by the continued subculture but was not changed by calcium treatment. On the other hand, the concentrations of cellular p53 were similar in both differentiation processes. However, telomerase activity was lost in NHOKs that had undergone differentiation by both calcium treatment and serial subculture. The results indicate that calcium-induced differentiation of NHOKs has similar characteristics to their serial subculture-induced differentiation, but that the differentiation processes are not identical, because calcium-induced differentiation does not concur with either replicative senescence or the gradually increased concentration of p16(INK4A).

Staphylococcus lugdunensis--a potential pathogen in oral infection.

OBJECTIVE: The purpose of this study was to investigate the pathogenicity of Staphylococcus lugdunensis in acute oral infection. STUDY DESIGN: S. lugdunensis was isolated from patients with acute oral infections and from healthy control subjects. Antibiotic susceptibility, in vitro cellular toxicity, in vivo virulence, and hemolytic activity testing and dot blot analysis were performed. The statistical significance of in vitro cellular toxicity was determined by means of analysis of variance. RESULTS: Isolated from the infected patients, S. lugdunensis showed resistance to penicillin, ampicillin, methicillin, cephalothin, and clindamycin, exhibited virulence in vivo, and showed delta-like hemolysin activity. Four of the 6 strains of S. lugdunensis gave synergistic hemolysis. In dot blot analysis, S. lugdunensis showed a positive reaction to the probe of the delta-hemolysin gene in S. aureus. CONCLUSIONS: The results suggest that S. lugdunensis may be a potential pathogen in acute oral infection.

Retinoic acid extends the in vitro life span of normal human oral keratinocytes by decreasing p16(INK4A) expression and maintaining telomerase activity.

Retinoic acid (RA) plays an important role in the regulation of cell growth and differentiation. To investigate whether RA extends in vitro the life span of human epithelial cells, we examined the effect of all-trans RA on both the cumulative population-doubling level (PDL) and the replicative senescence of cultured oral keratinocytes. When proliferating oral keratinocytes were cultured in medium containing 1 nM of all-trans RA, the in vitro life span of the cells was increased 1.5- to 1.8-fold compared to the vehicle control and the replicative senescence of the cells was significantly inhibited. Since the replicative senescence of human epithelial cells is associated with a steady increase of p16(INK4A) and a loss of telomerase activity, we expected that RA could delay the replicative senescence of oral keratinocytes by decreasing p16(INK4A) expression and/or inhibiting the loss of telomerase activity. To test this possibility, we examined the expression of replicative senescence-associated genes and the telomerase activities of different PDL numbers of oral keratinocytes exposed to 1 nM of all-trans RA. The protein level of cellular p16(INK4A) in the RA-treated oral keratinocytes was gradually but significantly enhanced by an increased PDL number; however, the level was significantly lower than that of the vehicle control at all of the same PDL numbers. In contrast, the telomerase activity was maintained in oral keratinocytes with increasing PDL numbers induced by RA treatment. Summarizing, these results indicate that RA induces the in vitro life-span extension of oral keratinocytes, which is linked to a decreased cellular level of p16(INK4A) and the maintenance of telomerase activity.