Effects of bisphenol F, bisphenol S, and bisphenol AF on cultured human osteoblasts.

Bisphenol A (BPA) analogs, like BPA, could have adverse effects on human health including bone health. The aim was to determine the effect of BPF, BPS and BPAF on the growth and differentiation of cultured human osteoblasts. Osteoblasts primary culture from bone chips harvested during routine dental work and treated with BPF, BPS, or BPAF for 24 h at doses of 10-5, 10-6, and 10-7 M. Next, cell proliferation was studied, apoptosis induction, and alkaline phosphatase (ALP) activity. In addition, mineralization was evaluated at 7, 14, and 21 days of cell culture in an osteogenic medium supplemented with BP analog at the studied doses. BPS treatment inhibited proliferation in a dose-dependent manner at all three doses by inducing apoptosis; BPF exerted a significant inhibitory effect on cell proliferation at the highest dose alone by an increase of apoptosis; while BPAF had no effect on proliferation or cell viability. Cell differentiation was adversely affected by treatment with BPA analogs in a dose-dependent, observing a reduction in calcium nodule formation at 21 days. According to the results obtained, these BPA analogs could potentially pose a threat to bone health, depending on their concentration in the organism.

Effect of NSAIDs on the aminopeptidase activity of cultured human osteoblasts.

Aminopeptidases (APs) are involved in various physiological and pathological processes. In tumor tissues the expression of APs, cyclooxygenase-2 and its metabolites are increased. The objective was to determine the effect of certain NSAIDs on the AP activity of osteoblasts. Primary cultures of osteoblast were treated with different concentrations of indomethacin, meloxicam, naproxen, nimesulide, and piroxicam. The AP activity was fluorimetrically determined using aminoacyl-ß-naphthylamides (aa-ßNAs) as substrates: Ala-ßNA, Arg-ßNA, Gly-ßNA, Leu-ßNA, Lys-ßNA, Met-ßNA, and Phe-ßNA. The five NSAIDs showed an inhibitory effect of AP activity against the study substrates depending on the dose tested. Meloxicam and piroxicam had the highest inhibitory effect on enzymatic activity, with an IC50 of around 70 µM. Our results suggest that the physiological alteration of osteoblasts in the presence of NSAIDs may be a consequence of AP inhibition, suggesting a potential clinical role for these drugs against cancer in combination with chemotherapeutic agents.

Retrospective study of the association between epidural analgesia during labour and complications for the newborn.

OBJECTIVE: our objective was to determine the association between epidural analgesia and different variables. BACKGROUND: the effect on newborns of epidural analgesia administered to the mother during labour remains under debate. METHOD: this association was retrospectively investigated in a cohort of 2399 children born in a Spanish public hospital. Only full-term (>37 weeks of gestation) deliveries were included. Other exclusion criteria were: induced delivery (medical or obstetric indication), elective caesarean section, or the presence of an important pregnancy risk factors (hypertension, diabetes, severe disease, toxaemia, retarded intrauterine growth, chronologically prolonged pregnancy, prolonged membrane rupture (>24 hours), oligoamnios, or polyhydramnios). The Mann-Whitney U test and Fisher׳s exact test were applied to determine the relationship between variables. KEY CONCLUSIONS: Apgar index values at one minute and five minutes were slightly but significantly lower in neonates whose mothers had received epidural analgesia. Neonatal intensive care unit admission was significantly more frequent in the epidural versus non-epidural group. Resuscitation was significantly more frequent in the epidural versus non-epidural group. Early breast feeding onset was more frequent in the non-epidural group. The adverse effect of epidural analgesia on early lactation remained significant after adjusting for NICU admission and the need for resuscitation in a logistic regression analysis. Epidural analgesia may have adverse effects on newborns, although the risks are low, and further research is required to elucidate the causal nature of this relationship.

Repercussions of NSAIDS drugs on bone tissue: the osteoblast.

Non-steroidal anti-inflammatory drugs (NSAIDs) can act by modulating the behavior of osteoblasts, including their proliferation, differentiation, adhesion, and migration, but not all NSAIDs have these effects. Our objective was to update the information on this issue in a review of the literature in order to offer guidance on the prescription of the appropriate NSAID(s) to patients requiring bone tissue repair. To review current knowledge of this issue by searching for all relevant publications since 2001 in the MEDLINE, EMBASE and Cochrane Library databases, we used the following descriptors: bone tissue, osteoblast, NSAIDs, Anti-inflammatory drugs. Published studies show that most NSAIDs have an adverse effect on osteoblast growth by cell cycle arrest and apoptosis induction. The effect on differentiation varies according to the drug, dose, and treatment time. Osteoblast adhesion is increased and migration decreased by some NSAIDs, such as indomethacin and diclofenac. The antigenic profile or phagocytic function can also be modulated by NSAIDs. In general, NSAIDs have an adverse effect on bone tissue and given the routine administration of NSAIDs to individuals requiring bone repair, in which the osteoblast has an essential role, this effect on bone should be borne in mind.

Therapeutic doses of nonsteroidal anti-inflammatory drugs inhibit osteosarcoma MG-63 osteoblast-like cells maturation, viability, and biomineralization potential.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are frequently used to reduce pain and inflammation. However, their effect on bone metabolisms is not well known, and results in the literature are contradictory. The present study focusses on the effect of dexketoprofen, ketorolac, metamizole, and acetylsalicylic acid, at therapeutic doses, on different biochemical and phenotypic pathways in human osteoblast-like cells. Osteoblasts (MG-63 cell line) were incubated in culture medium with 1-10 µM of dexketoprofen, ketorolac, metamizole, and acetylsalicylic acid. Flow cytometry was used to study antigenic profile and phagocytic activity. The osteoblastic differentiation was evaluated by mineralization and synthesis of collagen fibers by microscopy and alkaline phosphatase activity (ALP) by spectrophotometric assay. Short-term treatment with therapeutic doses of NSAIDs modulated differentiation, antigenic profile, and phagocyte activity of osteoblast-like cells. The treatment reduced ALP synthesis and matrix mineralization. However, nonsignificant differences were observed on collagen syntheses after treatments. The percentage of CD54 expression was increased with all treatments. CD80, CD86, and HLA-DR showed a decreased expression, which depended on NSAID and the dose applied. The treatments also decreased phagocyte activity in this cellular population. The results of this paper provide evidences that NSAIDs inhibit the osteoblast differentiation process thus reducing their ability to produce new bone mineralized extracellular matrix.

Use of platelet-rich plasma to treat pressure ulcers: a case study.

BACKGROUND: Pressure ulcers (PUs) are prevalent and chronic wounds that require significant time to heal and the search for new treatments to reduce healing time is ongoing. We describe our experience with platelet-rich plasma to facilitate PU healing. CASE: An 86-year-old woman residing in a long-term care facility developed a grade III PU on her right heel that exhibited no signs of healing despite topical therapy over a 4-month period. Her PU was treated with platelet-rich plasma generated from her own blood, with a follow-up every 3 days for a period of 8 weeks. CONCLUSIONS: The platelet-rich plasma-treated PU closed completely at 54 days. We found platelet-rich plasma easy to apply and inexpensive. Additional research is needed to evaluate the efficacy of this intervention in patients with nonhealing PUs.

Effect of aspirin on cell growth of human MG-63 osteosarcoma line.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used in bone tissue repair treatment for their pharmacological action. The objective of this study was to determine the effect of aspirin, on osteoblast growth, using MG63 cell line as osteoblast model. MTT spectrophotometry results showed that 20, 100, and 1000 µM aspirin doses have an inhibitory effect on growth. Cell cycle analysis revealed that aspirin doses of 100 and 1000 µM arrest the cell cycle in phase GO/G1. Parallel apoptosis/necrosis studies showed no changes in comparison to control cells after treatment with 1 or 10 µM aspirin but a significantly increased percentage of cells in apoptosis at doses of 20, 100, and 1000 µM. We highlight that treatment of osteoblast-like cells with 1000 µM aspirin increased not only the percentage of cells in apoptosis but also the percentage of necrotic cells, which was not observed in aspirin treatments at lower doses.