There is little doubt that serotonin influences bone biology. Bone loss in elderly patients on long-term selective serotonin receptor inhibitor (SSRI) or tricyclic (TCA) anti-depressant (AD) medication is considered to be secondary to a more sedentary lifestyle. However, a recent report suggested that in mice treated with SSRIs or TCAs the disturbances in normal bone mass was unrelated to the activity levels of the animal (Warden 2010). This could imply that psychoactive agents have a direct effect on normal bone cell metabolism. We have tested this hypothesis in vitro. Two SSRIs (fluoxetine hydrochloride (FLU) and citalopram hydrobromide (CIT)) and two TCAs (amitriptyline hydrochloride (AMI) and clomipramine hydrochloride (CLO)) in various doses at, above and below serum levels in treated patients (0.06μM–10μM) were added to rat osteoblast-like UMR106 cells and the effect on cell proliferation (DNA content per well) and alkaline phosphatase (AlkP) activity (soluble reaction product) assessed. After 72 hours treatment with SSRI or TCA (0.6μM), there was significant reduction in AlkP activity. DNA content was significantly reduced in all cases, except FLU. These data demonstrate a direct effect of ADs on bone cell behaviour

We analysed the effects of commonly used medications on human osteoblastic cell activity in vitro, specifically proliferation and tissue mineralisation. A list of medications was retrieved from the records of patients aged > 65 years filed in the database of the largest health maintenance organisation in our country (> two million members). Proliferation and mineralisation assays were performed on the following drugs: rosuvastatin (statin), metformin (antidiabetic), metoprolol (β-blocker), citalopram (selective serotonin reuptake inhibitor [SSRI]), and omeprazole (proton pump inhibitor (PPI)). All tested drugs significantly stimulated DNA synthesis to varying degrees, with rosuvastatin 5 µg/ml being the most effective among them (mean 225% (. sd. 20)), compared with metformin 10 µg/ml (185% (. sd.  10)), metoprolol 0.25 µg/ml (190% (. sd. 20)), citalopram 0.05 µg/ml (150% (. sd. 10)) and omeprazole 0.001 µg/ml (145% (. sd. 5)). Metformin and metoprolol (to a small extent) and rosuvastatin (to a much higher extent) inhibited cell mineralisation (85% (. sd. 5)). Our results indicate the need to evaluate the medications prescribed to patients in terms of their potential action on osteoblasts. Appropriate evaluation and prophylactic treatment (when necessary) might lower the incidence and costs associated with potential medication-induced osteoporosis. Cite this article: Bone Joint J 2013;95-B:1575–80

Platelet-rich plasma is a new inductive therapy which is being increasingly used for the treatment of the complications of bone healing, such as infection and nonunion. The activator for platelet-rich plasma is a mixture of thrombin and calcium chloride which produces a platelet-rich gel.

We analysed the antibacterial effect of platelet-rich gel in vitro by using the platelet-rich plasma samples of 20 volunteers. In vitro laboratory susceptibility to platelet-rich gel was determined by the Kirby-Bauer disc-diffusion method. Baseline antimicrobial activity was assessed by measuring the zones of inhibition on agar plates coated with selected bacterial strains.

Zones of inhibition produced by platelet-rich gel ranged between 6 mm and 24 mm (mean 9.83 mm) in diameter. Platelet-rich gel inhibited the growth of Staphylococcus aureus and was also active against Escherichia coli. There was no activity against Klebsiella pneumoniae, Enterococcus faecalis, and Pseudomonas aeruginosa. Moreover, platelet-rich gel seemed to induce the in vitro growth of Ps. aeruginosa, suggesting that it may cause an exacerbation of infections with this organism. We believe that a combination of the inductive and antimicrobial properties of platelet-rich gel can improve the treatment of infected delayed healing and nonunion.