Potential Preventive Treatment Research Articles

Subject-specific planning of femoroplasty: A combined evolutionary optimization and particle diffusion model approach

A potential effective treatment for prevention of osteoporotic hip fractures is augmentation of the mechanical properties of the femur by injecting it with agents such as (PMMA) bone cement – femoroplasty. The operation, however, is only in research stage and can benefit substantially from computer planning and optimization. We report the results of computational planning and optimization of the procedure for biomechanical evaluation. An evolutionary optimization method was used to optimally place the cement in finite element (FE) models of seven osteoporotic bone specimens. The optimization, with some inter-specimen variations, suggested that areas close to the cortex in the superior and inferior of the neck and supero-lateral aspect of the greater trochanter will benefit from augmentation. We then used a particle-based model for bone cement diffusion simulation to match the optimized pattern, taking into account the limitations of the actual surgery, including limited volume of injection to prevent thermal necrosis. Simulations showed that the yield load can be significantly increased by more than 30%, using only 9ml of bone cement. This increase is comparable to previous literature reports where gross filling of the bone was employed instead, using more than 40ml of cement. These findings, along with the differences in the optimized plans between specimens, emphasize the need for subject-specific models for effective planning of femoral augmentation.

Effects of CO2 laser irradiation on tooth enamel coated with biofilm

CO2 laser irradiation of tooth enamel can inhibit demineralization of tooth enamel, by changing enamel composition and resistance to acid attack. The aim of this work was to examine these effects of CO2 laser irradiation on enamel covered by biofilm. Streptococcus mutans was grown on bovine enamel surfaces for 48 hours to form a mature biofilm. Samples were irradiated by CO2 laser (wavelength of 10.6 µm) at a power of 0.08 W in a super-pulse mode for 1 second and 24 pulses/second, with an energy density of 0.77 J/cm(2) per pulse. Untreated controls and laser treated samples with and without biofilm were examined for the morphology of the biofilm and the enamel surface by scanning electron microscopy (SEM). Structural biofilm viability was assessed using confocal laser scanning microscopy with live/dead staining. The biofilm was removed in a sonication water bath and the non-treated and irradiated enamel samples were chemically analyzed using energy dispersive X-ray spectrometry (EDS) and Fourier transform infrared spectroscopy (FTIR). Irradiated samples showed a melt zone with micro-cracks in the center of the irradiating beam position, which was smaller when irradiated enamel was covered by biofilm. Confocal microscopy images demonstrated higher proportion of dead bacteria at the margins of the irradiated spot area, while at the spot center the bacteria were evaporated exposing the enamel surface to direct laser irradiation. EDS analysis showed an increase in Ca/P ratio after irradiation of enamel covered with biofilm. FTIR analysis showed an approximately 40% carbonate loss in the irradiated enamel samples, including those with biofilms. Biofilms protect enamel surfaces from possible morphological irradiation damage without interfering with the resultant chemical changes that may increase the enamel resistance to acid attack. Therefore, under certain exposure regimens that are thermally and mechanically safe for enamel, CO2 laser irradiation of biofilms on dental hard tissues is suggested as a potential novel preventive treatment for controlling dental caries.

Omalgia in Laparoscopic Kidney Surgery

Minimal invasive surgery has well-known advantages. The majority of procedures performed on the kidney are now-a-days laparoscopic, with several advantages over laparotomy: decreased perioperative morbidity and mortality, smaller incisions, faster recovery, shorter hospital stays and earlier return to active life. Postoperative pain is the most common complaint and an important issue following laparoscopic surgery. There are different theories proposed to explain omalgia: distension of the peritoneal blood vessels and nerves during pneumoperitoneum, the associated inflammatory reaction (release of proinflammatory cytokines), rate of CO2 infusion; distension of the triangular and round ligament; time of exposure to the gas; gas retention inducing irritation of the phrenic nerve; nerve injury during patient positioning (shoulder abduction) and diaphragm injury. Debate still exists on how to minimize it. We review the different etiologic mechanisms and proven and potential preventive measures and treatments on how to avoid postoperatory pain: proper patient positioning, pulmonary recruitment maneuvers, intraperitoneal normal saline infusion, using gabapentin, pregabalin, irrigation with bupivacaine, using NSAIDs, opioids and hydrocortisone.

Translational Research Using a Mouse Model of Intracranial Aneurysm

We have developed a mouse model of intracranial aneurysm that recapitulates key features of human intracranial aneurysms. In this model, spontaneous aneurysmal rupture occurs with a predictable time course. Aneurysmal rupture in this model can be easily detected by assessing neurological symptoms. Similar to human intracranial aneurysms, intracranial aneurysms in this model show an infiltration with inflammatory cells. This mouse model can be used to study the mechanisms and the potential preventive treatments for aneurysmal rupture.

Electrocautery-induced cavernous nerve injury in rats that mimics radical prostatectomy in humans

To investigate the early and delayed effects of cavernous nerve electrocautery injury (CNEI) in a rat model, with the expectation that this model could be used to test rehabilitation therapies for erectile dysfunction (ED) after radical prostatectomy (RP). In all, 30 male Sprague-Dawley rats were randomly divided equally into two groups (15 per group). The control group received CNs exposure surgery only and the experimental group received bilateral CNEI. At 1, 4 and 16 weeks after surgery (five rats at each time point), the ratio of maximal intracavernosal pressure (ICP) to mean arterial pressure (MAP) was measured in the two groups. Neurofilament expression in the dorsal penile nerves was assessed by immunofluorescent staining and Masson's trichrome staining was used to assess the smooth muscle to collagen ratio in both groups. At the 1-week follow-up, the mean ICP/MAP was significantly lower in the CNEI group compared with the control group, at 9.94% vs 70.06% (P < 0.05). The mean ICP/MAP in the CNEI group was substantially increased at the 4- (35.97%) and 16-week (37.11%) follow-ups compared with the 1-week follow-up (P < 0.05). At all three follow-up time points, the CNEI group had significantly decreased neurofilament staining compared with the control group (P < 0.05). Also, neurofilament expressions in the CNEI group at both 4 and 16 weeks were significantly higher than that at 1 week (P < 0.05), but there was no difference between 4 and 16 weeks (P > 0.05). The smooth muscle to collagen ratio in the CNEI group was significantly lower than in the control group at the 4- and 16-week follow-ups (P < 0.05), and the ratio at 16 weeks was further reduced compared with that at 4 weeks (P < 0.05). In the CNEI rat model, we found the damaging effects of CNEI were accompanied by a decline in ICP, reduced numbers of nerve fibres in the dorsal penile nerve, and exacerbated fibrosis in the corpus cavernosum. This may provide a basis for studying potential preventative measures or treatment strategies to ameliorate ED caused by CNEI during RP.

Maternal exposure to bisphenol A may increase the risks of Parkinson’s disease through down-regulation of fetal IGF-1 expression

So far, the pathogenesis of Parkinson’s disease (PD) remains unclear. Current studies implicate environmental toxins may be potential causes of fetal origin of PD. BPA is a member of the family of estrogenic chemicals existing widely in environment. Significant evidences from animal experimentation have demonstrated that BPA interfere with fetal neurodevelopment. Based on previous reports and our research on EB derived from hESCs, we speculate that maternal exposure to low-dose BPA during gestational period may decrease IGF-1 expression, thus hinder the development of fetal DA neurons, and finally increase the risks of fetal origin of PD. Our hypothesis may shed new light on the pathogenesis of PD and lead to potential preventive treatments.

A Particle Model for Prediction of Cement Infiltration of Cancellous Bone in Osteoporotic Bone Augmentation

Femoroplasty is a potential preventive treatment for osteoporotic hip fractures. It involves augmenting mechanical properties of the femur by injecting Polymethylmethacrylate (PMMA) bone cement. To reduce the risks involved and maximize the outcome, however, the procedure needs to be carefully planned and executed. An important part of the planning system is predicting infiltration of cement into the porous medium of cancellous bone. We used the method of Smoothed Particle Hydrodynamics (SPH) to model the flow of PMMA inside porous media. We modified the standard formulation of SPH to incorporate the extreme viscosities associated with bone cement. Darcy creeping flow of fluids through isotropic porous media was simulated and the results were compared with those reported in the literature. Further validation involved injecting PMMA cement inside porous foam blocks — osteoporotic cancellous bone surrogates — and simulating the injections using our proposed SPH model. Millimeter accuracy was obtained in comparing the simulated and actual cement shapes. Also, strong correlations were found between the simulated and the experimental data of spreading distance (R2 = 0.86) and normalized pressure (R2 = 0.90). Results suggest that the proposed model is suitable for use in an osteoporotic femoral augmentation planning framework.

Curcumin: a natural substance with potential efficacy in Alzheimer&amp;rsquo;s disease

Curcumin is a component of turmeric, a spice used in many types of cooking. Epidemiological evidence suggesting that populations that eat food with a substantial amount of curcumin were at lower risk of Alzheimer’s disease (AD) led to the idea that this compound might have a neuroprotective effect. Curcumin has substantial antioxidant and anti-inflammatory effects, and is being used as a potential preventative agent or treatment for many types of cancer. There is evidence to suggest that the addition of curcumin to cultured neuronal cells decreases brain inflammation and protects against β-amyloid-induced neurotoxicity. Curcumin also protects against toxicity when β-amyloid is administered to produce animal models of AD. Curcumin decreases β-amyloid formation from amyloid precursor protein, and also inhibits aggregation of β-amyloid into pleated sheets. Studies in transgenic mice with overproduction of β-amyloid demonstrate a neuroprotective effect of curcumin as well. Cognitive function was also improved in these animal models. Clinical trials of curcumin in AD have not been very promising. It is possible that this is due to poor oral bioavailability of curcumin in humans, and thus several approaches are being developed to improve delivery systems or to create analogs that will mimic the neuroprotective effects and easily reach the brain. The lack of efficacy of curcumin in humans with AD may also result from treating for too short a time or starting treatment too late in the course of the disease, where substantial neuronal death has already occurred and cannot be reversed. Curcumin may be beneficial in protecting against development or progression of AD if taken over the long term and started before symptoms of AD become apparent.

Prevention of Schizophrenia: An Impossible Dream?

Prevention of Schizophrenia: An Impossible Dream?

A hypothesized mechanism for the cardiovascular risk associated with antipsychotic drug exposure and a potential preventive treatment

A hypothesized mechanism for the cardiovascular risk associated with antipsychotic drug exposure and a potential preventive treatment

The type 2 CCK/gastrin receptor antagonist YF476 acutely prevents NSAID-induced gastric ulceration while increasing iNOS expression

YF476 differs from the proton pump inhibitor (PPI) esomeprazole in mode of action by antagonizing the type 2 receptor of cholecystokinin/gastrin (CCK-2R). YF476 protection against diclofenac-induced gastric ulcers was compared to esomeprazole and correlated with plasma levels of hormones related to gastric pH (gastrin, ghrelin, and somatostatin), gastric gene expression of these hormones, their receptors, and inducible nitric oxide synthase (iNOS). YF476 or esomeprazole pretreatments were followed by diclofenac. Four hours later, gastric tissue was excised and analyzed for ulcer index. An intragastrically implanted Bravo capsule measured pH for 5days during YF476 plus pentagastrin treatment. Changes in gene expression were assayed for gastrin, ghrelin, and somatostatin; their receptors; and iNOS. YF476 acutely (within 4h) protected against diclofenac-induced gastric ulcers equivalent to esomeprazole. Gastric pH recorded during 5days in the presence of pentagastrin was 1.83 (±0.06). YF476 raised pH to 3.67 (±0.09) and plasma ghrelin, gastrin, and somatostatin increased. YF476 increased gene expression of somatostatin receptor and gastrin, while ghrelin receptor decreased; transcripts coding ghrelin, somatostatin, and CCK-2R remained unchanged. In the presence of diclofenac, esomeprazole increased expression of all these transcripts and that of iNOS, while YF476 yielded only decreased CCK-2R and increased iNOS transcripts. YF476 is a potential new preventative treatment for patients at risk of nonsteroidal antiinflammatory drug (NSAID)-induced ulceration. Gastric gene expressions of ghrelin, gastrin, and somatostatin and their receptors differ between esomeprazole and YF476. Despite these differences and different modes of action to raise gastric pH, both drugs acutely increase iNOS, suggesting iNOS expression parallels pH.

Oxidative stress in the etiology of age-associated decline in glucose metabolism.

One of the most common pathologies in aging humans is the development of glucose metabolism dysfunction. The high incidence of metabolic dysfunction, in particular type 2 diabetes mellitus, is a significant health and economic burden on the aging population. However, the mechanisms that regulate this age-related physiological decline, and thus potential preventative treatments, remain elusive. Even after accounting for age-related changes in adiposity, lean mass, blood lipids, etc., aging is an independent factor for reduced glucose tolerance and increased insulin resistance. Oxidative stress has been shown to have significant detrimental impacts on the regulation of glucose homeostasis in vitro and in vivo. Furthermore, oxidative stress has been shown to be modulated by age and diet in several model systems. This review provides an overview of these data and addresses whether increases in oxidative stress with aging may be a primary determinant of age-related metabolic dysfunction.

Effect of experimental photopolymerized coatings on the hydrophobicity of a denture base acrylic resin and on Candida albicans adhesion

ObjectiveThis study investigated the effect of experimental photopolymerized coatings, containing zwitterionic or hydrophilic monomers, on the hydrophobicity of a denture base acrylic resin and on Candida albicans adhesion. MethodsAcrylic specimens were prepared with rough and smooth surfaces and were either left untreated (control) or coated with one of the following experimental coatings: 2-hydroxyethyl methacrylate (HE); 3-hydroxypropyl methacrylate (HP); and 2-trimethylammonium ethyl methacrylate chloride (T); and sulfobetaine methacrylate (S). The concentrations of these constituent monomers were 25%, 30% or 35%. Half of the specimens in each group (control and experimentals) were coated with saliva and the other half remained uncoated. The surface free energy of all specimens was measured, regardless of the experimental condition. C. albicans adhesion was evaluated for all specimens, both saliva conditioned and unconditioned. The adhesion test was performed by incubating specimens in C. albicans suspensions (1×107cell/mL) at 37°C for 90min. The number of adhered yeasts were evaluated by XTT (2,3-bis[2-methoxy-4-nitro-5-sulfophenyl]-5-[{phenylamino}carbonyl]-2H-tetrazolium-hydroxide) method. ResultsFor rough surfaces, coatings S (30 or 35%) and HP (30%) resulted in lower absorbance values compared to control. These coatings exhibited more hydrophilic surfaces than the control group. Roughness increased the adhesion only in the control group, and saliva did not influence the adhesion. The photoelectron spectroscopy analysis (XPS) confirmed the chemical changes of the experimental specimens, particularly for HP and S coatings. ConclusionsS and HP coatings reduced significantly the adhesion of C. albicans to the acrylic resin and could be considered as a potential preventive treatment for denture stomatitis.

Intervention of PKC-θ as an immunosuppressive regimen

PKC-θ is selectively enriched in T cells and specifically translocates to immunological synapse where it mediates critical T cell receptor signals required for T cell activation, differentiation, and survival. T cells deficient in PKC-θ are defective in their ability to differentiate into inflammatory effector cells that mediate actual immune responses whereas, their differentiation into regulatory T cells (Treg) that inhibits the inflammatory T cells is enhanced. Therefore, the manipulation of PKC-θ activity can shift the ratio between inflammatory effector T cells and inhibitory Tregs, to control T cell-mediated immune responses that are responsible for autoimmunity and allograft rejection. Indeed, PKC-θ-deficient mice are resistant to the development of several Th2 and Th17-dependent autoimmune diseases and are defective in mounting alloimmune responses required for rejection of transplanted allografts and graft-versus-host disease. Selective inhibition of PKC-θ is therefore considered as a potential treatment for prevention of autoimmune diseases and allograft rejection.

On the Use of Cavinton and Cerebrolysin in the Preventive Treatment of Alzheimer’s Disease1

The first issue of Zhurnal Nevrologii i Psikhiatrii im. S. S. Korsakova [S. S. Korsakov Journal of Neurology and Psychiatry] for 2010 included an article by a group of authors entitled “Potential preventive treatment of Alzheimer’s disease: results of a three-year prospective open comparative study of the efficacy and safety of courses of cerebrolysin and Cavinton in elderly patients with mild cognitive deficit syndrome,” addressing a comparison of the efficacies of these agents in moderate cognitive dysfunction. Cerebrolysin is a nootropic agent. It is registered in the Russian Federation for the treatment of Alzheimer’s disease, dementia syndromes of various etiologies, and chronic cerebrovascular failure. 2 Cavinton is a member of the pharmacological group of cerebral circulatory correctors and was registered in the Russian Federation for the treatment of acute and chronic cerebral circulatory failure (transient ischemia, progressive stroke, post-stroke states, vascular dementia, cerebrovascular atherosclerosis, post-traumatic and hypertensive encephalopathies, vertebrobasilar failure), as well as for the treatment of mental and neurological disorders (memory impairment, vertigo, headache, aphasia, apraxia, motor disorders) in patients with cerebrovascular failure. 2 The study inclusion criteria listed by the authors point directly to the search, using specific clinical psychological methods, for the moderate cognitive deficit symptoms typical of Alzheimer’s disease. In combination with low points

Controversies surrounding the clinical potential of cinnamon for the management of diabetes

Obesity levels have increased significantly in the past five decades and are predicted to continue rising, resulting in important health implications. In particular, this has translated to an increase in the occurrence of type II diabetes mellitus (T2D). To alleviate associated problems, certain nutraceuticals have been considered as potential adjuncts or alternatives to conventional prescription drugs. Cinnamon, a commonly consumed spice originating from South East Asia, is currently being investigated as a potential preventative supplement and treatment for insulin resistance, metabolic syndrome and T2D. Extensive in vitro evidence has shown that cinnamon may improve insulin resistance by preventing and reversing impairments in insulin signalling in skeletal muscle. In adipose tissue, it has been shown that cinnamon increases the expression of peroxisome proliferator-activated receptors including, PPARγ. This is comparable to the action of commonly used thiazolinediones, which are PPAR agonists. Studies have also shown that cinnamon has potent anti-inflammatory properties. However, numerous human clinical trials with cinnamon have been conducted with varying findings. While some studies have showed no beneficial effect, others have indicated improvements in cholesterol levels, systolic blood pressure, insulin sensitivity and postprandial glucose levels with cinnamon. However, the only measurement consistently improved by cinnamon consumption is fasting glucose levels. While it is still premature to suggest the use of cinnamon supplementation based on the evidence, further investigation into mechanisms of action is warranted. Apart from further characterization of genetic and epigenetic changes in model systems, systematic large-scale clinical trials are required. In this study, we discuss the mechanisms of action of cinnamon in the context of T2D and we highlight some of the associated controversies.

Mangafodipir Protects against Hepatic Ischemia-Reperfusion Injury in Mice

Introduction and AimMangafodipir is a contrast agent used in magnetic resonance imaging that concentrates in the liver and displays pleiotropic antioxidant properties. Since reactive oxygen species are involved in ischemia-reperfusion damages, we hypothesized that the use of mangafodipir could prevent liver lesions in a mouse model of hepatic ischemia reperfusion injury. Mangafodipir (MnDPDP) was compared to ischemic preconditioning and intermittent inflow occlusion for the prevention of hepatic ischemia-reperfusion injury in the mouse.MethodsMice were subjected to 70% hepatic ischemia (continuous ischemia) for 90 min. Thirty minutes before the ischemic period, either mangafodipir (10 mg/kg) or saline was injected intraperitoneally. Those experimental groups were compared with one group of mice preconditioned by 10 minutes' ischemia followed by 15 minutes' reperfusion, and one group with intermittent inflow occlusion. Hepatic ischemia-reperfusion injury was evaluated by measurement of serum levels of aspartate aminotransferase (ASAT) activity, histologic analysis of the livers, and determination of hepatocyte apoptosis (cytochrome c release, caspase 3 activity). The effect of mangafodipir on the survival rate of mice was studied in a model of total hepatic ischemia.ResultsMangafodipir prevented experimental hepatic ischemia-reperfusion injuries in the mouse as indicated by a reduction in serum ASAT activity (P<0.01), in liver tissue damages, in markers of apoptosis (P<0.01), and by higher rates of survival in treated than in untreated animals (P<0.001). The level of protection by mangafodipir was similar to that observed following intermittent inflow occlusion and higher than after ischemic preconditioning.ConclusionsMangafodipir is a potential new preventive treatment for hepatic ischemia-reperfusion injury.

Expanding the role of statins in postoperative atrial fibrillation

p p A Atrial fibrillation (AF) is a growing public health problem, predicted to impact as many as 15 million people by 2050. In addition to its well-known associated risks in an outpatient population, isolated perioperative AF (POAF) following cardiac surgery also contributes to increased mortality, increased length of hospital stay, and increased health-care costs. Various strategies to reduce POAF in cardiac surgery patients have been shown to be effective in reducing POAF and health-care costs. Many potential preventive treatments of AF and POAF focus on the modulation of the specific pathways that create the environment for AF to occur. In rapid atrial pacing animal models of AF, inhibition of the renin–angiotensin– aldosterone system with angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers attenuates the development of atrial hypertrophy and fibrosis. Both angiotensin-receptor blockers and angiotensin-converting enzyme inhibitors have been shown to reduce the incidence of new-onset AF in post hoc analyses in randomized controlled trials for the treatment of hypertension and congestive heart failure. Also, the use of angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers has been associated with lower rates of POAF in cardiac surgery; however, prospective randomized trials testing the use of renin– angiotensin–aldosterone system inhibition to prevent POAF after cardiac surgery failed to show a convincing benefit. Corticosteroids and nonsteroidal anti-inflammatory drugs can inhibit the inflammatory mediators associated with AF. They have been shown in limited series to help reduce POAF after cardiac surgery but are associated with higher rates of AF with chronic use. Amiodarone and sotalol are beneficial in reducing POAF after cardiac surgery, likely owing to their direct antiarrhythmic effects. Beta-blockers also are helpful in the prevention of POAF after cardiac surgery. Statins have been shown in multiple trials and observational series to reduce the development of AF and POAF in patients undergoing cardiac surgery. In ARMYDA-3, treatment with atorvastatin 80 mg resulted in a 61% reduction in POAF. A meta-analysis showed that statins were effective

Recovery of Corneal Sensitivity, Calcitonin Gene-Related Peptide–Positive Nerves, and Increased Wound Healing Induced by Pigment Epithelial–Derived Factor Plus Docosahexaenoic Acid After Experimental Surgery

To assess function of regenerated corneal nerves in correlation with epithelial wound healing after experimental nerve damage in rabbits treated with pigment epithelial-derived factor (PEDF) plus docosahexaenoic acid (DHA). An 8-mm stromal dissection was performed in the right eyes of adult New Zealand rabbits. Treatment with PEDF+DHA was for 6 weeks. Corneal sensation was measured weekly by Cochet-Bonnet esthesiometer. After 8 weeks, immunofluorescence with βIII-tubulin, calcitonin gene-related peptide, and substance P antibodies was performed to quantify nerves. Also, rabbits were treated with PEDF+DHA for 4 weeks after lamellar keratectomy, followed by 8-mm epithelial debridement and epithelial defect assessment. One week after surgery, corneas were stained with anti-Ki67 antibody to assess cell proliferation. Eight weeks after surgery, calcitonin gene-related peptide-positive nerve fibers in the PEDF+DHA group were similar to normal rabbit corneas but were decreased in the vehicle. Substance P was localized in the subepithelial plexus but appeared in epithelial cells after nerve injury regardless of treatment. Five weeks after surgery, an increase in corneal sensitivity occurred in the PEDF+DHA group and reached normal values by 8 weeks. Pigment epithelial-derived factor plus DHA increased epithelial wound healing after lamellar keratectomy. One week after epithelial injury, Ki67-positive cells increased in the limbal area. Pigment epithelial-derived factor plus DHA promotes regeneration of calcitonin gene-related peptide-positive corneal nerves, accelerating wound healing and return of corneal sensitivity. Pigment epithelial-derived factor plus DHA represents a new approach to regenerate nerves and a potential treatment for prevention of severe dry eye after surgery or diseases of the ocular surface.

A protective effect of Curcuma comosa Roxb. on bone loss in estrogen deficient mice

Ethnopharmacological relevance Curcuma comosa Roxb. or Wan chak motluk is an indigenous medicinal herb and has traditionally been used among postmenopausal women for relief of unpleasant menopausal symptoms. Aim of the study Estrogen deficiency is a causative factor in the development of osteoporosis in menopausal women. Phytoestrogens, non-steroidal plant-derived compounds which have an array of beneficial effects, are considered as an effective alternative compound in preventing bone loss caused by the deficiency of estrogen. The present study determined the potential effect of Curcuma comosa Roxb. ( C. comosa) hexane extract containing phytoestrogens in protecting bone loss induced by ovariectomy in mice. Materials and methods Mature Swiss albino female mice were ovariectomized and treated with the C. comosa extract for 5 weeks. Bone calcium content, bone mass density, histology, and bone markers were evaluated. Results The ovariectomized mice showed a marked decrease in total bone calcium content and bone mass density of lumbar vertebrae 5–6, femur and tibia bone in comparison with the intact control mice. Bone histology demonstrated the poor development of endochondral bone formation in ovariectomized mice which correlated with a decrease in plasma bone alkaline phosphatase activity. Treatment with C. comosa protected against the loss of total bone calcium content and bone mass density in both trabecular and cortical bones, similar to results observed with estrogen treatment. In addition, C. comosa treatment resulted in less increase in uterine weight compared to estrogen treatment. Conclusion Our results suggest that C. comosa prevents bone loss induced by estrogen deficiency. Therefore, C. comosa would be a potential alternative treatment for prevention of postmenopausal osteoporosis.