Investigating the chemo-preventive role of noscapine in lung carcinoma via therapeutic targeting of human aurora kinase B.

Lung carcinoma is the major contributor to global cancer incidence and one of the leading causes of cancer-related mortality worldwide. Irregularities in signal transduction events, genetic alterations, and mutated regulatory genes trigger cancer development and progression. Selective targeting of molecular modulators has substantially revolutionized cancer treatment strategies with improvised efficacy. The aurora kinase B (AURKB) is a critical component of the chromosomal passenger complex and is primarily involved in lung cancer pathogenesis. Since AURKB is an important therapeutic target, the design and development of its potential inhibitors are attractive strategies. In this study, noscapine was selected and validated as a possible inhibitor of AURKB using integrated computational, spectroscopic, and cell-based assays. Molecular docking analysis showed noscapine occupies the substrate-binding pocket of AURKB with strong binding affinity. Subsequently, MD simulation studies confirmed the formation of a stable AURKB-noscapine complex with non-significant alteration in various trajectories, including RMSD, RMSF, Rg, and SASA. These findings were further experimentally validated through fluorescence binding studies. In addition, dose-dependent noscapine treatment significantly attenuated recombinant AURKB activity with an IC50 value of 26.6 µM. Cell viability studies conducted on A549 cells and HEK293 cells revealed significant cytotoxic features of noscapine on A549 cells. Furthermore, Annexin-PI staining validated that noscapine triggered apoptosis in lung cancer cells, possibly via an intrinsic pathway. Our findings indicate that noscapine-based AURKB inhibition can be implicated as a potential therapeutic strategy in lung cancer treatment and can also provide a novel scaffold for developing next-generation AURKB-specific inhibitors.

Structural insight into the binding mode of cefotaxime and meropenem to TEM-1, SHV-1, KPC-2, and Amp-C type beta-lactamases.

Antimicrobial resistance is an emerging threat to public health around the world. The study employs computational and biophysical methods to investigate the properties of cefotaxime and meropenem's binding to various beta-lactamases like TEM-1, SHV-1, KPC-2, and Amp-C. The enzyme kinetics of purified proteins revealed an increase in Michaelis constant (Km) value in the presence of meropenem and cefotaxime, indicating a decrease in enzyme affinity for nitrocefin. Proteins interact with meropenem/cefotaxime, causing quenching through complex formation. All proteins have one binding site, and binding constant (Kb) values are 104, indicating strong interaction. The study found that meropenem and cefotaxime had high fitness scores for Amp-C, KPC-2,TEM-1 and SHV-1, with binding energy ranging from -7.4 to -7.8, and hydrogen bonds between them. Molecular Dynamic simulation of protein-ligand complexes revealed cefotaxime-binding proteins have slightly lower Root Mean Square Deviation(RMSD) than meropenem-binding proteins, indicating stable association antibiotics with these proteins.

Immunomodulatory Effect of Phytoactive Compounds on Human Health: A Narrative Review Integrated with Bioinformatics Approach.

BACKGROUND: Immunomodulation is the modification of immune responses to control disease progression. While the synthetic immunomodulators have proven efficacy, they are coupled with toxicity and other adverse effects, and hence, the efforts were to identify natural phytochemicals with immunomodulatory potential. OBJECTIVE: The objective of this study is to understand the immunomodulatory properties of various phytochemicals and investigate them in Echinacea species extracts using an in silico approach. METHODOLOGY: Several scientific database repositories were searched using different keywords: "Phytochemicals," "Alkaloids," "Polyphenols," "Flavonoids," "Lectins," "Glycosides," "Tannins," "Terpenoids," "Sterols," "Immunomodulators," and "Human Immune System" without any language restriction. Additionally, the study specifically investigated the immunomodulatory properties of Echinacea species extracts using gene expression analysis of GSE12259 from NCBI-GEO through the Bioconductor package GEOquery and limma. RESULTS: A total of 182 studies were comprehensively analyzed to understand immunomodulatory phytochemicals. The in silico analysis highlighted key biological processes (positive regulation of cytokine production, response to tumor necrosis factor) and molecular functions (cytokine receptor binding, receptor-ligand activity, and cytokine activity) among Echinacea species extracts contributing to immune responses. Further, it also indicated the association of various metabolic pathways, i.e., pathways in cancer, cytokine-cytokine receptor interaction, NF-kappa B, PI3K-Akt, TNF, MAPK, and NOD-like receptor signaling pathways, with immune responses. The study revealed various hub targets, including CCL20, CCL4, GCH1, SLC7A11, SOD2, EPB41L3, TNFAIP6, GCLM, EGR1, and FOS. CONCLUSION: The present study presents a cumulative picture of phytochemicals with therapeutic benefits. Additionally, the study also reported a few novel genes and pathways in Echinacea extracts by re-analyzing GSE 12259, indicating its anti-inflammatory, anti-viral, and immunomodulatory properties.

The role of serum and glucocorticoid-regulated kinase 1 in cellular signaling: Implications for drug development.

Serum and glucocorticoid-regulated kinase 1 (SGK1) is a ubiquitously expressed protein belonging to the Ser/Thr kinase family. It regulates diverse physiological processes, including epithelial sodium channel activity, hypertension, cell proliferation, and insulin sensitivity. Due to its significant role in the pathogenesis of numerous diseases, SGK1 can be exploited as a potential therapeutic target to address challenging health problems. SGK1 is associated with the development of obesity, and its overexpression enhances the sodium-glucose co-transporter 1 activity, which absorbs intestinal glucose. This review highlighted the detailed functional significance of SGK1 signaling and role in different diseases and subsequent therapeutic targeting. We aim to provide deeper mechanistic insights into understanding the pathogenesis and recent advancements in the SGK1 targeted drug development process. Small-molecule inhibitors are being developed with excellent binding affinity and improved SGK1 inhibition with desired selectivity. We have discussed small molecule inhibitors designed explicitly as potent SGK1 inhibitors and their therapeutic implications in various diseases. We further addressed the therapeutic potential and mechanism of action of these SGK1 inhibitors and provided a strong scientific foundation for developing effective therapeutics.

Probing Baicalin as potential inhibitor of Aurora kinase B: A step towards lung cancer therapy.

Cell cycle regulators play pivotal roles as their dysregulation, leads to atypical proliferation and intrinsic genomic instability in cancer cells. Abnormal expression and functioning of Aurora kinase B (AURKB) are associated with cancer pathogenesis and thus exploited as a potential therapeutic target for the development of anti-cancer therapeutics. To identify effective AURKB inhibitors, a series of polyphenols was investigated to check their potential to inhibit recombinant AURKB. Their binding affinities were experimentally validated through fluorescence binding studies. Enzyme inhibition assay revealed that Mangiferin and Baicalin significantly inhibited AURKB activity with an IC50 values of 20.0 µM and 31.1 µM, respectively. To get atomistic insights into the binding mechanism, molecular docking and MD simulations of 100 ns were performed. Both compounds formed many non-covalent interactions with the residues of the active site pocket of AURKB. In addition, minimal conformational changes in the structure and formation of stable AURKB-ligand complex were observed during MD simulation analysis. Finally, cell-based studies suggested that Baicalin exhibited in-vitro cytotoxicity and anti-proliferative effects on lung cancer cell lines. Conclusively, Baicalin may be considered a promising therapeutic molecule against AURKB, adding an additional novel lead to the anti-cancer repertoire.

Integrated spectroscopic and MD simulation approach to decipher the effect of pH on the structure function of Staphylococcus aureus thymidine kinase.

Staphylococcus aureus is a major human pathogen responsible for a variety of clinical infections, becoming increasingly resistant to antibiotics. To address this challenge, there is a need to identify new cellular targets and innovative approaches to expand treatment options. One such target is thymidine kinase (TK), a crucial enzyme in the pyrimidine salvage pathway, which plays a key role in the phosphorylation of thymidine, an essential component in DNA synthesis and repair. In this study, we have successfully cloned, expressed, and purified the TK protein. A comprehensive investigation into how different pH levels affect the structure and functional activity of TK, using a combination of spectroscopy, classical molecular dynamics simulations, and enzyme activity assays was conducted. Our study revealed that variation in pH disrupts secondary and tertiary structures of TK with noticeable aggregate formation at pH 5.0. Enzyme activity studies demonstrated that TK exhibited its maximum kinase activity within the physiological pH range. These findings strongly suggest a connection between structural changes and enzymatic activity, which was further supported by the agreement between the spectroscopic features we measured and the results of our MD simulations. Our study provides a deeper insight into the structural features of TK, which could potentially be harnessed for the development of therapeutic strategies aimed at combatting infectious diseases. Conformational dynamics plays an essential role in the design and development of effective inhibitors. Considering the effects of pH on the conformational dynamics of TK, our findings may be implicated in the development of potent and selective inhibitors.Communicated by Ramaswamy H. Sarma.

Exploring the molecular underpinning of psoriasis and its associated comorbidities through network approach: cross talks of genes and pathways.

Patients with psoriasis often complain of several linked disorders including autoimmune and cardiometabolic diseases. Understanding of molecular link between psoriasis and associated comorbidities would be of great interest at the point of patient care management. Integrative unbiased network approach, indicates significant unidirectional gene overlap between psoriasis and its associated comorbid condition including obesity (31 upregulated and 26 downregulated), ischemic stroke (14 upregulated and 2 downregulated), dyslipidaemia (5 upregulated, 5 downregulated), atherosclerosis (8 upregulated and 1 downregulated) and type II diabetes (5 upregulated, 5 downregulated). The analysis revealed substantial gene sharing among the different psoriasis-associated comorbidities. Molecular comorbidity index determining the strength of the interrelation between psoriasis and its comorbidities indicates prevalence of dyslipidaemia followed by type II diabetes among psoriasis patients. The Jaccard coefficient indices revealed psoriasis shared maximum number of biological pathways with dyslipidaemia followed by type 2 diabetes, ischemic stroke, obesity and atherosclerosis. Moreover, pathway annotation highlighted nearly 45 shared pathways amongst psoriasis and its comorbidities and a substantial number of shared pathways was found among multi-morbidities. Overall, the present study established conceivable link between psoriasis and comorbid diseases. The shared genes and overlapped pathways may be explored as a common productive target for psoriasis and its comorbid conditions. Supplementary Information: The online version contains supplementary material available at 10.1007/s13205-023-03533-y.

Investigating the Role of Antibiotics on Induction, Inhibition and Eradication of Biofilms of Poultry Associated Escherichia coli Isolated from Retail Chicken Meat.

Background: Widespread use of antibiotics as growth promoters and prophylactic agents has dramatic consequences for the development of antibiotic resistance. In this study, we investigated effects of selected antibiotics on bacterial biofilms and performed extensive antibiotic and VF profiling of poultry-meat associated E. coli strains. Methods: Antibiotic susceptibility was performed by a disc diffusion method, followed by molecular screening of resistance and virulence determinants. Further biofilm formation assays, MIC-p, MIC-b, MBIC and MBEC, were performed using standard tissue culture plate method. Results: In total, 83 (75%) samples were confirmed as E. coli from poultry sources, 26 different antibiotics were tested, and maximum numbers of the isolates were resistant to lincomycin (100%), while the least resistance was seen against cefotaxime (1%) and polymyxin B (1%). Overall, 48% of the isolates were ESBL producers and 40% showed carbapenemase activity; important virulence genes were detected in following percentages: fimH32 (39%), papC21 (25%), iutA34 (41%), kpsMT-II23 (28%), papEF9 (11%), papGII22 (27%) and fyuA13 (16%). Colistin showed remarkable anti-biofilm activity, while at sub-MIC levels, gentamicin, ceftriaxone and enrofloxin significantly (p < 0.01) inhibited the biofilms. A strong induction of bacterial biofilm, after exposure to sub-minimal levels of colistin clearly indicates risk of bacterial overgrowth in a farm environment, while use of colistin aggravates the risk of emergence of colistin resistant Enterobacteriaceae, a highly undesirable public health scenario.

The interaction analysis between human serum albumin with chlorpyrifos and its derivatives through sub-atomic docking and molecular dynamics simulation techniques.

Chlorpyrifos (CPF) is an extensively used organophosphate pesticide for crop protection. However, there are concerns about it contaminating the environment and human health, with estimated three lakh deaths annually. The molecular modeling protocol was assisted in redesigning thirteen well-known CPF linkers and inserting them at five selectable CPF (R1-R5) positions of CPF to get 258 CPF derivatives. CPF and its derivatives were optimized using LigPrep and docked to a grid centralized on Trp214 using extra precision glide docking. The Binding free energy of complexes was calculated using molecular mechanics/generalized born surface area (MM-GBSA). CPF and CPFD-225 have glide scores of - 3.08 and - 6.152 kcal/mol, respectively, with human serum albumin and ΔG bind for CPF (- 33.041817 kcal/mol) (- 52.825 kcal/mol) for CPF-D225. The top ten CPF derivatives showed at least ninefold better binding free energy than the CPF proposed for polyclonal antibody production. Subsequently, molecular docking studies revealed that CPF and its derivatives could bind to human serum albumin (HSA). Furthermore, using the Desmond package, a 100-ns molecular dynamics (MD) simulation was performed on the potential binding site. The final systems of CPF-HSA and CPF-222D complexes consist of 76,014 and 76,026 atoms, respectively. The physical stability of both the systems (CPF-HSA and CPF-222D) was analyzed by considering the overall potential energy, RMSF, RMSD, Hydrophobic interactions, and water-mediated patterns, which showed total energy of - 141,610 kcal/mol and - 140,150 kcal/mol, respectively. Supplementary Information: The online version contains supplementary material available at 10.1007/s13205-022-03344-7.

A comparative in silico study to detect the effect of food-additives on metabolic protein and its perturbations compensated by osmolytes.

Since its inception, food additive has been an integral part of the food processing industry with various commercial roles. Besides its advantages, various studies have already highlighted its long-term adverse effects on human health. However, in terms of protein structures and functions, the innate mechanism that triggers these effects has not been elucidated in previously reported studies. Our work takes an in silico approach to delve into structural implications resulting from these additives with three well studied metabolic proteins-lysozyme, bovine serum albumin (BSA) and ribonuclease A. Three classes of food additives- synthetic color, preservatives, and phosphate-containing, are taken here to understand their effects on the aforementioned metabolic proteins. Conventional molecular docking and dynamics (MD) studies reveal that these additives induce significant structural perturbations. Among them, carmoisine brings about the most secondary structural changes for lysozyme and ribonuclease A, whereas sodium tripolyphosphate affects BSA the most. To restore the secondary structural loss, we further examine the roles of osmolytes through cross-docking and higher timescale MD simulations. These studies unravel that application of osmolytes like raffinose and trehalose triggers structural restoration for BSA, lysozyme and ribonuclease A, and highlight their roles as co-formulants to alleviate the adverse effects of food additives.

Biomedical features and therapeutic potential of rosmarinic acid.

For decades, the use of secondary metabolites of various herbs has been an attractive strategy in combating human diseases. Rosmarinic acid (RA) is a bioactive phenolic compound commonly found in plants of Lamiaceae and Boraginaceae families. RA is biosynthesized using amino acids tyrosine and phenylalanine via enzyme-catalyzed reactions. However, the chemical synthesis of RA involves an esterification reaction between caffeic acid and 3,4-dihydroxy phenyl lactic acid contributing two phenolic rings to the structure of RA. Several studies have ascertained multiple therapeutic benefits of RA in various diseases, including cancer, diabetes, inflammatory disorders, neurodegenerative disorders, and liver diseases. Many previous scientific papers indicate that RA can be used as an anti-plasmodic, anti-viral and anti-bacterial drug. In addition, due to its high anti-oxidant capacity, this natural polyphenol has recently gained attention for its possible application as a nutraceutical compound in the food industry. Here we provide state-of-the-art, flexible therapeutic potential and biomedical features of RA, its implications and multiple uses. Along with various valuable applications in safeguarding human health, this review further summarizes the therapeutic advantages of RA in various human diseases, including cancer, diabetes, neurodegenerative diseases. Furthermore, the challenges associated with the clinical applicability of RA have also been discussed.

Therapeutic targeting of TANK-binding kinase signaling towards anticancer drug development: Challenges and opportunities.

TANK-binding kinase 1 (TBK1) plays a fundamental role in regulating the cellular responses and controlling several signaling cascades. It regulates inflammatory, interferon, NF-κB, autophagy, and Akt pathways. Post-translational modifications (PTM) of TBK1 control its action and subsequent cellular signaling. The dysregulation of the TBK1 pathway is correlated to many pathophysiological conditions, including cancer, that implicates the promising therapeutic advantage for targeting TBK1. The present study summarizes current updates on the molecular mechanisms and cancer-inducing roles of TBK1. Designed inhibitors of TBK1 are considered a potential therapeutic agent for several diseases, including cancer. Data from pre-clinical tumor models recommend that the targeting of TBK1 could be an attractive strategy for anti-tumor therapy. This review further highlighted the therapeutic potential of potent and selective TBK1 inhibitors, including Amlexanox, Compound II, BX795, MRT67307, SR8185 AZ13102909, CYT387, GSK8612, BAY985, and Domainex. These inhibitors may be implicated to facilitate therapeutic management of cancer and TBK1-associated diseases in the future.

Assessment of in vitro and in vivo effect of Quercetin 3-Glucoside, Oxyresveratrol and Quercetin O-Hexoside against Leishmania tropica

Abstract The aim was to scrutinize the in vivo and in vitro activities against Leishmania tropica with compounds of Oxyresveratrol, Quercetin O-Hexoside, and Quercetin 3-Glucoside. The in vitro outcomes against Leishmania were analyzed for 24-48 hours on L. tropica KWH23 promastigotes with compounds materials having 50 - 200 µg/mL concentration with negative control and standard drug Amphotericin B. The compounds were analyzed in L. tropica infected BALB/c mice against Leishmania tropica. The Quercetin 3-Glucoside shows mean inhibition of extracellular promastigotes after 48 hours at 50, 100, 150, 200 µg/mL were 91.02 ± 0.12, 94.50 ± 0.07, 96.15 ± 0.17 and 97.01 ± 0.08 % respectively. In BALB/c mice, the intracellular amastigotes were 91% cured at 200 µg/mL and mean lesion size decreased to 0.41 ± 0.21 mm (p < 0.01). The result shows that Quercetin 3-Glucoside possesses significant anti-leishmanial activity.

Impact of Deleterious Mutations on Structure, Function and Stability of Serum/Glucocorticoid Regulated Kinase 1: A Gene to Diseases Correlation.

Serum and glucocorticoid-regulated kinase 1 (SGK1) is a Ser/Thr protein kinase involved in regulating cell survival, growth, proliferation, and migration. Its elevated expression and dysfunction are reported in breast, prostate, hepatocellular, lung adenoma, and renal carcinomas. We have analyzed the SGK1 mutations to explore their impact at the sequence and structure level by utilizing state-of-the-art computational approaches. Several pathogenic and destabilizing mutations were identified based on their impact on SGK1 and analyzed in detail. Three amino acid substitutions, K127M, T256A, and Y298A, in the kinase domain of SGK1 were identified and incorporated structurally into original coordinates of SGK1 to explore their time evolution impact using all-atom molecular dynamic (MD) simulations for 200 ns. MD results indicate substantial conformational alterations in SGK1, thus its functional loss, particularly upon T256A mutation. This study provides meaningful insights into SGK1 dysfunction upon mutation, leading to disease progression, including cancer, and neurodegeneration.

Mechanistic insights into the role of serum-glucocorticoid kinase 1 in diabetic nephropathy: A systematic review.

Aberrant expression of serum-glucocorticoid kinase 1 (SGK1) contributes to the pathogenesis of multiple disorders, including diabetes, hypertension, obesity, fibrosis, and metabolic syndrome. SGK1 variant is expressed in the presence of insulin and several growth factors, eventually modulating various ion channels, carrier proteins, and transcription factors. SGK1 also regulates the enzymatic activity of Na+ K+ ATPase, glycogen synthase kinase-3, ubiquitin ligase Nedd4-2, and phosphomannose mutase impacting cell cycle regulation, neuroexcitation, and apoptosis. Ample evidence supports the crucial role of aberrant SGK1 expression in hyperglycemia-mediated secondary organ damage. Diabetic nephropathy (DN), a dreadful microvascular complication of diabetes, is the leading cause of end-stage renal failures with high morbidity and mortality rate. The complex pathogenesis of DN encompasses several influencing factors, including transcriptional factors, inflammatory markers, cytokines, epigenetic modulators, and abnormal enzymatic activities. SGK1 plays a pivotal role by controlling various physiological functions associated with the occurrence and progression of DN; therefore, targeting SGK1 may favorably influence the clinical outcome in patients with DN. This review aimed to provide mechanistic insights into SGK1 regulated DN pathogenesis and summarize the evidence supporting the therapeutic potential of SGK1 inhibition and its consequences on human health.

Protein-protein interaction and in silico mutagenesis studies on IL17A and its peptide inhibitor.

Protein-protein interactions of Interleukin-17 (IL17) play vital role in the autoimmune and inflammatory diseases, such as rheumatoid arthritis, multiple sclerosis, and psoriasis. Potent therapeutics for these diseases could be developed by blocking or modulating these interactions through biologics, peptide inhibitors and small molecule inhibitors. Unlike biologics, peptide inhibitors are cost effective and can be orally available. Peptide inhibitors do not require a binding groove as that of small molecules either. Therefore, crystal structure of IL17A in complex with a high affinity peptide inhibitor (HAP) (1-IHVTIPADLWDWIN-14) is investigated with an aim to find hot spots that could improve its potency. An in silico mutagenesis strategy was implemented using FoldX PSSM to scan for positions tolerant to amino acid substitution. Three positions T4, A7, and N14 showed improved stability when mutated with 'F/M/Y', 'P' and 'F/M/Y', respectively. A set of 31 mutant peptides are designed through combinations of these tolerant mutations using Build Model application of FoldX. Binding affinity and interactions of 31 peptides are assessed through protein-peptide docking and binding free energy calculations. Two peptides namely, P1 ("1-IHVTIPPDLWDWIY-14") and P2 ("1-IHVMIPPDLWDWIF-14") showed better binding affinity to IL17A dimerization site compared to HAP. Interactions of P1, P2 and HAP are also analyzed through 100 ns molecular dynamics simulations using GROMACS v5.0. The results revealed that the P2 peptide likely to offer better potency compared to HAP and P1. Therefore, the P2 peptide can be synthesized to develop oral therapies for autoimmune and inflammatory diseases with further experimental evaluations. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13205-021-02856-y.

Recent Advances and Implication of Bioengineered Nanomaterials in Cancer Theranostics.

Cancer is one of the most common causes of death and affects millions of lives every year. In addition to non-infectious carcinogens, infectious agents contribute significantly to increased incidence of several cancers. Several therapeutic techniques have been used for the treatment of such cancers. Recently, nanotechnology has emerged to advance the diagnosis, imaging, and therapeutics of various cancer types. Nanomaterials have multiple advantages over other materials due to their small size and high surface area, which allow retention and controlled drug release to improve the anti-cancer property. Most cancer therapies have been known to damage healthy cells due to poor specificity, which can be avoided by using nanosized particles. Nanomaterials can be combined with various types of biomaterials to make it less toxic and improve its biocompatibility. Based on these properties, several nanomaterials have been developed which possess excellent anti-cancer efficacy potential and improved diagnosis. This review presents the latest update on novel nanomaterials used to improve the diagnostic and therapeutic of pathogen-associated and non-pathogenic cancers. We further highlighted mechanistic insights into their mode of action, improved features, and limitations.

Evaluation of Disease Related Knowledge in Patients of Osteoporosis: An Observational Study.

OBJECTIVE: Osteoporosis is a systemic skeletal disease characterized by low bone mass and micro-architectural deterioration of bone tissue which results in consequent increase in bone fragility and susceptibility to fracture and more common in post-menopausal women and elderly people. This study was aimed to assess the knowledge of osteoporosis among patients in tertiary healthcare systems, as well as their knowledge of associated lifestyle, risk factors, and preventive measures. METHODS: A cross-sectional study design was used to determine the knowledge of outpatients towards osteoporosis. The survey was carried out in a tertiary care hospital Federal Government Polyclinic Hospital, Islamabad. This study included patients visiting various outpatient departments of Federal Government Polyclinic Hospital, Islamabad. A structured questionnaire was used as a tool to collect the data from the participants. The compiled data was analyzed by using the Statistical Package for Social Sciences (SPSS) software version 21.0. Chi-square test was performed to determine association level among study variables. Multiple regression was used to predict the impact of two or more independent variables on dependent variable. p-value of < .05 was considered to be significant. RESULTS: The mean score of knowledge was 8.73 ± 3.72. 159 (63.6%) respondents had poor knowledge, 78 (31.2%) had moderate knowledge and 13 (5.2%) had good knowledge. The results showed that most respondents had poor knowledge. Differences were statistically significant when age, gender, marital status and education were analyzed (P < .001). CONCLUSION: According to the results of all aspects of current study, it was concluded that mostly patients had inadequate knowledge regarding their disease which leads to an increased risk and progression of osteoporosis.