Introduction. The Infrapatellar fat pad (IPFP) represents an emerging alternative source of adipose-derived mesenchymal stem cells (ASCs). We compared the characteristics and differentiation capacity of ASCs isolated from IPFP and SC. Materials and Methods. ASCs were harvested from either IPFP or SC. IPFPs were collected from patients undergoing total knee arthroplasty (TKA), whereas subcutaneous tissues were collected from patients undergoing lipoaspiration. Immunophenotypes of surface antigens were evaluated. Their ability to form colony-forming units (CFUs) and their differentiation potential were determined. The ASCs karyotype was evaluated. Results. There was no difference in the number of CFUs and size of CFUs between IPFP and SC sources. ASCs isolated from both sources had a normal karyotype. The mesenchymal stem cells (MSCs) markers on flow cytometry was equivalent. IPFP-ASCs demonstrated significantly higher expression of SOX-9 and RUNX-2 over ASCs isolated from SC (6.19 ± 5.56-, 0.47 ± 0.62-fold; p value = 0.047, and 17.33 ± 10.80-, 1.56 ± 1.31-fold; p value = 0.030, resp.). Discussion and Conclusion. CFU assay of IPFP-ASCs and SC-ASCs harvested by lipoaspiration technique was equivalent. The expression of key chondrogenic and osteogenic genes was increased in cells isolated from IPFP. IPFP should be considered a high quality alternative source of ASCs.

Osteoarthritis (OA) is a multi-factorial disease and genetic factor is one of the important etiologic risk factors. Various genetic polymorphisms have been elucidated that they might be associated with OA. Recently, several studies have shown an association between Growth Differentiation Factor 5(GDF5) polymorphism and knee OA. However, the role of genetic predisposing factor in each ethnic group cannot be replicated to all, with conflicting data in the literatures. Therefore, the aim of this study was to investigate the association between GDF5 polymorphism and knee OA in Thai population. One hundred and ninety three patients aged 54-88 years who attended Ramathibodi Hospital were enrolled. Ninety cases with knee OA according to American College of Rheumatology criteria and one hundred and three cases in control group gave informed consent. Blood sample (5 ml) were collected for identification of GDF5 (rs143383) single nucleotide polymorphism by PCR/RFLP according to a standard protocol. This study protocol was approved by the Ethics Committee on human experimentation of Ramathibodi Hospital Faculty of Medicine, Mahidol University. Odds ratios (OR) and 95% confidence intervals were calculated for the risk of knee OA by genotype (TT, TC and CC) and allele (T/C) analyses. The baseline characteristics between two groups including job, smoking and activity were not different, except age and BMI. The entire cases and controls were in Hardy-Weinberg equilibrium (p > 0.05). The OA knee group (n = 90) had genotypic figure which has shown by TT 42.2% (n = 38), TC 45.6% (n = 41) and CC 12% (n = 11), whereas the control group (n = 103) revealed TT 32% (n = 33), TC 45.6% (n = 47), and CC 22.3% (n = 23), respectively. Genotypic TT increased risk of knee OA as compared to CC [OR = 2.41 (P = 0.04, 95%CI = 1.02-5.67)]. In the allele analysis, the T allele was found to be significantly associated with knee OA [OR = 1.53 (P = 0.043, 95%CI = 1.01-2.30)]. These data suggested that GDF5 polymorphism has an association with knee OA in Thai ethnic. This finding also supports the hypothesis that OA has an important genetic component in its etiology, and GDF5 protein might play important role in the pathophysiology of the disease.

Introduction: It has been reported that cells or growth factors might improve bone regeneration in nonunion. However, the intrinsic potential of the nonunion tissue to regenerate bone is still unclear; in particular, it is not known whether there are progenitor cells within the nonunion. Thus, in this study, a clinically relevant model has been developed to investigate the nature of the cells in atrophic nonunion tissue and to assess their regenerative potential. Materials and Methods: Seventeen Wistar rats underwent the procedure to induce an atrophic nonunion at the tibial midshaft by stripping the periosteum and endosteum as well as creating a small (1.0 mm) noncritical gap. The fracture was stabilized with an external fixator. The proliferation ability of bone marrow-derived cells and nonunion tissue-derived cells was determined using colony forming assays. The differentiation potential of nonunion tissue-derived cells was also investigated. Results: Noncritical size defect nonunions were successfully induced in all of the animals. The typical characteristics of atrophic nonunions were demonstrated by radiography, micro-CT, and histology. An atrophic nonunion stimulated a systemic response in the bone marrow with an increase in bone marrow-derived mesenchymal stem cells. In contrast, cells derived from the nonunion gap were not able to form colonies. This indicated that the quiescent or inactive cells in the tissue at the atrophic nonunion gap could be induced to differentiate under osteogenic and chondrogenic conditions, but not under adipogenic conditions. Thus, these cells had the characteristics of osteochondral progenitor cells. Discussion: Although there was an increase in the systemic response in the atrophic nonunion model, the intrinsic potential of local tissue from the atrophic nonunion site was impaired. The cells derived from nonunion tissue could be stimulated to differentiate into bone under appropriate conditions. This suggested that there are progenitor cells in atrophic nonunion tissue, which have an intrinsic ability to regenerate bone, but the microenvironment in the atrophic nonunion site might be retarding their function. Consequently, physical or biological agents (such as growth factors or cells) are needed to reactivate the endogenous progenitor cells to make them regenerate bone in atrophic nonunions.

Ankle fractures are common in the elderly. However, their association with osteoporosis remains controversial. This systematic review aims to determine the relationship between ankle fracture and bone mineral density (BMD), and to investigate the risk of subsequent fractures after ankle fracture. MEDLINE and Scopus publications were searched from inception to March and April 2019, respectively. Articles were selected by 2 independent reviewers for cross-sectional, cohort, or case-control studies comparing BMD or subsequent fracture risk in low-energy ankle fractures patients with that of the normal population. Data extraction was performed by 2 investigators. Discrepancies were resolved with the third reviewer. Quality assessment was conducted using the modified Newcastle-Ottawa Scale. Overall, 19 articles were included. The quality assessment showed a generally low-to-moderate risk of bias among studies, mainly due to potential confounders and inadequate follow-up. Of 13 studies exploring BMD in ankle fractured-patients, lower central and peripheral BMD was found in 3 and 2 studies, respectively. The risk of subsequent fracture was examined in 11 studies with relative risks ranging from 0.7 to 4.59. An increased risk of any subsequent fractures in women, both genders, and men was found in 5, 2, and 1 articles, respectively. Despite the lack of clear association with BMD, the contribution of ankle fracture to increased subsequent fracture risk and its associated microarchitectural changes cannot be overlooked. Moreover, its potential role as an early predictor of future fracture may promote secondary prevention. Further studies with longer follow-up and stricter confounder control are recommended.