Stromal cell-derived factor-1 promotes osteoblastic differentiation of human bone marrow mesenchymal stem cells via the lncRNA-H19/miR-214-5p/BMP2 axis.

BACKGROUND: Stromal cell-derived factor-1 (SDF-1) plays an important role in the osteoblastic differentiation of human bone marrow mesenchymal stem cells (hBMMSCs), but the specific mechanism remains unclear. Our study aimed to clarify the role of the lncRNA-H19/miR-214-5p/BMP2 axis in the osteoblastic differentiation of hBMMSCs induced by SDF-1. METHODS: We used reverse-transcriptase polymerase chain reaction, western blotting, alkaline phosphatase activity test, and Alizarin red staining to evaluate the osteoblastic differentiation of primary hBMMSCs and the luciferase reporter assay to determine if lncRNA-H19 binds with miR-214-5p. RESULTS: Our results indicated that SDF-1 (50 ng/mL) promotes the osteoblastic differentiation of hBMMSCs, significantly upregulates osteoblastogenic genes (OCN, OSX, RUNX2, and ALP), and increases Alizarin red staining, alkaline phosphatase activity, and lncRNA-H19 expression. Luciferase reporter assay verified that lncRNA-H19 binds with and represses miR-214-5p, thereby upregulating BMP2 expression. Use of miR-214-5p inhibitor or overexpression of lncRNA-H19 can promote the osteoblastic differentiation of hBMMSCs, but miR-214-5p or shH19 inhibits the osteoblastic differentiation of hBMMSCs. Treatment with an miR-214-5p inhibitor could rescue the inhibitory effect of shH19 on the osteoblastic differentiation of hBMMSCs. CONCLUSIONS: Taken together, SDF-1 promotes the osteoblastic differentiation of hBMMSCs through the lncRNA-H19/miR-214-5p/BMP2 axis. Increased osteoblastic differentiation by an miR-214-5p inhibitor reveals a new possible strategy for the treatment of bone defect and osteoporosis.

Bevacizumab did not reduce the risk of anemia associated with chemotherapy: an up-to-date meta-analysis.

PURPOSE: The risk of anemia due to bevacizumab-based chemotherapy has not been well described, and new randomized controlled trials (RCTs) have been reported in recent years. We therefore conducted an up-to-date meta-analysis of RCTs to fully characterize the risk of anemia with bevacizumab. METHODS: We carried out an electronic search of Medline, Embase, and The Cochrane Central Register of Controlled Trials to investigate the effects of RCTs on bevacizumab treatment on cancer patients up to October 2014, and random or fixed-effect meta-analytical models were used to assess the risk ratio (RR) of anemia due to the use of bevacizumab according to the heterogeneity of included studies. RESULTS: A total of 13,173 patients were included in this analysis from 18 RCTs. Among those patients receiving bevacizumab and chemotherapy, the incidences of all-grade and high-grade (grade 3 and above) anemia were 24% (95% confidence interval (CI) 13-41%) and 4.0% (95% CI 3.0-6.0%), respectively. Bevacizumab-containing therapy did not significantly decreased the risk of developing all-grade anemia (RR 0.872, 95% CI 0.739-1.029, P = 0.104) and high-grade anemia (RR 0.850, 95% CI 0.720-1.002, P = 0.053), which is not in agreement with previous meta-analysis. On subgroup analysis, we did not find significant risk differences based on bevacizumab dosage, tumor types, and concomitant drugs. When stratified by dose level, a significantly decreased risk of high-grade anemia with bevacizumab was obtained in a lower dose level (2.5 mg/kg/week, RR 0.773, 95% CI 0.611-0.978, P = 0.031) compared to control group. CONCLUSIONS: Bevacizumab did not significantly reduce the risk of anemia with chemotherapy in cancer patients.

Patellar denervation with electrocautery in total knee arthroplasty without patellar resurfacing: a meta-analysis.

PURPOSE: The impact of patellar denervation with electrocautery in total knee arthroplasty (TKA) on post-operative outcomes has been under debate. This study aims to conduct a meta-analysis and systematic review to compare the benefits and risks of circumpatellar electrocautery with those of non-electrocautery in primary TKAs. METHODS: Comparative and randomized clinical studies were identified by conducting an electronic search of articles dated up to September 2012 in PubMed, EMBASE, Scopus, and the Cochrane databases. Six studies that focus on a total of 849 knees were analysed. A random-effects model was conducted using the inverse-variance method for continuous variables and the Mantel-Haenszel method for dichotomous variables. RESULTS: There was no significant difference in the incidence of anterior knee pain between the electrocautery and non-electrocautery groups. In term of patellar score and Knee Society Score, circumpatellar electrocautery improved clinical outcomes compared with non-electrocautery in TKAs. The statistical differences were in favour of the electrocautery group but have minimal clinical significance. In addition, the overall complications indicate no statistical significance between the two groups. CONCLUSIONS: This study shows no strong evidence either for or against electrocautery compared with non-electrocautery in TKAs. LEVEL OF EVIDENCE: Therapeutic study (systematic review and meta-analysis), Level III.

Fibrodysplasia Ossificans Progressiva: A Case Report.

Fibrodysplasia ossificans progressiva (FOP) is a rare autosomal dominant genetic disorder characterized by congenital great toe malformations and progressive ectopic ossification. We report a typical case of FOP in a 22-year-old female patient presenting with limited movement of the left knee joint, which began following trauma in 2019. Clinical examination revealed a large mass behind the left knee, bilateral great toe deformities, and no palpable superficial lymph nodes, without systemic pain or other discomfort. Imaging and genetic testing further supported the diagnosis of FOP, demonstrating high-density ossification within soft tissues and a mutation in the ACVR1 gene. Treatment involved a combination of methylprednisolone and alendronate sodium vitamin D3 tablets, which yielded some therapeutic efficacy. The discussion emphasizes clinical diagnosis, pathogenesis, and treatment strategies for FOP, including injury prevention, rehabilitation exercises, and pharmacological interventions. Despite the lack of definitive treatment options, timely diagnosis and comprehensive management can effectively alleviate symptoms and improve the quality of life for affected individuals.

IRTKS promotes osteogenic differentiation by inhibiting PTEN phosphorylation.

Insulin stimulates osteoblast proliferation and differentiation as an anabolic agent in bone. Insulin Receptor Tyrosine Kinase Substrate (IRTKS) is involved in insulin signaling as an adapter for insulin receptors (IR). Here, we showed that IRTKS levels were significantly decreased in bone marrow mesenchymal stem cells (BMSCs) derived from the bone marrow of patients with osteoporosis. Based on relevant experiments, we observed that IRTKS promoted the proliferation, migration, and osteoblast differentiation of BMSCs and MC3T3-E1 cells. In addition, we identified a Phosphatase and Tensin homolog deleted on chromosome 10 (PTEN) as a potential active substrate of IRTKS. We demonstrated a direct interaction between IRTKS and PTEN using co-immunoprecipitation. Subsequently, we confirmed that the SH3 domain of IRTKS directly binds to the C-terminal tail of PTEN. Further experimental results demonstrated that PTEN attenuated the promoting effects of IRTKS on the proliferation, migration, and osteoblast differentiation of BMSCs and MC3T3-E1 cells. In conclusion, this study suggests that IRTKS contributes to osteogenic differentiation by inhibiting PTEN phosphorylation and provides a potential therapeutic target for osteoporosis patients.

Human ß-defensin 3 inhibits antibiotic-resistant Staphylococcus biofilm formation.

BACKGROUND: Implantation-associated infections have increased significantly with the recent widespread use of medical implants. Treatments for these infections are not always successful because these infections are sometimes caused by multiantibiotic-resistant organisms. It is therefore particularly urgent to provide doctors with more effective antimicrobial agents against these antibiotic-resistant organisms. Human ß-defensin 3 (hBD-3) has been shown to have strong broad-spectrum antibacterial activity. However, its effect on methicillin-resistant Staphylococcus epidermidis (MRSE) and methicillin-resistant Staphylococcus aureus (MRSA) in medical implant biofilm formation has not been reported. METHODS: In this study, we evaluated the effects of hBD-3 on S epidermidis ATCC 35984 (methicillin-resistant strain), MRSE287, and MRSA (ATCC43300) by evaluating bacterial adhesion, biofilm formation, and maturation. In addition, we used the spread plate method, confocal laser scanning microscopy, scanning electron microscopy, and real-time polymerase chain reaction to evaluate the effect of hBD-3. RESULTS: After evaluating biofilm adhesion and formation, we found that the number of each strain on the titanium surface was decreased in those groups exposed to 1MIC (minimum inhibitory concentration) of hBD-3 and was significantly lower than the number of colonies of the control. In the initial maturation of the biofilm, the numbers of each strain on the titanium surface from the 2MIC to 6MIC groups were significantly lower than the control. When the concentrations were further increased, hBD-3 was significantly effective against drug-resistant bacteria from the biofilms. CONCLUSIONS: HBD-3 has the potential to eliminate the biofilm formation of Staphylococcus, especially antibiotic-resistant strains, effectively.

Fixed- versus mobile-bearing unicondylar knee arthroplasty: are failure modes different?

PURPOSE: An ongoing controversy exists on whether mobile-bearing design is superior over fixed-bearing design in unicondylar knee arthroplasties (UKAs). The present study conducted a systematic review to ascertain differences in performance between fixed- and mobile-bearing designs in UKAs. METHODS: A literature search was performed in PubMed, Embase, Scopus and the Cochrane Library. A total of 9 comparative studies involving 915 knees comparing outcomes of mobile-bearing UKAs with fixed-bearing UKAs were included in the current analysis. Outcomes of interest included knee function, quality of life, radiographic outcomes, reasons and incidence of reoperation, timing of failures, and survivorship. RESULTS: The results presented no significant differences between the two designs in terms of knee scores, range of motion, limb alignment, implant positioning, incidence of radiolucent lines and overall reoperation rates. However, their differences have been noted in their modes and timing of failures. Early failures are related to the risk of bearing dislocation in the mobile-bearing design. In contrast, later failures are related to the risk of polyethylene wear in the fixed-bearing design. CONCLUSIONS: The available evidence has not confirmed the advantage of mobile-bearing UKAs over fixed-bearing UKAs but pointed out specific modes of failure.

Unsaturated bond recognition leads to biased signal in a fatty acid receptor.

Individual free fatty acids (FAs) play important roles in metabolic homeostasis, many through engagement with more than 40G protein-coupled receptors. Searching for receptors to sense beneficial omega-3 FAs of fish oil enabled the identification of GPR120, which is involved in a spectrum of metabolic diseases. Here, we report six cryo-electron microscopy structures of GPR120 in complex with FA hormones or TUG891 and Gi or Giq trimers. Aromatic residues inside the GPR120 ligand pocket were responsible for recognizing different double-bond positions of these FAs and connect ligand recognition to distinct effector coupling. We also investigated synthetic ligand selectivity and the structural basis of missense single-nucleotide polymorphisms. We reveal how GPR120 differentiates rigid double bonds and flexible single bonds. The knowledge gleaned here may facilitate rational drug design targeting to GPR120.

Pravastatin Reduces Matrix Metalloproteinases Expression and Promotes Cholesterol Efflux in Osteoarthritis Chondrocytes.

Background: Chondrocyte metabolic disorder plays an important role in the development of osteoarthritis (OA). The use of statins in the treatment of OA has also been widely studied, but the mechanism is still confusing. The present study aims to investigate the effects of statin on osteoarthritis chondrocytes and its underlying mechanism. Major findings. An untargeted metabolomics study revealed that the treatment of statins significantly changed the metabolites of articular cartilage tissues collected from female osteoarthritis patients, and might be involved in the glycerophospholipid metabolism pathway. In vitro study showed that 5-50 µmol/L of pravastatin exerts no cytotoxicity on human chondrocytes. Besides, 50 µmol/L of pravastatin caused a significant decrease in the expression of matrix metalloproteinase (MMP)-1 and MPP-13, and intracellular cholesterol in interleukin-1ß (IL-1ß)-induced human chondrocytes. Furthermore, at both mRNA and protein levels, the expression of the proteins related to the cholesterol efflux pathway (liver X receptor and cholesterol efflux regulatory protein) were significantly up-regulated by 50 µmol/L of pravastatin in IL-1ß-induced human chondrocytes. Conclusion: Pravastatin can reduce the expression of MMPs in IL-1ß-induced human chondrocytes and protect the chondrocyte matrix. The mechanism may be related to promoting the expression of proteins related to the cholesterol efflux pathway and reducing the level of cellular cholesterol.

TGF-ß1-induced bone marrow mesenchymal stem cells (BMSCs) migration via histone demethylase KDM6B mediated inhibition of methylation marker H3K27me3.

Mesenchymal stem cells (MSCs) are widely used in clinical research and therapy. Since the number of MSCs migration is extremely crucial at the lesion site, exploring the mechanisms to enhance the migration of MSCs is necessary. Therefore, this study focused on the epigenetic mechanisms in MSCs migration. TGF-ß1 stimulated bone marrow mesenchymal stem cells (BMSCs) to promote cell migration at lesion sites in vitro and in vivo. The mRNA and protein levels of several migration-related genes (N cadherin, CXCR4, FN1) were enhanced. The trimethylation marker H3K27me3 recruitment on the promoter of these genes were studied to dissect the epigenetic mechanisms. TGF-ß1 elevated the levels of KDM6B leading to removal of repression marker H3K27me3 in the promoter region of N cadherins and FN1. Congruently, knockdown of demethylase KDM6B substantially affected the TGF-ß1 induced BMSCs migration. This promoted the down-regulation of various migration-related genes. Collectively, epigenetic regulation played an important role in BMSCs migration, and H3K27me3 was at least partially involved in the migration of BMSCs induced by TGF-ß1.

[Founder effect of two families with TGFBI related Thiel-Behnke corneal dystrophy].

OBJECTIVE: To investigate the transforming growth factor beta induced (TGFBI; BIGH3) gene mutation and founder effect of two large Chinese families clinically diagnosed as Thiel-Behnke corneal dystrophy. METHODS: Fifteen members including 13 affected and 2 healthy in family A, 14 members including 6 affected and 8 healthy in family B, as well as 20 other unrelated healthy individuals were tested for TGFBI gene mutation. Haplotype analysis and clinical examination were also carried out in the two families. RESULTS: In exon 12 of the TGFBI gene, 1664G to A change was detected in all the patients, which leads to an amino acid replacement of arginine with glutamine (p.Arg555Gln). Members of the two families share some similar haplotypes. CONCLUSION: Genetic analysis is helpful in the diagnosis of corneal dystrophy. The two families may come from a same ancestor.

Reduced Staphylococcus aureus biofilm formation in the presence of chitosan-coated iron oxide nanoparticles.

Staphylococcus aureus can adhere to most foreign materials and form biofilm on the surface of medical devices. Biofilm infections are difficult to resolve. The goal of this in vitro study was to explore the use of chitosan-coated nanoparticles to prevent biofilm formation. For this purpose, S. aureus was seeded in 96-well plates to incubate with chitosan-coated iron oxide nanoparticles in order to study the efficiency of biofilm formation inhibition. The biofilm bacteria count was determined using the spread plate method; biomass formation was measured using the crystal violet staining method. Confocal laser scanning microscopy and scanning electron microscopy were used to study the biofilm formation. The results showed decreased viable bacteria numbers and biomass formation when incubated with chitosan-coated iron oxide nanoparticles at all test concentrations. Confocal laser scanning microscopy showed increased dead bacteria and thinner biofilm when incubated with nanoparticles at a concentration of 500 µg/mL. Scanning electron microscopy revealed that chitosan-coated iron oxide nanoparticles inhibited biofilm formation in polystyrene plates. Future studies should be performed to study these nanoparticles for anti-infective use.

Increased osteoblast function in vitro and in vivo through surface nanostructuring by ultrasonic shot peening.

Surface topography has significant influence on good and fast osseointegration of biomedical implants. In this work, ultrasonic shot peening was conducted to modify titanium to produce nanograined (NG) surface. Its ability to induce new bone formation was evaluated using an in vivo animal model. We demonstrated that the NG surface enhanced osteoblast adhesion, proliferation, differentiation, and mineralization in in vitro experiments compared to coarse-grained titanium surface. Push-out test, histological observations, fluorescent labeling, and histomorphometrical analysis consistently indicated that the NG surfaces developed have the higher osseointegration than coarse-grained surfaces. Those results suggest that ultrasonic shot peening has the potential for future use as a surface modification method in biomedical application.

Comparison of fixed- and mobile-bearing total knee arthroplasty with a mean five-year follow-up: A meta-analysis.

Controversy exists regarding the clinical and radiological differences in outcomes between fixed-bearing (FB) and mobile-bearing (MB) total knee arthroplasties (TKAs) at the mid- or long-term follow-up. We therefore conducted a meta-analysis and systematic review of randomized controlled trials (RCTs) that have evaluated FB and MB TKAs. We searched the Cochrane Central Register of Controlled Trials (CENTRAL) in the Cochrane Library, Medline and Embase. The data, including demographic information, methodological quality, duration of follow-up, clinical and radiographical outcomes, patient preferences and complications, were extracted. The methodological quality of the studies was assessed in accordance with the guidelines presented in the Cochrane Handbook for Systematic Reviews of Interventions. Nine trials, studying 1,821 knees, were eligible for data extraction and meta-analysis. The Knee Society score and the maximum knee flexion demonstrated no difference between the FB and MB groups (P=0.47 and P=0.72, respectively). Similarly, no difference was revealed between the groups for radiological outcomes or general health results. An increased number of high-quality RCTs with long-term follow-ups are required to validate the results.

The bone tissue compatibility of a new Ti35Nb2Ta3Zr alloy with a low Young's modulus.

Titanium (Ti) alloys of the ß-type are highly attractive metallic materials for biomedical applications due to their low elastic modulus, high corrosion resistance and notable biocompatibility. A new ß-type Ti35Nb2Ta3Zr alloy with a low Young's modulus of approximately 48 GPa was previously fabricated. In the present study, the biocompatibility of this alloy was evaluated. In an in vitro assay, the Ti35Nb2Ta3Zr alloy did not markedly affect the adhesion of MG63 osteoblast cells, but it increased their proliferation, alkaline phosphatase (ALP) activity, calcium deposition and mRNA expression of osteogenic genes (i.e., ALP, osteocalcin, osteopontin). In an in vivo study, no marked histological differences were observed between the new bone formed on the surface of Ti35Nb2Ta3Zr and that formed on the surface of control Ti6Al4V rods placed in the medullary canal of rabbit femurs. Additionally, no significant differences were observed in the failure load of Ti35Nb2Ta3Zr and Ti6Al4V in pull-out tests. In conclusion, the Ti35Nb2Ta3Zr alloy with a lower elastic modulus closer to that of human bone has significant bone tissue compatibility equal to that of Ti6Al4V, which has been widely used in orthopedic applications.

Ultrasonically enhanced rifampin activity against internalized Staphylococcus aureus.

Staphylococcus aureus (S. aureus) is the principle causative agent of osteomyelitis, accounting for 80% of all human cases. S. aureus internalized in osteoblasts escapes immune response, including engulfment by phagocytes. It also escapes the action of a number of antibiotics. Ultrasound increases cell membrane permeability to a number of drugs. Following an internalization assay, we used low-frequency, low-power ultrasound combined with the antibiotic rifampin to target S. aureus internalized in human osteoblasts. Tryptic soy agar (TSA) was used to quantitate the antibacterial effect of rifampin combined with low-frequency ultrasound. A Cell Counting Kit-8 (CCK-8) assay was used to evaluate cell viability following exposure to ultrasound. Our data revealed that rifampin successfully penetrates into osteoblasts and kills internalized S. aureus in osteoblasts, while low-frequency ultrasound promotes this process. Ultrasound had a negative impact on the cell viability of osteoblasts; however, this damage was slight and reversible. Ultrasound-enhanced antibiotic efficiency to bacteria internalized in the osteoblasts may contribute to the control of chronic infection to reduce recurrence.

Corrosion resistance and in vitro response of a novel Ti35Nb2Ta3Zr alloy with a low Young's modulus.

ß type titanium alloys have attracted much attention in the biomedical field because they consist of non-cytotoxic elements, show high corrosion resistance, and are biologically compatible. In this study, a novel ß type titanium alloy (Ti35Nb3Zr2Ta) with a Young's modulus of 48 GPa was fabricated and the alloy's corrosion resistance and in vitro response were determined. The results indicate that the novel alloy exhibits comparable corrosion resistance when compared with Ti6Al4V, but in vitro experiments show that osteoblasts attach, spread, proliferate, and differentiate better on Ti35Nb2Ta3Zr than on Ti6Al4V. The high corrosion resistance and satisfactory biocompatibility make the novel Ti35Nb3Zr2Ta alloy a promising biomaterial for surgical implants.

Ultrasound-targeted microbubble destruction enhances human ß-defensin 3 activity against antibiotic-resistant Staphylococcus biofilms.

The infection of orthopedic implantation devices with Staphylococcus is a serious concern within the biomaterial community. Treatments are not always successful because of antibiotic-resistant bacteria and serious biofilm infections. Human ß-defensin 3 (hBD-3) is considered to be the most promising class of defensin antimicrobial peptides and its effect on antibiotic-resistant Staphylococcus biofilms, combined with ultrasound (US)-targeted microbubble (MB) destruction (UTMD), has not been reported. In the study, we found that biofilm densities, the percentage of live cells and the viable counts of two tested Staphylococcus recovered from the biofilm were significantly decreased in the maximum concentration hBD-3 combined with UTMD compared with those of any other groups. Furthermore, results suggested that UTMD could also enhance 1MIC hBD-3 activity inhibiting the biofilm-associated genes expression of icaAD and the methicillin-resistance genes expression of MecA by simultaneously promoting the icaR expression. UTMD may have great potential for improving antibiotic activity against biofilm infections.

Staphylococcus aureus supernatant induces the release of mouse ß-defensin-14 from osteoblasts via the p38 MAPK and NF-κB pathways.

Mammalian ß-defensins are small cationic peptides of approximately 2-6 kDa that have been implicated in mediating innate immune defenses against microbial infection. Previous studies have reported that mouse ß-defensin-14 (MBD­14), based on structural and functional similarities, appears to be an ortholog of human ß-defensin-3 (HBD-3). The aim of this study was to identify the signaling pathways that contribute to the expression of MBD-14 in mouse osteoblasts (OBs) upon contact with methicillin-resistant Staphylococcus aureus (S. aureus) supernatant (SAS) to provide a theoretical basis for the use of MDB-14 as a therapeutic agent in the treatment of intramedullary infection with S. aureus in vivo. The bacterial exoproducts released by S. aureus mainly include a large amount of enterotoxins. Using mouse OBs, the release and regulation of MBD-14 was evaluated by real-time polymerase chain reaction (PCR) and enzyme­linked immunosorbent assay (ELISA) following exposure to SAS. The activation of the p38 mitogen­activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK) and nuclear factor-κB (NF-κB) pathways was determined by western blot analysis. OBs treated with lipopolysaccharide (LPS) were used as the positive control. The results revealed that SAS significantly promoted the phosphorylation of p38 MAPK, NF-κB and the inhibitory subunit of NF-κBα (IκBα) in a time-dependent manner. The treatment of OBs with SB203580 (an inhibitor of p38 MAPK) and pyrrolidine dithiocarbamate (PDTC, an inhibitor of NF-κB) prior to stimulation with SAS significantly inhibited the phosphorylation and mRNA expression of p38 MAPK and NF-κB p65, simultaneously reducing the release of MBD-14. Our findings suggest that the release of MBD-14 is mediated at least in part through the activation of p38 MAPK and NF-κB in response to S. aureus­secreted bacterial exoproducts. Moreover, our data demonstrate the innate immune capacity of OBs under conditions of bacterial challenge to enhance the local expression of this MBD-14, a peptide with anti­staphylococcal activity.

A novel classification to guide total hip arthroplasty for adult acetabular dysplasia.

In the field of hip arthroplasties, the secondary fixation of the implants depends directly on the quality of the primary stability. A good acetabular fit and metaphyseal filling between the prostheses and implants improve the initial stabilization, and optimize the transmission of forces to the bone. A precise knowledge of the three-dimensional acetabular or femoral shape is essential to the selection of adapted implants. A total of 63 patients diagnosed with developmental dysplasia were analyzed by three-dimensional computed tomography (3DCT), and the preoperative radiographic and 3DCT images were used to assess the acetabular/femoral deformities and variations of the hips. All joints were classified as Crowe type I, and bilateral measurements were taken for 10 patients. The acetabular abnormalities were classified according to the type of deficiency and the section angles of the acetabulum, with 26 hips (36%) classified as an anterior deficiency, 13 hips (18%) as a posterior deficiency and 34 hips (46%) as a lateral deficiency. The femoral side deformities were divided into three types according to the anteversion angle of the femur. A gradual increase in anteversion angle led to secondary rotational anomalies, and a narrowing of the canal at the isthmus. A total of 35 hips (48%) were classified as an F1 type deficiency, femur anteversion angle (FAVA) <30°; 32 hips (44%) as F2-type, 30°≤ FAVA ≤40°, with mild abnormalities of the femoral canal rotation and the diameter of the isthmus; and 6 hips (8%) as F3 type, FAVA >40°, with significant abnormalities of the femoral canal rotation and the diameter of the isthmus. This novel classification for adult acetabular dysplasia may provide a useful guide for surgery, and enable an improved selection of a suitable prosthesis.