Painful Hip Arthroplasty: What Should We Find? Diagnostic Approach and Results

IntroductionIdentifying the source of pain is paramount for determining appropriate treatment and ensuring successful outcome in terms of management and relief of pain. The difficulty is that each surgeon has his or her own way of seeing the problem, and there is no consensus for the evaluation of these patients. The study hypothesis was that it is possible to find the cause of the pain in most cases.Patients and methodsAll patients consulting for unexplained painful hip arthroplasty were included and followed a decision tree to assess the cause of the pain. The primary endpoint was the final diagnosis. Secondary endpoints were subgroup comparison between main causes and assessment of risk factors.ResultsTwo hundred one hips of 194 patients were included as unexplained painful hip arthroplasty 6 months postoperatively. Final diagnoses comprised periarticular pain in 53 cases (26.4%): 40 cases of trochanteric bursitis, 5 of iliopsoas tendinitis, 5 of abductor deficiency, 1 of ischial tuberosity tendinitis, and 2 of heterotopic ossification; projected pain in 49 (24.4%): 45 cases of back pain with or without neuropathy, 3 of knee osteoarthritis, and 1 of metabolic neuropathy; wear in 40 (19.9%), in the polyethylene liner; loosening in 20 (10.0%): loosening of the femoral component in 8 and that of the cup in 12; material problems in 17 (8.5%): trunnionosis in 13 and metallosis in metal-on-metal implants in 4; no diagnosis in 7 hips (3.5%); infection in 6 (3.0%), all chronic; instability without real dislocation in 3 (1.5%); misplacement in 3 (1.5%), all for leg-length discrepancy; fracture in 2 (1.0%): 1 of greater trochanter and 1 of ilio-ischiopubic ramus; complex regional pain syndrome in 1 (0.5%).DiscussionTo our knowledge, this is the first study on the causes of painful hip arthroplasty in clinical practice, whether leading to revision or not. A systematic approach, including physical examination, radiographic assessment and laboratory studies, is needed to find the cause of the pain. It is important to understand the pain so that it can be treated appropriately. Revision surgery can sometimes help—but the worst thing is to make the patient worse.Level of Evidencelevel 4, retrospective study.     

Toll‐Like Receptor 2 Knockdown Modulates Interleukin (IL)‐6 and IL‐8 but not Stromal Derived Factor‐1 (SDF‐1/CXCL12) in Human Periodontal Ligament and Gingival Fibroblasts

Background: Fibroblasts are now seen as active components of the immune response because these cells express Toll‐like receptors (TLRs), recognize pathogen‐associated molecular patterns, and mediate the production of cytokines and chemokines during inflammation. The innate host response to lipopolysaccharide (LPS) from Porphyromonas gingivalis is unusual inasmuch as different studies have reported that it can be an agonist for Toll‐like receptor 2 (TLR2) and an antagonist or agonist for Toll‐like receptor 4 (TLR4). This study investigates and compares whether signaling through TLR2 or TLR4 could affect the secretion of interleukin (IL)‐6, IL‐8, and stromal derived factor‐1 (SDF‐1/CXCL12) in both human gingival fibroblasts (HGF) and human periodontal ligament fibroblasts (HPDLF). Methods: After small interfering RNA‐mediated silencing of TLR2 and TLR4, HGF and HPDLF from the same donors were stimulated with P. gingivalis LPS or with two synthetic ligands of TLR2, Pam2CSK4 and Pam3CSK4, for 6 hours. IL‐6, IL‐8, and CXCL12 mRNA expression and protein secretion were evaluated by quantitative polymerase chain reaction and enzyme‐linked immunosorbent assay, respectively. Results: TLR2 mRNA expression was upregulated in HGF but not in HPDLF by all the stimuli applied. Knockdown of TLR2 decreased IL‐6 and IL‐8 in response to P. gingivalis LPS, or Pam2CSK4 and Pam3CSK4, in a similar manner in both fibroblasts subpopulations. Conversely, CXCL12 remained unchanged by TLR2 or TLR4 silencing. Conclusion: These results suggest that signaling through TLR2 by gingival and periodontal ligament fibroblasts can control the secretion of IL‐6 and IL‐8, which contribute to periodontal pathogenesis, but do not interfere with CXCL12 levels, an important chemokine in the repair process.     

MyD88 or TRAM Knockdown Regulates Interleukin (IL)‐6, IL‐8, and CXCL12 mRNA Expression in Human Gingival and Periodontal Ligament Fibroblasts

Background: In a previous report, it was shown that Toll‐like receptor (TLR) 2 knockdown modulates interleukin (IL)‐6 and IL‐8 but not the chemokine CXCL12, an important mediator with inflammatory and proangiogenic effects, in human gingival fibroblasts (HGF) and human periodontal ligament fibroblasts (HPDLF). This study investigates whether knocking down two important TLR adaptor molecules, such as myeloid differentiation protein 88 (MyD88) and TRIF‐related adaptor molecule (TRAM), could affect mRNA expression of IL‐6, IL‐8, and CXCL12 in HGF and HPDLF. Methods: After small interfering (si) RNA‐mediated silencing of MyD88 or TRAM, HGF and HPDLF were stimulated with Porphyromonas gingivalis (Pg) lipopolysaccharide (LPS) or two synthetic ligands of TLR2 (Pam2CSK4 and Pam3CSK4) for 6 hours. IL‐6, IL‐8, and CXCL12 mRNAs were evaluated by quantitative polymerase chain reaction. Results: Knockdown of MyD88 or TRAM partially impaired the IL‐8 mRNA upregulation in both fibroblast subpopulations. Similarly, IL‐6 upregulation was partially prevented by siMyD88 or siTRAM in HGF stimulated with Pg LPS, as well as in both fibroblast subtypes challenged with Pam2CSK4. Conversely, constitutive CXCL12 mRNA levels were upregulated by MyD88 or TRAM knockdown in non‐stimulated cells. Conclusions: These results suggest that TLR adaptor molecules knockdown, such as MyD88 or TRAM, can decrease IL‐6 and IL‐8 mRNA and increase CXCL12 mRNA expression in HGF and HPDLF. This can be an important step for better understanding the mechanisms that control the inflammatory cytokine and chemokine expression, which in turn contributes to periodontal pathogenesis.     

Titanium surfaces with nanotopography modulate cytokine production in cultured human gingival fibroblasts

Implant topography is an important factor that influences many cell types. To understand the role of topography in the inflammatory events, we evaluated the response of human gingival fibroblasts (HGFs) by the release pattern of cytokines. HGFs were cultured on Ti discs for 24 and 48 h. Four different surface treatments were used: machining method (turned), blasting followed by an acid-etching method (BAE), oxidative nanopatterning (ON) method, and an association of blasting followed by an acid-etching plus oxidative nanopatterning (BAE+ON) method. Extracellular levels of IL-6, IL-8, transforming growth factor beta (TGF-β), IL-4, and IL-10 were measured by enzyme-linked immunosorbant assay. Increased levels of IL-6 and IL-8 were observed in all surfaces after 24 h which decreased after 48 h. BAE, ON, and BAE+ON surfaces showed a reduction in IL-6 levels compared with the turned after 48 h (p < 0.05). On one hand, IL-8 production was lower in BAE+ON in comparison to the turned surface (p < 0.05). On the other hand, IL-4 showed increased levels with 48 h, which were significantly different between turned, BAE, and ON surfaces, but not with BAE+ON. Additionally, TGF-β and IL-10 production were not detected. This study indicates that nanotopography might be important in the modulation of the inflammatory response in cultured HGFs. ? 2012 Wiley Periodicals, Inc. J Biomed Mater Res Part A 100A:2629-2636, 2012.     

Understanding the impact of divalent cation substitution on hydroxyapatite: an in vitro multiparametric study on biocompatibility

Hydroxyapatite (HA), a stable and biocompatible material for bone tissue therapy, may present a variable stoichiometry and accept a large number of cationic substitutions. Such substitutions may modify the chemical activity of HA surface, with possible impact on biocompatibility. In this work, we assessed the effects of calcium substitution with diverse divalent cations (Pb(2+), Sr(2+), Co(2+), Zn(2+), Fe(2+), Cu(2+), or Mg(2+)) on the biological behavior of HA. Physicochemical analyses revealed that apatite characteristics related to crystallinity and calcium dissolution/uptake rates are very sensitive to the nature of cationic substitution. Cytocompatibility was evaluated by mitochondrial activity, membrane integrity, cell density, proapoptotic potential, and adhesion tests. With the exception of Zn-HA, all the substituted HAs induced some level of apoptosis. The highest apoptosis levels were observed for Mg-HA and Co-HA. Cu-HA was the only material to impair simultaneously mitochondrial activity, membrane integrity, and cell density. The highest relative cell densities after exposure to the modified HAs were observed for Mg-HA and Zn-HA, while Co-HA significantly improved cell adhesion onto HA surface. These results show that changes on surface dissolution caused by cationic substitution, as well as the increase of metal species released to biological media, were the main responsible factors related to alterations on HA biocompatibility.     

Serum markers as an aid in the diagnosis of pulmonary fungal infections in AIDS patients

Introduction

The etiology of pulmonary infections in HIV patients is determined by several variables including geographic region and availability of antiretroviral therapy.

Treatment of experimental periodontitis in rats using repeated adjunctive antimicrobial photodynamic therapy

The aim of this study was to histologically and histometrically evaluate the influence of repeated adjunctive antimicrobial photodynamic therapy (aPDT) on bone loss (BL) in furcation areas in rats. Periodontitis was induced by placing a ligature around the mandibular molar in 75 rats. The animals were divided into five groups: the SS group was treated with saline solution (SS); the SRP group received scaling and root planing (SRP); the aPDT1 group received SRP as well as toluidine blue (TBO) and low-level laser therapy (LLLT; InGaAlP, 660 nm; 4.94 J/cm²/point) postoperatively at 0 h; the aPDT2 group received SRP as well as TBO and LLLT postoperatively at 0, 24, 28, and 72 h; and the aPDT3 group received SRP, TBO, and LLLT postoperatively at 0, 48, 96, and 144 h. The area of BL in the furcation region of the molar was histometrically analyzed. Data were analyzed statistically (P?<?0.05). Animals treated with a single episode of aPDT showed less BL at days 7 and 30 than those who received only SRP treatment. No significant differences were found among the aPDT groups (P?>?0.05). Repeated aPDT did not improve BL reduction when compared to a single episode of aPDT.