Therapy of chronic extensor mechanism deficiency after total knee arthroplasty using a monofilament polypropylene mesh.

Introduction: Lesions of the quadriceps or patellar tendon after total knee arthroplasty (TKA) are a rare but serious complication which, if left untreated, can lead to loss of function of the knee joint. While acute and subacute extensor mechanism disruptions may have several causes, chronic deficiencies are often related to multiple prior revision surgeries for joint infection or aseptic TKA failure. Up to date, biological allograft reconstruction showed unsatisfying results. The use of a monofilament polypropylene mesh is a promising approach for this pathological condition. The aim of the present study was to evaluate clinical, functional and patient reported outcomes of this procedure in patients with chronic extensor mechanism deficiency. Materials and Methods: Twenty-eight patients with chronic extensor mechanism deficiency (quadriceps tendon rupture n = 9, patellar tendon rupture n = 19) after TKA were included in this retrospective study. None of the patients were lost to follow-up. Surgical reconstruction was performed at one institution between 2014 and 2020 with a monofilament polypropylene mesh (Marlex Mesh, Bard, Murray Hill, USA). The mean age at the time of surgery was 69 years. Patients presented with a mean BMI of 33 kg/m2. The mean follow-up period was 23 months. Results: The 2-year survivorship free of mesh revision was 89% [95% confidence interval (CI): 75% to 100%]. Three patients (11%) had to undergo revision because of mechanical mesh failure and received another polypropylene mesh. No further revisions were performed thereafter. Flexion was 87° (range, 30-120°) on average. The majority of patients (75%, 21/28) had a full active extension. The mean active extension lag after surgery was 4 degrees (range, 0-30°). Discussion: We observed a substantial improvement of extensor mechanism function. The majority of patients had full extension and showed good clinical results. A failure rate of over 50% has been published for alternative procedures. Thus, the use of the described augmentation technique represents a reasonable treatment option for chronic extensor mechanism disruptions of the patellar tendon as well as the quadriceps tendon after total knee arthroplasty. However, there might be a potentially higher risk for infection persistence in periprosthetic joint infection cases due to the presence of a foreign material.

Saliva proteomic patterns in patients with molar incisor hypomineralization.

Molar incisor hypomineralization (MIH) is an endemic pediatric disease with an unclear pathogenesis. Considering that saliva controls enamel remineralization and that MIH is associated with higher saliva flow rate, we hypothesized that the protein composition of saliva is linked to disease. To test this, we enrolled 5 children aged 6-14 years with MIH showing at least one hypersensitive molar and 5 caries-free children without hypomineralization. Saliva samples were subjected to proteomic analysis followed by protein classification in to biological pathways. Among 618 salivary proteins identified with high confidence, 88 proteins were identified exclusively in MIH patients and 16 proteins in healthy controls only. Biological pathway analysis classified these 88 patient-only proteins to neutrophil-mediated adaptive immunity, the activation of the classical pathway of complement activation, extracellular matrix degradation, heme scavenging as well as glutathione -and drug metabolism. The 16 controls-only proteins were associated with adaptive immunity related to platelet degranulation and the lysosome. This report suggests that the proteaneous composition of saliva is affected in MIH patients, reflecting a catabolic environment which is linked to inflammation.

Combination of von Willebrand disease type 1 and partial factor XII deficiency in children: clinical evidence for a diminished bleeding tendency.

Factor XII deficiency can be associated with a thrombotic and VWF deficiency with a haemorrhagic clinical course. To study the potential influence of factor XII deficiency on bleeding tendency in patients suffering from VWD we retrospectively compared the clinical outcome of children with either an isolated factor XII deficiency, an isolated VWD, or a combination of both. Patients with the combined coagulation defect showed significantly fewer bleeding events when compared to patients with isolated VWD, although ristocetin cofactor activities were reduced to a comparable degree. As far as aPTT values are concerned, there were no significant differences among the three groups. Whether this combination of thrombophilic and haemorrhagic coagulation disorders is only coincidental or the result of an active modulation of one of the two counteracting coagulation factors is not known at present.

Modified T-cell activation pattern during specific immunotherapy (SIT) in cat-allergic patients.

OBJECTIVE: The aim of the study was to analyse early effects of specific immunotherapy (SIT) on immune functions in cat-allergic patients. METHODS: Immunological responses of peripheral blood mononuclear cells from eight cat-allergic patients were analysed before and after SIT in comparison with 11 nonallergic controls. Cells were stimulated in vitro with either bacterial superantigen, mitogen, or cat allergen. Production of IL-12 and TH1/TH2 cytokines was analysed by ELISA and lymphocyte subset distribution was assessed by flow-cytometry. RESULTS: We found a significantly reduced secretion of IL-12 (P < 0.05) from cells of allergic individuals compared with the controls. This finding was associated with significantly lower IFN-gamma production after stimulation with allergen (P < 0.05) that did not increase during SIT. However, no significant differences were seen after stimulation with mitogen indicating an allergen specific IFN-gamma secretion response in allergic individuals. Prior to SIT IL-5 production was significantly higher in cells of allergic donors stimulated with allergen < 0.005 or mitogen (< 0.05). After reaching the maintenance dose for SIT, allergen-induced IL-5 production returned to normal levels, whereas it remained elevated after stimulation with mitogen. These changes were associated with a reduced frequency of CD45 RO T cells following SIT. CONCLUSION: These results suggest that SIT exerts early effects on allergen-specific T-cell responses with selective inhibition of the up-regulated TH2 immune response.

Granulomatous cheilitis and Crohn's disease in a 3-year-old boy.

Granulomatous cheilitis and Crohn's disease are disorders of unknown etiology. There are case reports describing their coincidence and pointing out the necessity of ruling out systemic disorders once the diagnosis of granulomatous cheilitis is made. However, such reports are few and the causal association of both diseases is controversial in the literature. We report the youngest patient so far, a 3-year-old boy, who had granulomatous cheilitis and Crohn's disease simultaneously. This coincidence so early in life strongly suggests that both represent manifestations of the same disease.

A subset of CD8+ T cells from allergic patients produce IL-4 and stimulate IgE production in vitro.

BACKGROUND AND OBJECTIVE: A subset of IL-4 producing CD8+ T cells was recently identified in HIV patients. Based on these findings we examined whether IL-4 producing CD8+ T cells would also be present in allergic patients and what would be the functional relevance of this T-cell population. METHODS: We investigated the role of CD8+ T cells in IgE production of allergic diseases by analysing the cytokine profile of individual CD4+ and CD8+ T cells. RESULTS: In allergic patients about twice as many CD4+ T cells and six times as many CD8+ T cells produced IL-4 as in non-allergic controls. In contrast the frequency of IFNgamma+ T-cell subsets did not significantly differ between the allergic and non-allergic individuals. The frequency of IL4+ CD8+ T cells correlated with the level of serum IgE. Coculture experiments with T cells or purified CD8+ T cells together with autologous B cells indicated that CD8+ T cells enhanced IgE in vitro, but not IgM production, even when they were physically separated from B cells. This effect could be partially blocked by addition of an IL-4 binding protein, a soluble IL-4 receptor indicating that IL-4 is involved in CD8+ T-cell mediated IgE production. CONCLUSIONS: These data indicate a positive role of IL-4 secreting CD8+ T cells in IgE regulation in allergic patients.

Role and modulation of T-cell cytokines in allergy.

Allergic sensitization and the development of effector functions are controlled by IL-4-secreting and IL-5-secreting type 2 T cells. Recent studies have provided new insights into the events triggering the development of type 1 and type 2 T cells, the discrimination of type 1 and type 2 effector T cells from various T-cell subsets, and the improvement of established and new therapeutic strategies, which are aimed at modulating such T-cell functions in the allergic patient.

Influence of cadmium ions on endothelin-1 binding and calcium signaling in rat glioma C6 cells.

Cadmium ions did not influence the binding of endothelin-1 (ET-1) to its receptor on the surface of rat glioma C6 and rat aorta A10 cells. This was studied (a) by the binding of 1251-ET-1 to intact cells in the absence or presence of cadmium (Cd2+) and (b) by analysis of the receptor/ET-1 complex after crosslinking with disuccinimidyl suberate (DSS) or ethylene glycol-bis-(succinimidyl succinate) (EGS) on SDS PAGE. Using Fura-2 and Quin-2 loaded C6 rat glioma cells, it was shown that Cd2+ ions strongly interfered with the ET-1 induced Ca(2+)-influx in C6 glioma cells (IC50 approximately 10 microM).

Downregulation of endothelin receptor mRNA synthesis in C6 rat astrocytoma cells by persistent measles virus and canine distemper virus infections.

Persistent infections of C6 rat astrocytoma cells with measles (subacute sclerosing panencephalitis [SSPE]) virus (C6/SSPE cells) or canine distemper virus (C6/CDV cells) cause a loss of endothelin-1 (ET-1) binding to its specific receptors (ETRA type) and subsequent ET-1-induced Ca2+ signaling. It was the aim of this study to investigate the underlying mechanism of this phenomenon in more detail. By using an RNase protection assay, it was found that ETRA mRNA disappears, whereas other cellular mRNA species, e.g., beta-actin mRNA, were not influenced. The data show that the loss of the ET-1 signaling pathway in C6/SSPE and C6/CDV cells is due to a receptor downregulation at the transcriptional level.

Relevance of mediators to cardiac parameters of isolated anaphylactic guinea-pig heart.

The release of histamine, eicosanoids and catecholamines were measured after induction of anaphylaxis in isolated guinea-pig hearts. The concentration-time profile of these mediators was compared with changes of cardiac parameters. The histamine and catecholamine levels of the coronary effluent were determined at 10 s intervals; thromboxane and prostacyclin levels at 60 s intervals. The release of histamine and norepinephrine were maximum between 20 and 30 s after the antigen challenge and decreased rapidly within 60 s. Thromboxane and prostacyclin increased to a maximum after 3 min and declined slowly within 10 min. The rise in histamine release was correlated with tachycardia. The release of thromboxane was correlated with the increase of coronary perfusion pressure. Cimetidine inhibited the tachycardia and clemastine reduced bradyarrhythmia. The inhibition of lipoxygenase and cyclooxygenase also reduced the rise in the perfusion pressure. These data suggest that different mediators are time-dependently involved in anaphylaxis-induced cardiac changes.