CAD-CAM resin-ceramic material wear: A systematic review.

STATEMENT OF PROBLEM: The increasing use of computer-aided design and computer-aided manufacturing (CAD-CAM) systems has led to the development of resin-ceramic materials that meet the requirements of minimally invasive dentistry, including the resin nanoceramic (RNC) and polymer-infiltrated ceramic network (PICN). The wear characteristics of these materials are unclear. PURPOSE: The purpose of this systematic review was to compare the wear resistance of resin-ceramic materials when compared with one another or with lithium disilicate glass-ceramics. MATERIAL AND METHODS: The PubMed, Scopus, and DOSS search engines were used to identify articles published between 2013 and 2021. Two independent researchers conducted the systematic review by following the preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines and by following a combination of keywords. RESULTS: Of a total of 310 articles, 26 were selected, including only 1 clinical study. Among these, 15 compared resin-ceramic materials with each other, while 11 compared resin-ceramic materials with lithium disilicate ceramics. Two types of wear were used to compare the materials: attrition and abrasion. The most commonly studied materials were 2 RNCs (Lava Ultimate and Cerasmart), 1 PICN (Vita Enamic), and 1 ceramic (IPS e.max CAD). Among the resin-ceramic materials, the PICN (Vita Enamic) showed less wear than the RNCs. Of the RNCs, Cerasmart had less attrition wear and less wear of the opposing teeth. CONCLUSIONS: Lithium disilicate glass-ceramics have a higher wear resistance than resin-ceramic materials, but they cause more wear of the opposing teeth.

Interferon α kinoid induces neutralizing anti-interferon α antibodies that decrease the expression of interferon-induced and B cell activation associated transcripts: analysis of extended follow-up data from the interferon α kinoid phase I/II study.

OBJECTIVE: IFN α Kinoid (IFN-K) is a therapeutic vaccine composed of IFNα2b coupled to a carrier protein. In a phase I/II placebo-controlled trial, we observed that IFN-K significantly decreases the IFN gene signature in whole blood RNA samples from SLE patients. Here, we analysed extended follow-up data from IFN-K-treated patients, in order to evaluate persistence of neutralizing anti-IFNα Abs antibodies (Abs), and gene expression profiling. METHODS: Serum and whole blood RNA samples were obtained in IFN-K-treated patients included in the follow-up study, in order to determine binding and neutralizing anti-IFNα Ab titres, and perform high-throughput transcriptomic studies. RESULTS: Neutralization studies of 13 IFNα subtypes demonstrated the polyclonal nature of the Ab response induced by IFN-K. Follow-up analyses in six patients confirmed a significant correlation between neutralizing anti-IFNα Ab titres and decrease in IFN scores compared to baseline. These analyses also revealed an inhibitory effect of IFNα blockade on the expression of B cell associated transcripts. CONCLUSIONS: IFN-K induces a polyclonal anti-IFNα response that decreases IFN- and B cell-associated transcripts. TRIAL REGISTRATION: ClinicalTrials.gov, clinicaltrials.gov, NCT01058343.

Modulation of anti-tumor necrosis factor alpha (TNF-α) antibody secretion in mice immunized with TNF-α kinoid.

Tumor necrosis factor alpha (TNF-α) blockade is an effective treatment for patients with TNF-α-dependent chronic inflammatory diseases, such as rheumatoid arthritis, Crohn's disease, and psoriasis. TNF-α kinoid, a heterocomplex of human TNF-α and keyhole limpet hemocyanin (KLH) (TNF-K), is an active immunotherapy targeting TNF-α. Since the TNF-K approach is an active immunization, and patients receiving this therapy also receive immunosuppressant treatment, we evaluated the effect of some immunosuppressive drugs on the generation of anti-TNF-α antibodies produced during TNF-K treatment. BALB/c mice were injected intramuscularly with TNF-K in ISA 51 adjuvant. Mice were also injected intraperitoneally with one of the following: phosphate-buffered saline, cyclophosphamide, methylprednisolone, or methotrexate. Anti-TNF-α and anti-KLH antibody levels were assessed by enzyme-linked immunosorbent assay and the anti-TNF-α neutralizing capacity of sera by L929 bioassay. Our results showed that current treatments used in rheumatoid arthritis, such as methylprednisolone and methotrexate, do not significantly alter anti-TNF-α antibody production after TNF-K immunization. In contrast, the administration of cyclophosphamide (200 mg/kg) after immunization significantly reduced anti-TNF-α antibody titers and their neutralizing capacity.

Interplay between TNF and regulatory T cells in a TNF-driven murine model of arthritis.

CD4(+)CD25(+)Foxp3(+) regulatory T cells (Treg) are involved in several autoimmune diseases, including rheumatoid arthritis. TNF-α blockers induce therapeutic benefits in rheumatoid arthritis via a variety of mechanisms. We aimed to characterize the impact on Treg of TNF-α overexpression in vivo and of TNF-α inhibiting treatments. We used human TNF-α transgenic mice as a model of strictly TNF-α-dependent arthritis. Our study showed that initial Treg frequency was lower in TNF-α transgenic mice than in wild-type mice. However, the course of arthritis was marked by elevation of Treg frequency and a dramatic increase in expression of TNFR2. Antagonizing TNF-α with either the anti-human TNF-α Ab (infliximab) or active immunotherapy (TNF-kinoid) increased the Treg frequency and upregulated CTLA-4, leading to enhancement of suppressor activity. Moreover, both anti-TNF-α strategies promoted the differentiation of a CD62L(-) Treg population. In conclusion, in an in vivo model of TNF-α-driven arthritis, Treg frequency increased with inflammation but failed to control the inflammatory process. Both passive and active TNF-α-inhibiting strategies restored the suppressor activity of Treg and induced the differentiation of a CD62L(-) Treg population.

Active immunization to tumor necrosis factor-alpha is effective in treating chronic established inflammatory disease: a long-term study in a transgenic model of arthritis.

INTRODUCTION: Passive blockade of tumor necrosis factor-alpha (TNF-alpha) has demonstrated high therapeutic efficiency in chronic inflammatory diseases, such as rheumatoid arthritis, although some concerns remain such as occurrence of resistance and high cost. These limitations prompted investigations of an alternative strategy to target TNF-alpha. This study sought to demonstrate a long-lasting therapeutic effect on established arthritis of an active immunotherapy to human (h) TNF-alpha and to evaluate the long-term consequences of an endogenous anti-TNF-alpha response. METHODS: hTNF-alpha transgenic mice, which spontaneously develop arthritides from 8 weeks of age, were immunized with a heterocomplex (TNF kinoid, or TNF-K) composed of hTNF-alpha and keyhole limpet hemocyanin after disease onset. We evaluated arthritides by clinical and histological assessment, and titers of neutralizing anti-hTNF-alpha antibody by enzyme-linked immunosorbent assay and L929 assay. RESULTS: Arthritides were dramatically improved compared to control mice at week 27. TNF-K-treated mice exhibited high levels of neutralizing anti-hTNF-alpha antibodies. Between weeks 27 and 45, all immunized mice exhibited symptoms of clinical deterioration and a parallel decrease in anti-hTNF-alpha neutralizing antibodies. A maintenance dose of TNF-K reversed the clinical deterioration and increased the anti-hTNF-alpha antibody titer. At 45 weeks, TNF-K long-term efficacy was confirmed by low clinical and mild histological scores for the TNF-K-treated mice. Injections of unmodified hTNF-alpha did not induce a recall response to hTNF-alpha in TNF-K immunized mice. CONCLUSIONS: Anti-TNF-alpha immunotherapy with TNF-K has a sustained but reversible therapeutic efficacy in an established disease model, supporting the potential suitability of this approach in treating human disease.