does triamcinolone acetonide cream lighten skin

Interferon (IFN)-γ, lipopolysaccharides and tumour necrosis factor (TNF) are especially well-known inducers of M1 macrophages. First, the classically activated (or M1) macrophages are activated through a cell-mediated immune response. Inactive macrophages are able to differentiate into different active subtypes. This effect might result from the marked influence of corticosteroids on macrophage differentiation. It remains unclear through which mechanisms corticosteroids exert this positive effect on macrophages and other joint tissues within the joint during OA development. The authors of that study also showed that corticosteroid therapy reduced cartilage destruction. More recently, in 2014, this finding was reproduced in a post-traumatic model of OA using intra-articular injections of dexamethasone. This finding suggests that TA somehow intervenes with synovial macrophage activation and might prevent subsequent TGF-β–induced osteophyte development. reported that TA quite effectively protected against osteophyte development in a pre-clinical model of OA. More specifically, triamcinolone acetonide (TA) injections are even more effective than other corticosteroids in reducing pain. Intra-articular injection with corticosteroids provides excellent results for OA-related pain and is an advocated treatment for individuals with knee OA. Pain management for patients with OA can be achieved through analgesia with agents such as paracetamol, non-steroidal anti-inflammatory drugs or intra-articular injection of corticosteroids. The latter is of special interest because pain management plays a pivotal role in clinical management of OA. Second, it is thought that enhanced growth factor and cytokine production by activated macrophages facilitates cartilage extracellular matrix (ECM) degradation, contributes to synovial fibrosis and induces pain. Due to TGF-β, synoviocytes increase their production of bone morphogenetic protein 2 (BMP2) and BMP4 as a consequence, osteophytes develop within the OA joint. These cytokines and growth factors are thought to detrimentally change the articular joint.įirst, activated synovial macrophages have been proposed to enhance transforming growth factor (TGF)-β production. During OA progression, synovial macrophages become activated and secrete many pro-inflammatory cytokines and growth factors. Osteoarthritis (OA) is characterized by deterioration of articular cartilage and extensive subchondral bone remodelling, as well as by inflammation within the synovial lining of the osteoarthritic joint. TA injections potently induce a CD163 +- and FRβ +-activated macrophage with anti-inflammatory characteristics such as reduced IL-10 production in vitro and lack of osteophytosis in vivo. Furthermore, TA-stimulated M2 macrophages showed enhanced IL-10 expression at the mRNA level. In vitro macrophage cultures showed that TA strongly induced monocyte differentiation towards CD163 + and FRβ + macrophages. There was no beneficial effect of TA against cartilage degradation or subchondral bone sclerosis. Despite stimulated macrophage activation, osteophyte formation was fully prevented. Our in vivo study showed that intra-articular injections with TA strongly enhanced FRβ + macrophage activation. These cultured macrophages were either M1- or M2-activated, and they were analyzed using fluorescence-activated cell sorting for CD163 and FRβ expression as well as for messenger RNA (mRNA) expression of interleukin (IL)-10. To further explain the outcomes of our in vivo study, TA on macrophages was also studied in vitro. Articular cartilage was analyzed at 6 and 12 weeks with ex vivo contrast-enhanced μCT and histology.

Synovial macrophage activation was measured in vivo using folate receptor β (FRβ)-targeted single-photon emission computed tomography/computed tomography. Untreated and TA-treated animals were longitudinally monitored for 12 weeks with in vivo micro–computed tomography (μCT) to measure subchondral bone changes. Osteoarthritis was induced in rat knees using papain injections and a running protocol. Furthermore, in vitro macrophage differentiation experiments were conducted to further explain working mechanisms of TA effects found in vivo. In this animal study, we investigated the in vivo effects of TA injections on macrophage activation, osteophyte development and joint degeneration. Although widely applied in clinical care, the mechanism through which TA exerts this effect remains unknown. TA injections might influence macrophage activation and subsequently reduce osteophytosis. Osteophyte formation is known to be facilitated by synovial macrophage activation. Triamcinolone acetonide (TA) is used for osteoarthritis management to reduce pain, and pre-clinical studies have shown that TA limits osteophyte formation.

Does triamcinolone acetonide cream lighten skin