[Oral manifestations of systemic sclerosis]. / Orale manifestaties van systemische sclerose.

Systemic sclerosis is a relatively rare connective tissue disorder, in which a severe and progressive fibrosis of the skin and sometimes also of internal organs often develops as a result of an increased deposition of collagen. Fibrosis of the salivary glands may cause hyposalivation and xerostomia. Fibrosis of the perioral skin reduces the maximum opening of the mouth, thereby hampering dental treatment and the maintenance of oral hygiene. Periodontitis and bone resorption ofthe jaws are more frequently observed in systemic sclerosis patients.

How to perform local soft-tissue glucocorticoid injections?

Inflammation of periarticular soft-tissue structures such as tendons, tendon sheaths, entheses, bursae, ligaments and fasciae is the hallmark of many inflammatory rheumatic diseases, but inflammation or rather irritation of these structures also occurs in the absence of an underlying rheumatic disease. In both these primary and secondary soft-tissue lesions, local glucocorticoid injection often is beneficial, although evidence in the literature is limited. This chapter reviews local injection therapy for these lesions and for nerve compression syndromes.

Lack of a role for transforming growth factor-beta in cytotoxic T lymphocyte antigen-4-mediated inhibition of T cell activation.

Similarities in the phenotypes of mice deficient for cytotoxic T lymphocyte antigen-4 (CTLA-4) or transforming growth factor-beta1 (TGF-beta1) and other observations have led to speculation that CTLA-4 mediates its inhibitory effect on T cell activation via costimulation of TGF-beta production. Here, we examine the role of TGF-beta in CTLA-4-mediated inhibition of T cell activation and of CTLA-4 in the regulation of TGF-beta production. Activation of AND TCR transgenic mouse T cells with costimulatory receptor-specific antigen presenting cells results in efficient costimulation of proliferation by CD28 ligation and inhibition by CTLA-4 ligation. Neutralizing antibody to TGF-beta does not reverse CTLA-4-mediated inhibition. Also, CTLA-4 ligation equally inhibits proliferation of wild-type, TGF-beta1(-/-), and Smad3(-/-) T cells. Further, CTLA-4 engagement does not result in the increased production of either latent or active TGF-beta by CD4(+) T cells. These results indicate that CTLA-4 ligation does not regulate TGF-beta production and that CTLA-4-mediated inhibition can occur independently of TGF-beta. Collectively, these data demonstrate that CTLA-4 and TGF-beta represent distinct mechanisms for regulation of T cell responses.