The SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, and osteitis) is a chronic, relapsing, inflammatory condition with skin and osteoarticular manifestations. Its etiology remains unclear, and various treatment regimens with steroids and nonsteroidal antiinflammatory drugs frequently fail to control the disease, while exposing patients to the side effects of these drugs. Because the SAPHO syndrome manifests as a destructive inflammatory bone disease, use of bisphosphonates that possess antiosteoclastic and probably antiinflammatory properties has been suggested to be helpful. To our knowledge, this is the first reported case of successful treatment with zoledronic acid of SAPHO syndrome that was resistant to conventional treatment.
Recently, a number of studies have pointed to a potential relationship between periodontitis (PO) and RA and vice versa. Both diseases are characterized by chronic inflammation, osseous destruction, damage of the supporting soft tissues, similar cellular immune responses and common immunogenetic findings. Although a definite, methodological report associating these diseases is missing from the literature, it is possible that both diseases share a common aetiopathogenic background. This background includes the post-translation modification citrullination, which guides the conversion of the amino acid arginine to citrulline in certain self-proteins, generating neo-epitope structures. This results in reduced self-tolerance, development of autoimmunity and the production of ACPAs. The current hypothesis suggests that certain oral bacteria induce the citrullination of proteins under the action of the enzyme peptidyl arginine deiminase (PAD), which exists in both Porphyromonas gingivalis and inflammatory cells. Antibodies against citrullinated proteins and peptides constitute a common serological finding in both RA and PO. The aim of this review is to map the immunological and serological profiles of PO, and to unveil the parameters that connect PO with the appearance of RA at clinical, prognostic and pathogenetic levels. Until now, there have been no reports sufficiently mapping the immunological profile of PO and defining its aetiopathogenic connection with RA, although a similarity between the immunological profile of PO and RA is highly expected.
We report 2 cases of leishmaniasis in patients with autoimmune rheumatic diseases
in Greece. To assess trends in leishmaniasis reporting in this patient
population, we searched the literature for similar reports from Europe. Reports
increased during 2004–2008, especially for patients treated with
anti–tumor necrosis factor agents.
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