Alterations in osteoblast metabolism are involved in the pathogenesis of typical subchondral bone changes in osteoarthritis (OA). Osteocalcin is a specific bone protein, synthesised by the osteoblasts, which can be considered a marker of metabolic activity of these cells. In this study we correlated osteocalcin production from human osteoblasts isolated from healthy and osteoarthritic subjects to the degree of cartilage damage, before and after stimulation with 1,25(OH)2-vitamin D3, the active metabolite of vitamin D3. We isolated human osteoblasts from cancellous bone of healthy subjects and from subchondral bone of osteoarthritic subjects and considered the osteoblasts corresponding to different degrees of cartilage damage as different cell populations. We determined the osteocalcin production in normal and osteoarthritic osteoblasts from maximal and minimal cartilage damage areas both under basal conditions and after vitamin D3 stimulation. Compared to normal osteoblasts, under basal conditions osteocalcin production is significantly greater in osteoarthritic osteoblasts, corresponding both to maximal and minimal damage joint areas. No differences were observed between osteoblasts from maximal and minimal damage areas. The response of osteoblasts to vitamin D3 stimulation appeared to be proportional to the degree of joint damage, as the vitamin D3-induced increase in osteocalcin is proportionally greater in maximally damaged osteoblasts compared to minimally damaged ones. Thus, after vitamin D3 stimulation, a significant increase in osteocalcin production by maximally damaged osteoblasts compared to the minimally damaged ones was observed. This study confirms abnormal osteoarthritic osteoblast behaviour and indicates that osteoblasts from different areas of the same affected joint may be metabolically different, supporting the hypothesis that subchondral osteoblasts may play an essential role in the pathogenesis of OA.

Psoriatic arthritis (PsA) is a well-known disease characterized by psoriasis and inflammatory joint disease, with distinct clinical and radiological features to differentiate it from other arthropathies. Whereas many cases of coexistence of arthritis and other autoimmune disorders with chromosomal abnormalities have been reported, the occurrence of PsA and Klinefelter syndrome has not been reported previously. A case of Klinefelter syndrome and PsA was reported. This case report emphasizes the role played by sex hormones and chromosomal abnormalities in the pathogenesis of autoimmune disorder, and to our knowledge, this is an uncommon case of a patient with Klinefelter syndrome who developed PsA.

Behçet's disease (BD) is a chronic relapsing-remitting inflammatory disorder of unknown origin, affecting multiple organs. Neurological involvement is one of the most devastating manifestations of BD and may be fatal. We report a 36-year-old woman with neuro-Behçet who was treated with low-dose pulse cyclophosphamide (St. Thomas' protocol) and methylprednisolone, with almost complete clinical remission.

Because of the increased incidence of tuberculosis (TB) in recent years, infective spondylitis is still a major problem in the world. In skeletal TB the spine is the most often involved and lumbosacral spine involvement is rare. Nowadays early diagnosis and new medical treatment can reduce the incidence of the serious skeletal sequelae and the number of surgery procedures in spinal TB. We present a case of TB spondylodiscitis characterized by a rapid and progressive clinical and radiological improvement after treatment with Neridronate and chemotherapic drugs. Our data suggest that in the treatment of the TB spondylodiscitis the combined use of these drugs is a good alternative to stimulate bone reparative process to the chemotherapy alone. To our knowledge this is first case of a patient with TB discitis treated with Neridronate. Further studies are necessary to confirm the effectiveness of Neridronate treatment added to antiTB drugs in spondylodiscitis.

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