MSC therapy may be a valid alternative treatment for chronic knee osteoarthritis. The intervention is simple, does not require hospitalization or surgery, provides pain relief, and significantly improves cartilage quality.

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Both treatment approaches were equally effective but the intraoperative ERCP group had less morbidity, a shorter hospital stay, and reduced costs. The lower morbidity in the intraoperative ERCP group resulted from the lower rate of papillotomy and lower rates of post-ERCP pancreatitis and cholecystitis. Total morbidity was principally related to the type of treatment approach used.

The diagnosis and the prompt treatment of early osteoarthritis (OA) represent vital steps for delaying the onset and progression of fully blown OA, which is the most common form of arthritis, involving more than 10 % of the world's population older than 60 years of age. Nonsurgical treatments such as physiotherapy, anti-inflammatory medications, and other disease-modifying drugs all have modest and short-lasting effect. In this context, the biological approaches have recently gained more and more attention. Growth factors, blood derivatives, such as platelet concentrates, and mesenchymal adult stem cells, either expanded or freshly isolated, are advocated amongst the most promising tool for the treatment of OA, especially in the early phases. Primarily targeted towards focal cartilage defects, these biological agents have indeed recently showed promising results to relieve pain and reduce inflammation in patients with more advanced OA as well, with the final aim to halt the progression of the disease and the need for joint replacement. However, despite of a number of satisfactory in vitro and pre-clinical studies, the evidences are still limited to support their clinical efficacy in OA setting.

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Joint surface incongruence resulting from osteochondritis dissecans (OCD) alters the articular physiologic congruence, increasing the contact stress on adjacent joint surfaces and accelerating wear and the cascade of joint degeneration. Accordingly, the restoration of articular surface integrity is of major importance, especially in young adults where, in lesions left untreated or following simple fragment excision, early osteoarthritis can be anticipated. Therefore, the treatment algorithm in unstable knee OCD of the young adult foresees surgical options to restore the articular surface. Several procedures have been proposed, including refixation of the detached fragment bone marrow stimulation, osteochondral autograft implantation, fresh osteochondral allograft transplantation, and cell-based or cell-free regenerative techniques. The aim of this review was to summarize the evidence for these surgical strategies, reporting their results and limitations. The overall evidence documents positive results for each of the assorted surgical procedures applied to treat unstable OCD, thus indicating support for their selected use to treat osteochondral defects paying particular attention to their specific indications for the lesion characteristics. The fixation of a good quality fragment should be pursued as a first option, while unfixable small lesions may benefit from autografts. For large lesions, available cell-based or cell-free osteochondral scaffold are a feasible solution but with limitation in terms of regenerated tissue quality. In this light, fresh allografts may offer articular surface restoration with viable physiologic osteochondral tissue providing a predictably successful outcome, and therefore they may currently represent the most suitable option to treat unstable irreparable OCD lesion in young adults. Level of evidence V.

Chromosomal imbalances were examined by comparative genomic hybridization in 30 cases of B-cell chronic lymphocytic leukemia (CLL) at diagnosis, in sequential samples from 17 of these patients, and in 6 large B-cell lymphomas transformed from CLL [Richter's syndrome (RS)] with no available previous sample. The most common imbalances in CLL at diagnosis were gains in chromosome 12 (30%), and losses in chromosomes 13 (17%), 17p (17%), 8p (7%), 11q (7%), and 14q (7%). The analysis of sequential samples showed an increased number of chromosomal imbalances in 6 of 10 (60%) patients with clinical progression and in 2 patients with stable stage C disease. No karyotypic evolution was observed in four cases with stable stage A disease and in one RS clonally unrelated to the previous CLL. Gains of 2pter, and 7pter, and losses of 8p, 11q, and 17p were recurrent alterations associated with karyotype progression. RS showed a higher number of gains, losses, total alterations, and losses of 8p and chromosome 9 than CLL at diagnosis. 17p losses were associated with p53 gene mutations and with a significantly higher number of chromosomal imbalances than tumors with normal chromosome 17 profile. However, no relationship was observed between 9p deletions and p16(INK4a) gene alterations. Losses of 17p and an increased number of losses at diagnosis were significantly associated with a shorter survival. These findings indicate that CLL has frequent chromosomal imbalances, which may increase during the progression of the disease and transformation into large cell lymphoma. Genetic alterations detected by comparative genomic hybridization may also be of prognostic significance.

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