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This retrospective study described the clinical and radiographic long-term outcomes of combined periodontal and orthodontic treatment (OT) with fixed appliances in patients with Stage IV periodontitis and pathologic tooth migration (PTM) in the anterior sextants. OT was performed in either one or both arches, using tooth-supported or skeletal anchorage, following completion of active periodontal treatment and accurate planning of tooth movement biomechanics. Twenty-nine patients were identified and retrospectively examined when presenting for a supportive periodontal care (SPC) appointment. The mean SPC duration was 8.9 years (range 5 to 12 years). All anterior-migrated teeth showed statistically significant periodontal improvement compared to baseline values and stable radiographic bone levels at the final follow-up. Residual probing depths were 2.9 ± 0.5 mm at the end of active periodontal treatment, and they remained stable at the completion of OT (2.9 ± 0.6 mm) and at the last follow-up visit (2.8 ± 0.5 mm). These findings suggest that OT is a safe and effective treatment in improving the long-term prognosis of teeth with PTM in Stage IV periodontitis provided that periodontal health has been re-established and maintained with individualized SPC sessions.

This retrospective study evaluated the effect of combined periodontal-orthodontic treatment in terms of clinical, radiographic, and patient-reported outcomes in 40 stage IV periodontitis patients with advanced attachment loss and pathologic migration of anterior teeth. Full-mouth periodontal parameters were recorded at baseline (after diagnosis; T0), at the end of active periodontal therapy (APT; T1), at completion of orthodontic tooth movement (OTM; T2), and at the last supportive periodontal care (SPC) visit (T3). Radiographic analysis was performed at T0, T2, and T3. A total of 115 teeth were lost during APT, including 5 molars at T2 (used as orthodontic anchorage) and 10 premolars at T3 (due to root fracture). All anterior migrated teeth were in function at T3 (mean duration: 9.5 years). Significant mean probing pocket depth reduction (1.5 ± 1.1 mm) and attachment level gain (0.9 ± 1.0 mm) were observed after APT, whereas OTM and SPC were associated with furthering small changes. The alveolar bone level at T3 was slightly increased from T0 values. Patient-reported outcome measurements significantly improved in terms of esthetics and masticatory function. OTM should be considered an essential part of the comprehensive treatment plan to change the prognosis of severely compromised teeth in stage IV periodontitis patients.

This retrospective study evaluated the long-term response of periodontal tissues and survival rate of teeth with advanced attachment loss and pathologic migration in 21 periodontitis patients treated with combined periodontal and orthodontic treatment. All anterior migrated teeth were in function at the end of 10 to 15 years of maintenance. Residual probing depths and clinical attachment levels improved after treatment and remained stable through the follow-up. A total of 55 hopeless teeth were lost during active therapy, as well as 6 molars over the course of the supportive periodontal therapy (for nonperiodontal reasons). In highly compliant patients, all migrated teeth with initial unfavorable prognosis showed long-term clinical stability.

Objectives: Hyperbaric oxygen therapy (HBOT) has been used as treatment for different clinical conditions, including fibromyalgia (FM). HBOT modulates brain activity, ameliorates chronic pain and modifies the ratio of immune cells. Clinical studies have provided evidence that FM is associated with immune system dysregulation. In the present study we aimed to evaluate the effect of HBOT on immune system and on the quality of life-style of FM patients., Methods: Patients with primary FM and controls were treated with HBOT. Physical, emotional and social assessment, quality of sleep, tender points, intensity score, WPI and symptom severity were evaluated before and after HBOT. Furthermore, a characterisation of CD4 T lymphocytes and their cytokine production was performed by flow cytometry. The expression of TNF-α, IFN-γ, IL-17, IL-9 and IL-22 was also assessed by RT-PCR. Finally, the serum levels of serotonin were evaluated by ELISA., Results: Our results confirm the participation of immune system in the pathogenesis of FM and highlight the impact of HBOT treatment, with particular regard to the changes on proinflammatory cytokines production by CD4 T cells subsets., Conclusions: FM patients show a Th1 signature and the activation of this subset is modulated by HBOT.

Dysbaric accidents are usually referred to compressed air-supplied diving. Nonetheless, some cases of decompression illness are known to have occurred among breath-hold (BH) divers also, and they are reported in the medical literature. A male BH diver (57 years old), underwater fishing champion, presented neurological disorders as dizziness, sensory numbness, blurred vision, and left frontoparietal pain after many dives to a 30-35 meters sea water depth with short surface intervals. Symptoms spontaneously regressed and the patient came back home. The following morning, pain and neurological impairment occurred again and the diver went by himself to the hospital where he had a generalized tonic-clonic seizure and lost consciousness. A magnetic resonance imaging of the brain disclofsed a cortical T1-weighted hypointense area in the temporal region corresponding to infarction with partial hemorrhage. An early hyperbaric oxygen therapy led to prompt resolution of neurological findings. All clinical and imaging characteristics were referable to the Taravana diving syndrome, induced by repetitive prolonged deep BH dives. The reappearance of neurological signs after an uncommon 21-hour symptom-free interval may suggest an atypical case of Taravana syndrome.

Cellular activity of the myosin light chain phosphatase (MLCP) determines agonist-induced force development of smooth muscle (SM). CPI-17 is an endogenous inhibitor protein for MLCP, responsible for mediating G-protein signaling into SM contraction. Fluctuations in CPI-17 expression occur in response to pathological stresses, altering excitation-contraction coupling in SM. Here, we determined the signaling pathways regulating CPI-17 expression in rat aorta tissues and the cell culture using a pharmacological approach. CPI-17 transcription was suppressed in response to the proliferative stimulus with platelet-derived growth factor (PDGF) through the ERK1/2 pathway, whereas it was elevated in response to inflammatory, stress-induced and excitatory stimuli with transforming growth factor-β, IL-1β, TNFα, sorbitol, and serotonin. CPI-17 transcription was repressed by inhibition of JNK, p38, PKC, and Rho-kinase (ROCK). The mouse and human CPI-17 gene promoters were governed by the proximal GC-boxes at the 5'-flanking region, where Sp1/Sp3 transcription factors bound. Sp1 binding to the region was more prominent in intact aorta tissues, compared with the SM cell culture, where the CPI-17 gene is repressed. The 173-bp proximal promoter activity was negatively and positively regulated through PDGF-induced ERK1/2 and sorbitol-induced p38/JNK pathways, respectively. By contrast, PKC and ROCK inhibitors failed to repress the 173-bp promoter activity, suggesting distal enhancer elements. CPI-17 transcription was insensitive to knockdown of myocardin/Kruppel-like factor 4 small interfering RNA or histone deacetylase inhibition. The reciprocal regulation of Sp1/Sp3-driven CPI-17 expression through multiple kinases may be responsible for the adaptation of MLCP signal and SM tone to environmental changes.

We previously reported that substantial amounts of IL-10, an immunomodulatory cytokine, are produced by cell suspensions of fresh human metastatic melanoma tissues. Production diminished with continuous culturing of cells, which suggests a pivotal interactive role between melanoma cells and the tumor microenvironment. In this study, we found that the culture media obtained from LPS-stimulated peripheral blood mononuclear cells induced IL-10 production by metastatic melanoma cells. Of the multiple cytokines present in the conditioned culture media, IL-6 was identified as the inducer of IL-10 production. A neutralizing antibody against IL-6 completely blocked the conditioned medium-induced IL-10 production. Metastatic melanoma cells that constitutively produce low amount of IL-10 increased IL-10 production in response to recombinant human IL-6 in a dose-dependent fashion. The response to exogenously added IL-6 was less significant in melanoma cells that produced high amounts of IL-6, probably due to pre-existing autocrine stimulation of IL-10 by endogenous IL-6. On the other hand, metastatic melanoma cells that do not constitutively produce IL-10 protein did not respond to exogenous IL-6. In IL-6-responsive melanoma cells, IL-6 increased STAT3 phosphorylation and inhibition of STAT3 signaling using siRNA or inhibitors for JAKs diminished IL-6-induced IL-10 production. In addition, inhibition of MEK and PI3K, but not mTOR, interfered with IL-10 production. Taken together, the data suggest that blocking of these signals leading to IL-10 production is a potential strategy to enhance an anti-melanoma immune response in metastatic melanoma.

Ca(2+) sensitivity of smooth muscle (SM) contraction is determined by CPI-17, an inhibitor protein for myosin light chain phosphatase (MLCP). CPI-17 is highly expressed in mature SM cells, but the expression level varies under pathological conditions. Here, we determined the expression of CPI-17 in embryonic SM tissues and arterial neointimal lesions using immunohistochemistry. As seen in adult animals, the predominant expression of CPI-17 was detected at SM tissues on mouse embryonic sections, whereas MLCP was ubiquitously expressed. Compared with SM alpha-actin, CPI-17 expression doubled in arterial SM from embryonic day E10 to E14. Like SM alpha-actin and other SM marker proteins, CPI-17 was expressed in embryonic heart, and the expression was down-regulated at E17. In adult rat, CPI-17 expression level was reduced to 30% in the neointima of injured rat aorta, compared with the SM layers, whereas the expression of MLCP was unchanged in both regions. Unlike other SM proteins, CPI-17 was detected at non-SM organs in the mouse embryo, such as embryonic neurons and epithelium. Thus, CPI-17 expression is reversibly controlled in response to the phenotype transition of SM cells that restricts the signal to differentiated SM cells and particular cell types.