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Purpose: Mast cells play an important role in innate and acquired immunity and are thought to be the cellular origin of most proteases and cytokines. Substance P (SP) and its receptor, NK-1R, play critical roles in immune regulation in human and animal models of inflammation. Methods: We used mature human cord blood mast cells (HCBMC) differentiated from cord blood CD34+ precursor activated with SP in culture. Results: Our data indicate that Substance P strongly activates mature HCBMC in releasing CXCL8 expression and secretion (Control: 1.200 ± 1.0; SP: 4.10 ± 0.90; P < 0.01). Moreover, in a RT-PCR, HCBMC expressed CXCL8 mRNA after Substance P activation. Since calcium ionophore A23187 is a pharmacological activator that raises cytosolic free calcium ion concentraion and stimulates mast cells in the production and secretion of proinflammatory compounds, it was used as positive control. In addition, we found that HCBMCs generate the transcription of histidine decarboxylase (HDC), the enzyme responsible for the generation of histamine from histidine, after SP treatment. Since CXCL8 is a member of the CXC chemokine subfamily with potent chemotactic activity and is a primary inflammatory cytokine we conclude that our results, obtained from HCBMC cultures, a good and valid model in vitro, support the concept that the neurogenic system modulates inflammatory events by Substance P-mediated HCBMC chemokine CXCL8 release. Conclusion: The expression, synthesis and release of CXCL8 suggest an increase of inflammatory process in vivo mediated by the recruitment and infiltration of inflammatory cells in inflamed tissues.

The main therapeutic approaches for inflammatory periodontal diseases include the mechanical treatment of root surfaces. Multi-center clinical trials have demonstrated that the adjunctive use of a chlorhexidine (CHX) chip is effective in improving clinical results compared to scaling and root planing (SRP) alone. However, some recent studies failed to confirm these clinical results, nor have any data been reported regarding the capability of the CHX chip in affecting the activity of alkaline phosphatase (ALP) in the gingival crevicular fluid (GCF). This enzyme has been related to a condition of destructive activity of periodontitis. The aim of this study is to provide further data on the clinical and biochemical effects of CHX chips when used as an adjunct to SRP. Eighty-two systemically healthy patients, aged 31-63, with moderate and advanced periodontitis were recruited from the departments of Periodontology of the University of Chieti. In each patient 2 experimental sites, located in two symmetric quadrants, were chosen with a probing depth ofor = 5 mm and bleeding on probing. The 2 sites were selected randomly at the split-mouth level; control sites received SRP alone, and test sites SRP plus 1 CHX chip. Clinical indices, including probing depth (PPD), clinical attachment level (CAL), bleeding on probing (BOP), and the ALP activity in GCF were evaluated at baseline and after 6 months. Alkaline phosphatase activity was assayed spectrophotometrically. The PPD and CAL were significantly lower at 6 months as compared to the baseline scores in both treatments (p less than 0.01). The PPD reduction was 2.7 mm in the CHX+SRP group and 1.9 mm in the SRP alone group. The CHX+SRP group showed a significantly greater gain of clinical attachment (mean: 1.4 mm) in comparison with the SRP group (mean: 0.9; p less than 0.05). No differences were observed in the decrease of the percent of BOP-positive sites between the experimental groups. Conversely, the CHX+SRP group underwent a significantly greater decrease (p less than 0.01) of the GCF-ALP activity 6 months after treatment in comparison with the SRP alone group. The adjunctive use of the CHX chip resulted in a significant improvement of pocket reduction and clinical attachment gain as compared with SRP alone. These results were concomitant with a significantly greater reduction of the GCF-ALP activity levels.

Osteochondroma is one of the most common benign tumors of the axial skeleton. Location of a solitary exostosis in the scapula is relatively rare. We report the case of an osteochondroma of the scapula in a 13-year-old boy. Because of the atypical location with nonspecific shoulder pain, the diagnosis is often made late. CT is necessary to determine the correct position of the osteochondroma. Despite the young age of the patient, surgical excision of the exostosis was performed, because of an arising thoracic pressure pain. The outcome was good, the patient noticed disappearance of previous painful symptoms, and a normal profile of the scapula was gained.

Background: Viscosupplementation (VS) with hyaluronic acid (HA) is largely used for knee osteoarthritis therapy, but the evidences for its usefulness in hip osteoarthritis (OA) are limited. Methods: In this review, an extensive search of published trials on VS in hip OA was performed. From the selected papers the following data were extracted: sample size, inclusion / exclusion criteria, treatment procedures, evaluation methods, follow-up duration and clinical outcomes. Results: The level of evidence was low in quite all the trials (no placebo controlled groups). A reduction of pain and an improvement of function after 3 months, persistent in the long term (12 - 18 months), was observed. Patients with mild morphological alterations responded better to therapy. Side effects were negligible, and were limited to pain and a sensation of heaviness in the injection site. No clear differences among Low (LMW) and High Molecular Weight (HMW) HA preparations were found in the clinical outcomes. However, for HMW-HA preparations, a lower number of injections was, in general, necessary in order to reach the therapeutic effect. Conclusions: Despite the initial promising results, some questions still remain open : 1) the characteristics of responders must be more precisely defined; 2) the treatment schedules, at present mainly based on the individual clinical experience, need a proper and accepted standardization. Finally, larger and placebo controlled trials are necessary to confirm the efficacy of VS in hip OA.

The intrinsic pathogenetic mechanisms of tendinopathies are largely unknown and whether inflammation or degeneration has the prominent role is still a matter of debate. Assuming that there is a continuum from physiology to pathology, overuse may be considered as the initial disease factor; in this context, microruptures of tendon fibers occur and several molecules are expressed, some of which promote the healing process, while others, including inflammatory cytokines, act as disease mediators. Neural in-growth that accompanies the neovessels explains the occurrence of pain and triggers neurogenic-mediated inflammation. It is conceivable that inflammation and degeneration are not mutually exclusive, but work together in the pathogenesis of tendinopathies.

Prostaglandin D2 PGD2 is a major cyclooxygenase metabolite of arachidonic acid produced by mast cells and it is released following allergen challenge in diseases, such as allergic diseases. PGD2 may act as a neuromodulator and as an allergic and inflammatory mediator. In allergic diseases, activated mast cell synthesizes prostaglandin D2 (first cyclo-oxygenate mediator) which has bronchoconstrictive and vasodilating effects and attracts several leukocytes. It has been found that activated mast cells, challenged with physiological and non- physiological secretagogues, release elevated histamine and tryptase and chymase, leukotrienes B4, C4 and D4, 5-hydroxyeicosatetraenoic acid, PGD2, Platelet Activating Factor (PAF), heparin, and high-molecular-weight neutrophil chemotactic factor and cytokines/chemokines. PGD2 exerts its biological activity through the DP and CRTH2 receptors and their cDNA cloning which were characterized 15 years ago. In this report, we revisited the biological effects of arachidonic acid compounds released by activated mast cells in allergic and inflammatory states.

Carpometacarpal osteoarthritis (CMC-OA) is a disabling condition, characterized by pain and functional impairment. The aim of the present study is to evaluate the efficacy of a single ultrasound-guided injection of hyaluronic acid (HA) in patients suffering from CMC-OA. Eighteen patients with CMC-OA, grade 2–3 Kellgren and Lawrence score, attending the Orthopaedic Department of the University Hospital of Chieti, were enrolled. They underwent clinical evaluation at baseline and after one month follow-up, evaluating: grading of pain (VAS at rest and during activities), function (Dreiser Index), grip and pinch strengths (Jamar dynamometer), as well as NSAIDs consumption. Each patient received a single ultrasound- guided injection of HA into the articular CMC joint. The results were that pain at rest and during activities decreased from 1.8 ± 1.07 to 0.5 ± 0.68 (p < 0.001) and from 8.05 ± 0.94 to 4.15 ± 1.42 (p < 0.001), respectively. Dreiser Functional Index showed a significant improvement (+11.59 %; p < 0.004), as well as pulp pinch strength (24.07 %; p < 0.001). The consumption of NSAIDs was also clearly reduced, from 16 to 7 patients (-45%) and from 2.45 ± 1.98 to 1.15 ± 1.30 tablets per week (p < 0.02). Mild local side effects, lasting less than 3 hours, were observed only in 2 cases. A single ultrasound guided injection of HA is a safe and effective procedure in CMC-OA, with a significant improvement in terms of pain and function. However, studies with larger samples and longer term follow-up are warranted.

To verify the potential involvement of the age-dependent modifications of EC-SOD activity in the impairment of plasma NO availability with advancing age, 40 healthy men divided into 4 age groups for the purpose of comparison (young: 27.4 +/- 1.5 years; middle: 50.8 +/- 2.2, years; old: 70.0 +/- 1.8 years; very old: 86.1 +/- 1.1 years) were enrolled in this study. Plasma samples were used for measurements of the stable end-product nitrite/nitrate (NOx), as an expression of NO availability, EC-SOD activity, thiobarbituric acid reactive substances (TBARS) as a marker of lipid peroxidation, low density lipoprotein (LDL) copper-mediated oxidation in vitro and total antioxidant capacity (TEAC). Our results indicated a significant age-related progressive decrease of plasma NOx content and EC-SOD activity and their values were positively correlated (r = 0.713, p < 0.001). Increased TBARS amount together with reduced lag time for in vitro oxidation of LDL and decreased content of TEAC were observed with advancing age. Finally, EC-SOD values were negatively correlated with plasma TBARS values (r = -0.855, p < 0.001). Findings of the present study suggest that the decrease of antioxidant defence strategies play a primary role by compromising NO availability in normally aged individuals, particularly through a progressive decrease of EC-SOD activity.