Short‐Term Effects of 2% Atorvastatin Dentifrice as an Adjunct to Periodontal Therapy: A Randomized Double‐Masked Clinical Trial

Background: The pleiotropic effects of statins, such as immunomodulation and anti‐inflammatory effects, may also improve periodontal conditions. The aim of the present study is to assess the effectiveness of a dentifrice medicated with 2% atorvastatin in improving clinical periodontal parameters as a complement to non‐surgical periodontal treatment (NSPT). Methods: A randomized, double‐masked clinical trial was performed with two parallel groups: 1) atorvastatin group (NSPT plus medicated 2% atorvastatin dentifrice) and 2) placebo group (NSPT plus placebo dentifrice). The effectiveness of these treatments was assessed using periodontal measurements obtained at baseline and 1 month later. The measurements were probing depth (PD), clinical attachment level (CAL), bleeding on probing (BOP), gingival index (GI), and periodontal inflamed surface area (PISA). Multiple linear regression models were used to compare outcome variables after adjusting for sex, diabetes, and tobacco use. Results: A total of 36 individuals participated in this study (atorvastatin group, n = 18; placebo group, n = 18). Both groups showed improvements in periodontal parameters. The atorvastatin group showed a decrease of 297.63 mm² in PISA (95% confidence interval = 76.04 to 519.23; P = 0.01), which was significantly greater than the reduction observed in the placebo group. There was also a significantly greater reduction in mean PD, percentage of sites with PD ≥5 mm, mean CAL, percentage of sites with CAL ≥5 mm, BOP, and GI in the atorvastatin group compared with the placebo group. Conclusion: NSPT plus 2% atorvastatin medicated dentifrice was more effective in improving clinical periodontal parameters than NSPT plus a placebo dentifrice.     

Growth hormone treatment for sustained pain reduction and improvement in quality of life in severe fibromyalgia

Functional defects in growth hormone (GH) secretion and its efficacy as a complementary treatment have been suggested for fibromyalgia. This study investigated the efficacy and safety of low-dose GH as an add-on therapy in patients with both severe FM and low insulin-like growth factor 1 levels. A total of 120 patients were enrolled in a multicenter, placebo-controlled study for 18 months. They were randomly assigned to receive either 0.006 mg/kg/day of GH subcutaneously (group A, n=60) or placebo (group B, n=60) for 6 months (blind phase). The placebo arm was switched to GH treatment from month 6 to month 12 (open phase), and a follow-up period after GH discontinuation was performed until month 18. Standard treatment for fibromyalgia (selective serotonin re-uptake inhibitors, opioids, and amitriptyline) was maintained throughout the study. Number and intensity of tender points, Fibromyalgia Impact Questionnaire (FIQ) with its subscales, and EuroQol 5 dimensions test (EQ5D) with visual analogue scale (VAS) were assessed at different time points. At the end of the study, 53% of group A patients obtained fewer than 11 positive tender points, vs 33% of group B patients (P<.05). 39.1% vs 22.4% reached more than 50% improvement in VAS (P<.05). Group A patients showed significantly improved FIQ scores (P=.01) compared with group B. Although GH discontinuation worsened all scores in both groups during follow-up, impairment in pain perception was less pronounced in the GH-treated group (P=.05). In this largest and longest placebo-controlled trial performed in FM (NCT00933686), addition of GH to the standard treatment is effective in reducing pain, showing sustained action over time.     

Effect of Topically Applied Cyclooxygenase-2-Selective Inhibitors on Arachidonic Acid- and Tetradecanoylphorbol Acetate-Induced Dermal Inflammation in the Mouse

The topical effects of cyclooxygenase-2 (COX-2)-selective inhibitors, flosulide (CGP 28238), L-745,337 and SC-57,666 were examined in AA- and TPA-induced ear dermal inflammation in the mouse. The doses that caused 50% inhibition in AA edema (ED₅₀) were 2.4, 0.45 and 0.35 mg/ear for flosulide, L-745,337 and SC-57,666, respectively. The respective ED_50s in TPA-edema were 1, 0.45 and 0.14. Indomethacin and zileuton showed higher activity than the COX-2-selective inhibitors in both models. Flosulide and L-745,337 inhibited the AA-induced increase in 6-keto-PGF₁, while SC-57,666 was inactive. 80% inhibition was seen with indomethacin while zileuton had no effect. COX-2 selective inhibitors and indomethacin had no effect on LTB₄ levels, while zileuton produced a 50% inhibition. The TPA-induced increase in 6-keto-PGF₁ was greatly inhibited by all COX-2 inhibitors while LTB₄was potentiated by both flosulide and L-745,337. Indomethacin inhibited 6-keto-PGF₁ and zileuton reduced 6-keto-PGF and strongly reduced LTB₄. The neutrophil influx induced by AA was lower than that of TPA. Myeloperoxidase (MPO) levels were lowered by flosulide and L-745,337 but not by SC-57,666. TPA-induced MPO increase was decreased by all COX-2 inhibitors. Indomethacin and zileuton had similar effect on AA and TPA-induced increase in MPO. The results indicate that COX-2-selective inhibitors showed lower topical anti-inflammatory activity than indomethacin or zileuton.     

Evaluation of the effect of probiotics in the treatment of peri-implant mucositis: a triple-blind randomized clinical trial

Objectives

To determine if the treatment of mucositis with mechanical debridement, 0.12% chlorhexidine, and a further application of Lactobacillus reuteri (L. reuteri) will result in an improvement of the clinical and microbiological parameters in comparison to the treatment with mechanical debridement and 0.12% chlorhexidine alone.

Material and methods

Fifty dental implants with mucositis in 50 patients were randomly assigned to one of the following groups: mechanical debridement, 0.12% chlorhexidine mouthwash, and the subsequent administration of a probiotic agent (test group) or mechanical debridement and 0.12% chlorhexidine mouthwash (control group). Data were analyzed to determine clinical and microbiological changes during treatment and after a follow-up period of 3 months.

Results

After the administration of 0.12% chlorhexidine, all clinical parameters improved in the test and the control group, observing a significant decrease in Full Mouth Plaque Index (FMPI), full mouth bleeding on probing (FMBOP), Plaque Index (PI), and bleeding on probing (BOP) at the implant. However, following the administration of probiotics or placebo, the clinical variables, except for probing pocket depth, slightly and progressively increased up to 3 months of follow-up, but without reaching baseline levels. From a microbiological point of view, no major alterations of the subgingival microflora were recorded at different time points between groups during the study.

Conclusions

Treatment with mechanical debridement, oral hygiene reinforcement, and administration of 0.12% chlorhexidine was effective in reducing mucositis, but it did not always result in complete resolution of inflammation. The administration of probiotics did not seem to provide an additional clinical or microbiological benefit.

Clinical relevance

The use of probiotics does not seem to provide an additional benefit in the treatment of peri-implant mucositis.

     

0.2% Chlorhexidine Mouthwash With an Antidiscoloration System Versus 0.2% Chlorhexidine Mouthwash: A Prospective Clinical Comparative Study

Background: The goal of this study is to evaluate the degree of staining and clinical efficacy of a chlorhexidine mouthwash with an antidiscoloration system (ADS) versus 0.2% chlorhexidine mouthwash (traditional). Secondary objectives are to evaluate the patient “compliance” factor according to patterns assigned by the clinician and to observe the side effects of the two mouthwashes. Methods: This comparative study is carried out on a sample of 15 non‐smoking patients with chronic periodontitis at the Department of Periodontology, the International University of Catalunya, Barcelona, Spain. All patients used either 0.2% chlorhexidine mouthwash (control group = bottle B) or chlorhexidine with ADS (test group = bottle A) for 15 days. Each patient first rinsed with a randomly assigned mouthwash for 15 days followed by a 15‐day washout period. Subsequently, each patient used a second mouthwash. Before each cycle, a full dental prophylaxis was performed. The plaque, gingival, and Brecx staining indexes were used. Results: The results showed less tooth staining with the test group (P <0.01). No statistically significant differences were observed in plaque (P = 0.1496) and gingival indexes (P = 0.1688). Eighty‐eight percent of patients followed the instructions outlined in the protocol. In terms of other adverse effects, two patients reported a bad taste with both mouthwashes. Conclusions: The test group with ADS had less staining than the control group during a usage period of 15 days. However, the two mouthwashes seemed to be equally effective as antiplaque and antigingivitis agents.     

Effect of Topically Applied Cyclosporin A on Arachidonic Acid (AA)- and Tetradecanoylphorbol Acetate (TPA)-Induced Dermal Inflammation in Mouse Ear

Topical cyclosporin A (CsA) was compared with dexamethasone, indomethacin and phenidone in edema, increases in vascular permeability, eicosanoids and cell-influx induced by arachidonic acid (AA) and tetradecanoylphorbol acetate (TPA) in mouse ears. CsA ED₅₀ on AA-edema (7.7 g/ear) was similar to dexamethasone and lower than indomethacin and phenidone. CsA ED₅₀ in TPA edema (21 g/ear) was higher than dexamethasone and lower than indomethacin or phenidone. All drugs equally reduce the AA-induced increase in vascular permeability, but CsA and dexamethasone had more activity on TPA. AA-increase in 6-keto-PGF₁ was reduced by dexamethasone, indomethacin and phenidone but not by CsA; only phenidone reduced LTB₄. TPA-increase in 6-keto-PGF₁ was reduced by CsA and indomethacin while CsA, dexamethasone and phenidone decreased LTB₄. CsA, indomethacin and phenidone, but not dexamethasone, suppressed AA-neutrophil influx. In TPA-ears all drugs produced similar reduction in neutrophil influx. CsA was shown to be a good topical anti-inflammatory drug.     

The contribution of sensory system functional connectivity reduction to clinical pain in fibromyalgia

Fibromyalgia typically presents with spontaneous body pain with no apparent cause and is considered pathophysiologically to be a functional disorder of somatosensory processing. We have investigated potential associations between the degree of self-reported clinical pain and resting-state brain functional connectivity at different levels of putative somatosensory integration. Resting-state functional magnetic resonance imaging was obtained in 40 women with fibromyalgia and 36 control subjects. A combination of functional connectivity-based measurements were used to assess (1) the basic pain signal modulation system at the level of the periaqueductal gray (PAG); (2) the sensory cortex with an emphasis on the parietal operculum/secondary somatosensory cortex (SII); and (3) the connectivity of these regions with the self-referential “default mode” network. Compared with control subjects, a reduction of functional connectivity was identified across the 3 levels of neural processing, each showing a significant and complementary correlation with the degree of clinical pain. Specifically, self-reported pain in fibromyalgia patients correlated with (1) reduced connectivity between PAG and anterior insula; (2) reduced connectivity between SII and primary somatosensory, visual, and auditory cortices; and (3) increased connectivity between SII and the default mode network. The results confirm previous research demonstrating abnormal functional connectivity in fibromyalgia and show that alterations at different levels of sensory processing may contribute to account for clinical pain. Importantly, reduced functional connectivity extended beyond the somatosensory domain and implicated visual and auditory sensory modalities. Overall, this study suggests that a general weakening of sensory integration underlies clinical pain in fibromyalgia.