A novel treatment modality for myogenous temporomandibular disorders using aromatherapy massage with lavender oil: A randomized controlled clinical trial.

OBJECTIVE: To investigate the effect of aromatherapy massage on pain intensity and maximal mouth opening (MMO) in patients with myogenous TMD. METHODS: Ninety-one patients were randomly assigned to three groups: Group L (aromatherapy massage with lavender oil, test), group P (massage with sweet almond oil, placebo), and group C (control). Participants were evaluated at T0 (before the intervention), T1 (immediately after the intervention), and T2 (2-month follow-up). Data were analyzed using one-way ANOVA, Tukey's HSD, and Kruskal-Wallis tests. RESULTS: For T1 and T2, group L showed the greatest MMO values (48.01 ± 0.85 mm; 45.67 ± 0.84 mm), while group C exhibited the lowest values (39.13 ± 0.49 mm; 39.66 ± 0.82 mm) (p < 0.001). For VAS, group L revealed the lowest pain values at T1 (2) and T2 (2) (p < 0.001). DISCUSSION: Aromatherapy massage with lavender oil was effective in the management of painful TMD conditions and limited mouth opening.

Effect of low-level gallium aluminum arsenide laser therapy on the chewing performance and pain perception of patients with systemic lupus erythematosus: A randomized controlled clinical trial.

OBJECTIVE: To evaluate the effect of low-level laser therapy (LLLT) on pain intensity (PI) and chewing performance (CP) in systemic lupus erythematosus (SLE) patients with myogenic temporomandibular disorder (TMD). METHODS: Ninety-one patients were randomly allocated to three groups: Group L (intervention), Group P (placebo), and Group C (control). Outcomes were PI (assessed with visual analog scale (VAS)) and CP (assessed with the geometric mean diameter (GMD) of crushed test food). Measurements were performed at T0 (before the LLLT), T1 (immediately after the LLLT), and T2 (1-month follow-up). Data were analyzed using Generalized Linear Models, Kruskal-Wallis, and Friedman tests. RESULTS: For T1 and T2, Group L demonstrated the lowest values for both GMD (6283.7 ± 257.2 µm; 6382.7 ± 303.7 µm) and VAS (5;6) (p < 0.001). CONCLUSION: LLLT was an effective therapeutic approach in reducing pain and improving CP for one month in SLE patients with myogenic TMD.

Development of a thermosensitive statin loaded chitosan-based hydrogel promoting bone healing.

Statins have been proposed as potential adjuvant to periodontal treatment due to their pleiotropic properties. A new thermosensitive chitosan hydrogel loaded with statins (atorvastatin and lovastatin) nanoemulsions was synthesized to allow a spatially controlled local administration of active compounds at lesion site. Spontaneous nano-emulsification method was used to synthesize statins loaded nanoemulsions. In vitro, atorvastatin and lovastatin loaded nanoemulsions were cytocompatible and were able to be uptake by oral epithelial cells. Treatment of Porphyromonas gingivalis infected oral epithelial cells and gingival fibroblasts with atorvastatin and lovastatin loaded nanoemulsions decreased significantly pro-inflammatory markers expression (TNF-α and IL-1ß) and pro-osteoclastic RANKL. Nevertheless, such treatment induced the expression of Bone sialoprotein 2 (BSP2) in osteoblast emphasizing the pro-healing properties of atorvastatin and lovastatin nanoemulsions. In vivo, in a calvarial bone defect model (2 mm), treatment with the hydrogel loaded with atorvastatin and lovastatin nanoemulsions induced a significant increase of the neobone formation in comparison with systemic administration of statins. This study demonstrates the potential of this statins loaded hydrogel to improve bone regeneration and to decrease soft tissue inflammation. Its use in the specific context of periodontitis management could be considered in the future with a reduced risk of side effects.

Identification of a Kavain Analog with Efficient Anti-inflammatory Effects.

Kavain, a compound derived from Piper methysticum, has demonstrated anti-inflammatory properties. To optimize its drug properties, identification and development of new kavain-derived compounds was undertaken. A focused library of analogs was synthesized and their effects on Porphyromonas gingivalis (P. gingivalis) elicited inflammation were evaluated in vitro and in vivo. The library contained cyclohexenones (5,5-dimethyl substituted cyclohexenones) substituted with a benzoate derivative at the 3-position of the cyclohexanone. The most promising analog identifed was a methylated derivative of kavain, Kava-205Me (5,5-dimethyl-3-oxocyclohex-1-en-1-yl 4-methylbenzoate.) In an in vitro assay of anti-inflammatory effects, murine macrophages (BMM) and THP-1 cells were infected with P. gingivalis (MOI = 20:1) and a panel of cytokines were measured. Both cell types treated with Kava-205Me (10 to 200 µg/ml) showed significantly and dose-dependently reduced TNF-α secretion induced by P. gingivalis. In BMM, Kava-205Me also reduced secretion of other cytokines involved in the early phase of inflammation, including IL-12, eotaxin, RANTES, IL-10 and interferon-γ (p < 0.05). In vivo, in an acute model of P. gingivalis-induced calvarial destruction, administration of Kava-205Me significantly improved the rate of healing associated with reduced soft tissue inflammation and osteoclast activation. In an infective arthritis murine model induced by injection of collagen-antibody (ArthriomAb) + P. gingivalis, administration of Kava-205Me was able to reduce efficiently paw swelling and joint destruction. These results highlight the strong anti-inflammatory properties of Kava-205Me and strengthen the interest of testing such compounds in the management of P. gingivalis elicited inflammation, especially in the management of periodontitis.

In-situ forming implants loaded with chlorhexidine and ibuprofen for periodontal treatment: Proof of concept study in vivo.

Control of infection and inflammation is crucial for the success of periodontal treatment. In this study, in-situ forming implants (ISFI) loaded with chlorhexidine dihydrochloride (CHX) and ibuprofen (IBU) were developed and tested to optimize periodontal treatment outcomes. Release profiles were promising. Exposure to 1.5% and 5.3% CHX-IBU loaded ISFI's release media decreased significantly the P. gingivalis growth up to 20-fold and 35-fold, respectively, after 48 h (p < 0.05). The metabolic activity assay of gingival epithelial cells (EC) demonstrated 1.5% CHX-IBU-loaded ISFI to be non-toxic, therefore, it was selected for further experimentation. Furthermore, significant down-regulation of TNF-α release (34% at 6 h and 43% at 24 h, p < 0.05) in P. gingivalis lipopolysaccharide (Pg-LPS) stimulated EC exposed to 1.5% CHX-IBU ISFI release medium was demonstrated by ELISA. In vivo, 1.5% CHX-IBU ISFI was injected into the periodontal pocket in an experimental periodontitis mouse model and the reduction in inflammation and improvement in periodontal wound healing was evaluated through inflammatory cell scoring and histomorphometry at 7- and 15-days post-treatment. The results indicate that CHX-IBU loaded ISFI could be efficient as adjuvant to periodontal therapy for the control of infection and inflammation. Moreover, other (e.g., pro-regenerative) drugs could be incorporated into ISFI to further improve periodontal treatment outcomes.

No evidence to support benefit of 14-day courses of amoxicillin-plus-metronidazole as adjunct to non-surgical periodontal treatment at three months.

Data sources Databases including Embase, MEDLINE, The Cochrane Central Register of Controlled Trials and the WHO International Clinical Trial Register Platform were screened by two reviewers. A manual search has been performed in references from included articles and relevant reviews.Study selection Blinded, placebo-controlled, randomised clinical trials (RCTs) with a minimum follow-up of three months were included. Primary outcomes were periodontal pocket depth (PD) and clinical attachment level (CAL) changes after non-surgical periodontal treatment with adjunctive use of amoxicillin/metronidazole vs placebo in periodontitis patients. Secondary outcomes were adverse events and compliance.Data extraction and synthesis Data were extracted and compiled in a spreadsheet. Studies were grouped according to duration (seven days or fourteen days) and dose of amoxicillin/metronidazole regimen (lower dose (mg): 250/200, 375/250, 375/500, 500/250 and higher dose (mg): 500/400, 500/500). Meta-analyses were performed using inverse-variance method. Random-effect models were applied and weighted mean differences were estimated for PD reduction and CAL changes at three months. Risk of bias was assessed using the Cochrane Collaboration tool.Results Eighteen studies were identified and included in the systematic review. Among them, 15 were pooled for meta-analysis. The use of a wide range of antibiotics concentrations (amoxicillin (from 250 to 500 mg) and metronidazole (from 200 to 500 mg)) was reported and the duration of antibiotic administration ranged from three to 14 days. Eleven studies were performed in chronic periodontitis patients and six in aggressive periodontitis patients. No significant differences were found regarding mean PD and mean CAL changes according to the duration or dose of administered antibiotics (Table 1). Risk differences for adverse events in the higher dose and longer duration groups were minimally greater (0.04 and 0.05 respectively).Conclusions Longer courses (14 days) of antibiotics adjuvant to non-surgical therapy do not appear to provide better results in terms of PD reduction or CAL gain at three months. No differences were found between high and low dose groups. In this context, 400/500 mg or 500/500 mg of amoxicillin/metronidazole three times per day should be recommended for seven days.

Reduction of Articular and Systemic Inflammation by Kava-241 in a Porphyromonas gingivalis-Induced Arthritis Murine Model.

Rheumatoid arthritis (RA) is an inflammatory disease that has been linked to several risk factors, including periodontitis. Identification of new anti-inflammatory compounds to treat arthritis is needed. We had previously demonstrated the beneficial effect of Kava-241, a kavain-derived compound, in the management of Porphyromonas gingivalis-induced periodontitis. The present study evaluated systemic and articular effects of Kava-241 in an infective arthritis murine model triggered by P. gingivalis bacterial inoculation and primed with a collagen antibody cocktail (CIA) to induce joint inflammation and tissular destruction. Clinical inflammation score and radiological analyses of the paws were performed continuously, while histological assessment was obtained at sacrifice. Mice exposed to P. gingivalis and a CIA cocktail and treated concomitantly with Kava-241 exhibited a reduced clinical inflammatory score and a decreased number of inflammatory cells and osteoclasts within joint. Kava-241 treatment also decreased significantly tumor necrosis factor alpha (TNF-α) in serum from mice injected with a Toll-like receptor 2 or 4 (TLR-2/4) ligand, P. gingivalis-lipopolysaccharide (LPS). Finally, bone marrow-derived macrophages infected with P. gingivalis and exposed to Kava-241 displayed reduced TLR-2/4, reduced mitogen-activated protein kinase (MAPK)-related signal elements, and reduced LPS-induced TNF-α factor (LITAF), all explaining the observed reduction of TNF-α secretion. Taken together, these results emphasized the novel properties of Kava-241 in the management of inflammatory conditions, especially TNF-α-related diseases such as infective RA.

Kava-241 reduced periodontal destruction in a collagen antibody primed Porphyromonas gingivalis model of periodontitis.

AIM: The aim of this study was to evaluate the effect of Kava-241, an optimized Piper methysticum Kava compound, on periodontal destruction in a collagen antibody primed oral gavage model of periodontitis. METHODS: Experimental periodontitis was induced by oral gavage of Porphyromonas gingivalis (P. gingivalis) + type II collagen antibody (AB) in mice during 15 days. Mice were treated with Kava-241 concomitantly or prior to P. gingivalis gavage and compared to untreated mice. Comprehensive histomorphometric analyses were performed. RESULTS: Oral gavage with P. gingivalis induced mild epithelial down-growth and alveolar bone loss, while oral gavage with additional AB priming had greater tissular destruction in comparison with gavage alone (p < .05). Kava-241 treatment significantly (p < .05) reduced epithelial down-growth (72%) and alveolar bone loss (36%) in P. gingivalis+AB group. This Kava-241 effect was associated to a reduction in inflammatory cell counts within soft tissues and an increase in fibroblasts (p < .05). CONCLUSION: Priming with type II collagen antibody with oral gavage is a fast and reproducible model of periodontal destruction adequate for the evaluation of novel therapeutics. The effect of Kava-241 shows promise in the prevention and treatment of inflammation and alveolar bone loss associated with periodontitis. Further experiments are required to determine molecular pathways targeted by this therapeutic agent.