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1.  Effects on the maxilla and cranial base caused by cervical headgear: A longitudinal study 
Objectives: The aim of this study is to test the possible orthopedic effects of cervical headgear on the cranial base and maxilla. Study design: a sample consisting of 79 subjects with skeletal class II malocclusion was divided into two groups. The experimental group was made up of 41 patients all treated with cervical headgear. The control group included a total of 38 non-treated patients. Each one of these groups was then subdivided according to age into one of three groups: prepubescent, pubescent or post-pubescent. Cephalometric parameters were compared in both groups in order to measure the cranial base angle and the vertical and sagittal position of the maxilla. Additionally, cephalometric superimpositions taken at the beginning and end of the study were compared. Results: results revealed significant differences in the cranial base angle and in the SNA angle (p<0.05). However, no differences were observed in the variables that measure the maxillomandibular relationship. While no changes were noted in the palatal plane slope, a flattening of the cranial base was found caused by the cervical headgear, in addition to a retrusion of point A that does not mean there was a reduction in the maxillomandibular relationship. Conclusions: cervical headgear treatment induces cephalometric flattening of the cranial base and a decrease of the SNA angle.
Key words:Orthodontics, cervical headgear, class II treatment, cephalometry, superimposition.
doi:10.4317/medoral.17698
PMCID: PMC3482532  PMID: 22322499
2.  Study of mandibular growth in patients treated with Fränkel´s functional regulator (1b) 
Objectives: The purpose of this study was to assess mandibular growth in patients with Class II division 1 malocclusions when treated with Fränkel´s functional regulator 1b. Study Design: The treatment group was made up of 43 patients that were divided into two groups: prepubescent (n:28), and pubescent (n:15). The control group included 40 patients who did not receive any kind of treatment and were likewise divided into a prepubescent group (n:19), and a pubescent group (n:21). A computerized cephalometric study was carried out and superimpositions were done in order to assess the antero-posterior, vertical and rotational movements of the mandible. A two-way ANOVA with interaction was done to compare the changes between the control group and the treatment group, while the Student t for independent samples was used to compare each age group. Results: The Gnathion and Gonion points showed significant differences in the whole sample (p<0.001) as well as in the prepubescent (p<0.001) and pubescent groups (p<0.05). Rotational changes of the mandible measured using the facial axis and mandibular plane showed no statistical differences between both groups (p>0.05). Conclusion: The results show that the FR produces vertical orthopedic growth in the mandible but not horizontal growth compared to non-treated Class II-type I malocclusion patients. No rotational changes were found in the mandible, but we did record mandibular growth along the inclination of the facial axis.
Key words:Fränkel appliance, orthodontics, functional appliances, mandibular growth.
doi:10.4317/medoral.17958
PMCID: PMC3482538  PMID: 22549680
3.  Cranial base and maxillary changes in patients treated with Frankel’s functional regulator (1b) 
Objectives: The purpose of this study was to assess cranial base and maxillary growth in patients with Class II-type I malocclusions when treated with Frankel’s functional regulator (FR-1b). Study Design: The treatment group was made up of 43 patients that were divided into two groups: prepubescent (n: 28), and pubescent (n: 15). The control group included 40 patients who did not receive any kind of treatment and were likewise divided into a prepubescent group (n: 19), and a pubescent group (n: 21). A computerized cephalometric study was carried out and superimpositions were done in order to assess the antero-posterior, vertical and rotational movement of the maxilla. Results: The results indicate that anterior cranial length is not affected by the regulator but the cranial deflection of the treatment group was diminished. Although a slight counterclockwise rotation effect on the upper jaw was observed due to treatment, no growth restriction of the maxilla in a vertical or antero-posterior direction was observed compared to other non-treated Class II-type I malocclusion patients. Conclusion: The functional regulator does not have any effect on anterior cranial length, but it does affect the angulation of the cranial base. According to our results, the appliance has demonstrated a flattening effect of the cranial base (p<0.05) in the treated sample. The functional regulator induces counterclockwise rotation rather than vertical or sagittal changes in the maxilla.
Key words:Orthodontics, frankel regulator, class II treatment, cephalometry, superimposition.
doi:10.4317/medoral.17631
PMCID: PMC3476035  PMID: 22322486
4.  Matrix metalloproteinase-8 deficiency increases joint inflammation and bone erosion in the K/BxN serum-transfer arthritis model 
Arthritis Research & Therapy  2010;12(6):R224.
Introduction
Rheumatoid arthritis is an autoimmune disease in which joint inflammation leads to progressive cartilage and bone erosion. Matrix metalloproteinases (MMPs) implicated in homeostasis of the extracellular matrix play a central role in cartilage degradation. However, the role of specific MMPs in arthritis pathogenesis is largely unknown. The aim of the present study was to investigate the role of Mmp-8 (collagenase-2) in an arthritis model.
Methods
Arthritis was induced in Mmp8-deficient and wildtype mice by K/BxN serum transfer. Arthritis severity was measured by a clinical index and ankle sections were scored for synovial inflammation, cartilage damage and bone erosion. cDNA microarray analysis, real-time PCR and western blot were performed to identify differential changes in gene expression between mice lacking Mmp8 and controls.
Results
Mmp8 deficiency increased the severity of arthritis, although the incidence of disease was similar in control and deficient mice. Increased clinical score was associated with exacerbated synovial inflammation and bone erosion. We also found that the absence of Mmp8 led to increased expression of IL-1β, pentraxin-3 (PTX3) and prokineticin receptor 2 (PROKR2) in arthritic mice joints.
Conclusions
Lack of Mmp-8 is accompanied by exacerbated synovial inflammation and bone erosion in the K/BxN serum-transfer arthritis model, indicating that this Mmp has a protective role in arthritis.
doi:10.1186/ar3211
PMCID: PMC3046537  PMID: 21190566
6.  Akt activity protects rheumatoid synovial fibroblasts from Fas-induced apoptosis by inhibition of Bid cleavage 
Introduction
Synovial hyperplasia is a main feature of rheumatoid arthritis pathology that leads to cartilage and bone damage in the inflamed joints. Impaired apoptosis of resident synoviocytes is pivotal in this process. Apoptosis resistance seems to involve defects in the extrinsic and intrinsic apoptotic pathways. The aim of this study was to investigate the association of PI3Kinase/Akt and the mitochondrial apoptotic pathway in the resistance of rheumatoid arthritis (RA) fibroblast like synovial cells (FLS) to Fas-mediated apoptosis.
Methods
Apoptosis was assessed by ELISA quantification of nucleosomal release, Hoechst staining and activated caspase-3/7 measure in cultured RA FLS stimulated with anti-Fas antibody. Two Phosphoinositol-3-kinase/protein Kinase B (PI3 Kinase) inhibitors, Wortmannine and LY294002, were used before anti-Fas stimulation. Proapoptotic BH3 interacting domain death agonist (Bid) was suppressed in RA FLS by small interfering RNA (siRNA) transfection. Bid was overexpressed by transfection with the pDsRed2-Bid vector. Phosphorylated Akt, caspase-9, and Bid expression were analysed by western blot.
Results
PI3 kinase inhibition sensitizes RA FLS to Fas-induced apoptosis by increasing cleavage of Bid protein. Bid suppression completely abrogated Fas-induced apoptosis and Bid overexpression highly increased apoptotic rate of RA FLS in association with cleavage of caspase-9.
Conclusions
In RA FLS, phosphorylation of Akt protects against Fas-induced apoptosis through inhibition of Bid cleavage. The connection between the extrinsic and the intrinsic apoptotic pathways are critical in this Fas- mediated apoptosis and points to PI3Kinase as potential therapeutic target for RA.
doi:10.1186/ar2941
PMCID: PMC2875667  PMID: 20187936
7.  Therapeutic Effect of a Poly(ADP-Ribose) Polymerase-1 Inhibitor on Experimental Arthritis by Downregulating Inflammation and Th1 Response 
PLoS ONE  2007;2(10):e1071.
Poly(ADP-ribose) polymerase-1 (PARP-1) synthesizes and transfers ADP ribose polymers to target proteins, and regulates DNA repair and genomic integrity maintenance. PARP-1 also plays a crucial role in the progression of the inflammatory response, and its inhibition confers protection in several models of inflammatory disorders. Here, we investigate the impact of a selective PARP-1 inhibitor in experimental arthritis. PARP-1 inhibition with 5-aminoisoquinolinone (AIQ) significantly reduces incidence and severity of established collagen-induced arthritis, completely abrogating joint swelling and destruction of cartilage and bone. The therapeutic effect of AIQ is associated with a striking reduction of the two deleterious components of the disease, i.e. the Th1-driven autoimmune and inflammatory responses. AIQ downregulates the production of various inflammatory cytokines and chemokines, decreases the antigen-specific Th1-cell expansion, and induces the production of the anti-inflammatory cytokine IL-10. Our results provide evidence of the contribution of PARP-1 to the progression of arthritis and identify this protein as a potential therapeutic target for the treatment of rheumatoid arthritis.
doi:10.1371/journal.pone.0001071
PMCID: PMC2034533  PMID: 17971849
8.  Partial protection against collagen antibody-induced arthritis in PARP-1 deficient mice 
Poly(ADP-ribose) polymerase-1 (PARP-1) is a nuclear DNA-binding protein that participates in the regulation of DNA repair and maintenance of genomic integrity. In addition, PARP-1 has a role in several models of inflammation disease, where its absence or inactivation confers protection. The aim of this study was to analyze the impact of selective PARP-1 suppression in collagen antibody-induced arthritis. We show that PARP-1 deficiency partially reduces the severity of arthritis, although the incidence of disease was similar in control and deficient mice. Decreased clinical scores were accompanied by partial reduction of histopathological findings. Interestingly, quantitative real-time PCR and ELISA analysis revealed that the absence of PARP-1 down-regulated IL-1β and monocyte chemotactic protein 1 expression in arthritic joints whereas tumor necrosis factor-α transcription was not impaired. Our results provide evidence of the contribution of PARP-1 to the progression of arthritis and identify this protein as a potential therapeutic target for the treatment of rheumatoid arthritis.
doi:10.1186/ar1865
PMCID: PMC1526570  PMID: 16356201

Results 1-8 (8)