Long-term stability of maxillary and mandibular arch dimensions when using rapid palatal expansion and edgewise mechanotherapy in growing patients.

OBJECTIVE: The purpose of this study was to assess the long-term stability of rapid palatal expansion (RPE) followed by full fixed edgewise appliances. METHODS: This study included 67 patients treated using Haas-type RPE and non-extraction edgewise appliance therapy at a single orthodontic practice. Serial dental casts were obtained at three different time points: pretreatment (T1), after expansion and fixed appliance therapy (T2), and at long-term recall (T3). The mean duration of the T1-T2 and T2-T3 periods was 4.8 ± 3.5 years and 11.0 ± 5.4 years, respectively. The dental casts were digitized, and the computed measurements were compared with untreated reference data. RESULTS: The majority of treatment-related increases in the maxillary and mandibular arch measurements were statistically significant (p < 0.05) and greater than expected for the untreated controls. Although many measurements decreased postretention (T2-T3), the net gains persisted for all of the measurements evaluated. CONCLUSIONS: The use of RPE therapy followed by full fixed edgewise appliances is an effective method for increasing maxillary and mandibular arch width dimensions in growing patients.

Association of Increased F4/80high Macrophages With Suppression of Serum-Transfer Arthritis in Mice With Reduced FLIP in Myeloid Cells.

OBJECTIVE: Macrophages are critical in the pathogenesis of rheumatoid arthritis (RA). We recently demonstrated that FLIP is necessary for the differentiation and/or survival of macrophages. We also showed that FLIP is highly expressed in RA synovial macrophages. This study was undertaken to determine if a reduction in FLIP in mouse macrophages reduces synovial tissue macrophages and ameliorates serum-transfer arthritis. METHODS: Mice with Flip deleted in myeloid cells (Flipf/f LysMc/+ mice) and littermate controls were used. Arthritis was induced by intraperitoneal injection of K/BxN serum. Disease severity was evaluated by clinical score and change in ankle thickness, and joints were examined by histology and immunohistochemistry. Cells were isolated from the ankles and bone marrow of the mice and examined by flow cytometry, real-time quantitative reverse transcriptase-polymerase chain reaction, or Western blotting. RESULTS: In contrast to expectations, Flipf/f LysMc/+ mice developed more severe arthritis early in the clinical course, but peak arthritis was attenuated and the resolution phase more complete than in control mice. Prior to the induction of serum-transfer arthritis, the number of tissue-resident macrophages was reduced. On day 9 after arthritis induction, the number of F4/80high macrophages in the joints of the Flipf/f LysMc/+ mice was not decreased, but increased. FLIP was reduced in the F4/80high macrophages in the ankles of the Flipf/f LysMc/+ mice, while F4/80high macrophages expressed an antiinflammatory phenotype in both the Flipf/f LysMc/+ and control mice. CONCLUSION: Our observations suggest that reducing FLIP in macrophages by increasing the number of antiinflammatory macrophages may be an effective therapeutic approach to suppress inflammation, depending on the disease stage.