Mild elevation of C-reactive protein in a young patient with severe periodontitis: a case report with 2 years of follow-up.

Periodontal inflammation is associated with systemic disease. Low-grade inflammation (LGI) is critical to the link between periodontal disease and several systemic disorders. C-reactive protein (CRP) is a common circulating biomarker for acute-phase immune responses, and it is closely related to LGI. The present case demonstrated excellent results using a comprehensive approach for periodontitis in a young woman with severe periodontitis and mild CRP elevation. A 21-year-old Japanese woman complained of tooth mobility and bleeding during tooth brushing. She was pre-obese (body mass index = 29.9), and she had a mildly elevated CRP level (5.2 mg/L). Of all periodontal sites, 34.5% had deep pockets (≥6 mm). The patient was diagnosed with stage III, grade C periodontitis and generalized aggressive periodontitis. Comprehensive periodontal treatments, including regenerative procedures for vertical bone loss and furcation involvement, were performed. Periodontal tissue inflammation was resolved, and periodontal regeneration was achieved. During the 2-year follow-up period, her teeth did not exhibit any signs of instability, attachment loss, or bone loss. Despite the weak nature of the evidence, this case suggests that CRP is valuable for assessing LGI, and it may potentially be considered during periodontal grading in the future.

Lactoferrin suppress the adipogenic differentiation of MC3T3-G2/PA6 cells.

Lactoferrin accelerates the differentiation of osteogenic and chondrogenic lineage cells, whereas it inhibits the myogenic and adipogenic differentiation of pluripotent mesenchymal cells; however, the effect of lactoferrin on the differentiation of preadipocytes is unknown. In this study, we examined the effect of lactoferrin on adipogenic differentiation using a mouse preadipocyte cell line, MC3T3-G2/PA6. The cells were cultured in differentiation medium with or without lactoferrin to induce cellular differentiation. The cell lineage was then determined by Oil Red O staining, real-time PCR screening for the mRNA expression of phenotype-specific markers, and Western blot analysis. The number of Oil Red O-positive lipid droplets decreased following treatment with lactoferrin, as did the mRNA expression of C/EBPalpha, PPARgamma, aP2, and adiponectin. Furthermore, our Western blot data revealed a decrease in PPARgamma expression attributable to lactoferrin exposure. These results suggest that lactoferrin suppresses the adipogenic differentiation of MC3T3-G2/PA6 cells.