Outcomes of hospitalizations attributed to periapical abscess from 2000 to 2008: a longitudinal trend analysis.

INTRODUCTION: Root canal therapy is a highly successful in-office treatment and preventive measure against periapical abscesses. Left untreated, periapical abscesses can have serious consequences that can lead to hospitalization. This study observes the trends of hospitalizations attributed to periapical abscesses. METHODS: A retrospective analysis of the Nationwide Inpatient Sample (years 2000-2008) was used; we selected cases with a primary diagnosis of a periapical abscess with/without sinus involvement. The demographic characteristics and outcomes were examined. Each individual hospitalization was the unit of analysis. RESULTS: During the 9-year study period, a total of 61,439 hospitalizations were primarily attributed to periapical abscesses in the United States. The average age was 37 years, and 89% of all hospitalizations occurred on an emergency/urgent basis. The mean length of stay was 2.96 days, and a total of 66 patients died in hospitals. Medicare, Medicaid, and private insurance plans paid for 18.7%, 25.2%, and 33.4% of hospitalizations, respectively. Uninsured patients accounted for 18.5% of hospitalizations. Significant predictors that influenced both hospital charges and length of stay included age, race, insurance status, a periapical abscess with sinus involvement, geographic region of country, the Charlson comorbidity index, and the year of study (P < .05). CONCLUSIONS: The current study highlights the increasing burden of hospitalization of patients with periapical abscesses over a 9-year study period from 2000 to 2008. The high-risk groups likely to seek a hospital setting for the treatment of periapical abscesses were identified as were groups associated with higher hospital charges and a longer length of stay.

Combinatorial effect of Si4+, Ca2+, and Mg2+ released from bioactive glasses on osteoblast osteocalcin expression and biomineralization.

Osteocalcin (OCN) expression is an essential osteogenic marker of successful bone regeneration therapies. This study hypothesizes that Si(4+) and Ca(2+) combinatorial released by bioactive glass enhance osteoblast biomineralization through up-regulation of OCN expression; and Mg(2+) release delays such enhancement. Osteoblasts (MC3T3-E1) were treated with ionic products of bioactive glass dissolution (6P53-b experimental bioactive glass and 45S5 commercial Bioglass™). Results showed that gene expressions, including OCN and its up-stream transcription factors (Runx2, ATF4, MSX1, SP7/OSX), growth factors and signaling proteins (BMP2, BMP6, SMAD3), were enhanced in both 45S5 and 6P53-b glass conditioned mediums (GCMs). This up-regulation led to enhanced mineral formation by 45S5 glass conditioned mediums ([GCM], Si(4+)+Ca(2+)) after 20 days, and by 45S5 GCM and 6P53-b GCM (Si(4+)+Ca(2+)+Mg(2+)) after 30 days. In examining the extracellular matrix generated by cells when exposed to each GCM, it was found that 45S5 GCM had slightly elevated levels of mineral content within ECM as compared to 6P53-b GCM after 30 days while control treatments exhibited no mineral content. The formation of well-defined mineralized nodules (distinct PO4(3-) [960 cm(-1)] and CO3(2-) [1072 cm(-1)] peaks from Raman Spectra) was observed for each GCM as the soluble glass content increased. In examining the individual and combined ion effects between Si(4+), Ca(2+), and Mg(2+), it was found Mg(2+) down-regulates OCN expression. Thus, ions released from both 45S5 and 6P53-b bioactive glasses up-regulate OCN expression and biomineralization while 6P53-b GCM Mg(2+) release down-regulated OCN expression and delayed osteoblast biomineralization. These results indicate that Si(4+), Ca(2+), and Mg(2+) combinatorially regulate osteoblast OCN expression and biomineralization.

Si and Ca individually and combinatorially target enhanced MC3T3-E1 subclone 4 early osteogenic marker expression.

This study tests the hypothesis that silicon and calcium ions combinatorially target gene expression during osteoblast differentiation. MC3T3-E1 subclone 4 osteoblast progenitors (transformed mouse calvarial osteoblasts) were exposed to Si(4+) (from Na(2)SiO(3)) and Ca(2+) (from CaCl(2):H(2)O) ion treatments both individually (0.4 mM each + control treatment) and combinatorially (0.4 mM Si(4+) + 0.4 mM Ca(2+) + control treatment) and compared to control treated (α-minimum essential medium, 10% fetal bovine serum, and 1% penicillin-streptomycin) cells. Cell proliferation studies showed no significant increase in cell density between treatments over 5 days of culture. Cellular differentiation studies involved addition of ascorbic acid (50 mg/L) for all treatments. Relative gene expression was determined for collagen type 1 (Col(I)α1/Col(I)α2), core-binding factor a (cbfa1/Runx2), and osteocalcin (OCN), which indicated osteoblast progenitor differentiation into a mineralizing phenotype. Increased Si(4+) or Ca(2+) ion treatments enhanced Col(I)α1, Col(I)α2, Runx2, and OCN expression, while increased Si(4+) + Ca(2+) ion treatments enhanced OCN expression. Moreover, it was found that a Si(4+)/Ca(2+) ratio of unity was optimal for maximal expression of OCN. Collagen fiber bundles were dense, elongated, and thick within extracellular matrices (ECM) exposed to Si(4+) and Si(4+) + Ca(2+) treatments, while collagen fiber bundles were sparse, short, and thin within Ca(2+) and control treated ECM. These results indicated that individual ions enhance multiple osteogenic gene expression, while combined ion treatments enhance individual gene expression. In addition, these results indicated that Si(4+) enhanced osteoblast gene expression and ECM formation at higher levels than Ca(2+). These results support the larger concept that ions (possibly released from bioactive glasses) could control bone formation by targeting osteoblast marker expression.