Results of this study support the need for a clinical tool to evaluate dental implant stability prior to loading, especially for implants placed in the maxilla. It appears that implant stability is weakest at 3 to 6 weeks in one-stage non-loaded dental implants. ISQ readings can be used to determine different healing phases and the stability of dental implants. However, it is difficult to define a general standardized range of ISQ readings for successful implant integration for various implant systems. Thus, RFA values/ISQ levels should be calibrated for each implant system separately. Further studies are needed to compare the early changes seen in immediately loaded dental implants and to determine whether there is any time in which the total recovery in ISQ levels may occur.

1259Sleep and Preterm Birth-Blair et al. INTRODUCTIONIn the United States, preterm birth affects 11.5% of deliveries and is the underlying cause of more than one third of infant deaths.1 A high proportion of surviving preterm infants suffer from severe physical and cognitive consequences, potentially requiring intensive medical and/or educational support throughout the lifespan.2 The morbidity and mortality associated with preterm birth pose significant drains on the financial and emotional resources of afflicted families, and on the nation as a whole, costing more than $26 billion annually in the United States. 3Inflammation is a causal mechanism in the initiation of preterm as well as term labor. 4 Inflammatory mediators can initiate contractions, encourage cervical ripening, and cause rupture of the membranes.4,5 Via these mechanisms, inflammation induced by infection or psychological stress may trigger early parturition. 6,7Importantly, poor sleep promotes inflammation.8 For example, in a population-based cohort of more than 5,000 adults, shorter sleep duration was associated with elevations in Study Objectives: Poor sleep promotes inflammation. In turn, inflammation is a causal mechanism in term as well as preterm parturition. In the United States, a persistent racial disparity in preterm birth exists, with African Americans showing ~1.5 times greater risk. This study examined associations among sleep quality, serum proinflammatory cytokines, and length of gestation in a racially diverse sample of 138 pregnant women. Design: Observational. Measurements: Women completed the Pittsburgh Sleep Quality Index (PSQI) and other psychosocial and behavioral measures during midpregnancy. Serum levels of interleukin (IL)-6, IL-8, IL-1β, and tumor necrosis factor (TNF)-α were determined by high-sensitivity assays. Birth outcomes were determined via medical record review. Results: Among African American women (n = 79), shorter gestation was predicted by poorer overall sleep (r s = −0.35, P = 0.002) as well the following PSQI subscales: subjective sleep quality (r s = −0.34, P = 0.002), sleep latency (r s = −0.27, P = 0.02), and sleep efficiency (r s = −0.27, P = 0.02). African American women with poor sleep quality (PSQI > 5) had 10.2 times the odds of preterm birth compared to those with good sleep quality. In contrast, among European American women (n = 53), gestational length was not significantly predicted by sleep quality (Ps > 0.12). Bootstrapping analyses showed that, among African Americans, IL-8 significantly mediated the association between sleep quality and length of gestation (indirect effect estimate −0.029; 95% confidence interval −0.06, −0.002). Conclusions:The data provide novel evidence that African American women exhibit greater inflammation in response to sleep disturbance than European American women and these effects correspond with length of gestation. Racial differences in susceptibility to sleep induced immune dysregulation may contribute to marked racial disparities in preterm birth.

It is possible to radiographically observe a gain of approximately 3 to 4 mm of bone from the sinus floor to the implant apex. The amount of initial alveolar bone height, presence of sinus membrane perforation, and the amount of exposed implant surface appear to play a role in the presence or absence of radiopacity within the elevated sinus floor, following 6 months of healing.

Psychological stress is associated with an increased expression of markers of peripheral inflammation, and there is a growing literature describing a link between periodontal pathogens and systemic inflammation. The hypothesis of the present work is that exposing mice to the social stressor, called social disruption (SDR), would enhance the inflammatory response to lipopolysaccharide (LPS) derived from the oral pathogen, Porphyromonas gingivalis. Mice were exposed to SDR for 2 hrs per day on 6 consecutive days. On the morning following the last cycle of SDR, mice were tested for anxiety-like behavior in the open field test and novel object test. The mice were sacrificed the following day and their spleens harvested. Spleen cells were stimulated with LPS derived from P. gingivalis in the absence or presence of increasing doses of corticosterone. Social disruption resulted in anxiety-like behavior, and the production of IL-1β and TNF-α was significantly higher in spleen cells from mice exposed to SDR in comparison to levels from non-stressed control mice. In addition, the viability of spleen cells from mice exposed to SDR was significantly greater than the viability of cells from non-stressed control mice, even in the presence of high doses of corticosterone. The use of cultures enriched for CD11b+ cells indicated that the stressor was affecting the activity of splenic myeloid cells. This study demonstrates that social stress enhances the inflammatory response to an oral pathogen and could provide a critical clue in the reported associations between stress, inflammation, and oral pathogens.