Comparison of temporal artery to rectal temperature measurements in children up to 24 months.

This descriptive study compared temporal artery (TA) and rectal temperature measurements, patient comfort during temperature measurements, and nursing time required to obtain temperature measurements. Study participants (n = 40) included children 0-24 months old with fever higher than 38°C, admitted to a freestanding children's hospital in the Midwest. Statistical analysis of 450 paired TA and rectal temperature measurements revealed a 0.776 correlation, mean difference of 0.03°C, and 94.7% of measurements differing by less than 1.0°C. Patient comfort, measured via the Face, Legs, Activity, Cry, Consolability Scale, was enhanced with TA thermometry compared to rectal. TA thermometry resulted in an 87% savings of nursing time.

B Cell IgD Deletion Prevents Alveolar Bone Loss Following Murine Oral Infection.

Periodontal disease is one of the most common infectious diseases of humans. Immune responses to infection trigger loss of alveolar bone from the jaw and eventual tooth loss. We investigated the contribution of B cell IgD to alveolar bone loss by comparing the response of B cell normal BALB/cJ mice and IgD deficient BALB/c-Igh-5(-/-J) mice to oral infection with Porphyromonas gingivalis, a gram-negative periodontopathic bacterium from humans. P. gingivalis-infected normal mice lost bone. Specific antibody to P. gingivalis was lower and oral colonization was higher in IgD deficient mice; yet bone loss was completely absent. Infection increased the proportion of CD69(+) activated B cells and CD4(+) T cells in immune normal mice compared to IgD deficient mice. These data suggest that IgD is an important mediator of alveolar bone resorption, possibly through antigen-specific coactivation of B cells and CD4(+) T cells.

An essential role for IL-17 in preventing pathogen-initiated bone destruction: recruitment of neutrophils to inflamed bone requires IL-17 receptor-dependent signals.

IL-17 and its receptor are founding members of a novel family of inflammatory cytokines. IL-17 plays a pathogenic role in rheumatoid arthritis (RA)-associated bone destruction. However, IL-17 is also an important regulator of host defense through granulopoiesis and neutrophil trafficking. Therefore, the role of IL-17 in pathogen-initiated bone loss was not obvious. The most common form of infection-induced bone destruction occurs in periodontal disease (PD). In addition to causing significant morbidity, PD is a risk factor for atherosclerotic heart disease and chronic obstructive pulmonary disease (COPD). Similar to RA, bone destruction in PD is caused by the immune response. However, neutrophils provide critical antimicrobial defense against periodontal organisms. Since IL-17 is bone destructive in RA but a key regulator of neutrophils, we examined its role in inflammatory bone loss induced by the oral pathogen Porphyromonas gingivalis in IL-17RA-deficient mice. These mice showed enhanced periodontal bone destruction, suggesting a bone-protective role for IL-17, reminiscent of a neutrophil deficiency. Although IL-17RA-deficient neutrophils functioned normally ex vivo, IL-17RA knock-out (IL-17RA(KO)) mice exhibited reduced serum chemokine levels and concomitantly reduced neutrophil migration to bone. Consistently, CXCR2(KO) mice were highly susceptible to alveolar bone loss; interestingly, these mice also suggested a role for chemokines in maintaining normal bone homeostasis. These results indicate a nonredundant role for IL-17 in mediating host defense via neutrophil mobilization.

Genetic control of the immune response in pathogenesis.

BACKGROUND: Epidemiological studies have suggested that there is a genetic component to susceptibility to chronic periodontitis. Studies in humans and in animal models have suggested that some of the important components may be polymorphisms in key immunological genes. METHODS: This paper summarizes previously published data from a mouse model in which alveolar bone loss is induced by oral infection with Porphyromonas gingivalis. Mice of different inbred immune-normal strains were used, as well as the F1 heterozygotes from crosses between strains. In addition, tissue expression of an array of immunological genes was measured in the gingiva and spleen of these mice by quantitative reverse transcription-polymerase chain reaction (QPCR). RESULTS: Not all strains of mice are susceptible to bone loss. Intercross experiments demonstrate that susceptibility is an inherited trait. A subset of immunological genes tested showed differential basal expression in the gingiva or spleens (or both). Tumor necrosis factor and osteoprotegerin mRNAs are more highly expressed in the gingiva and interleukin-1 mRNA is more highly expressed in both the gingiva and the spleens of susceptible mice than resistant mice. In the resistant mice, interleukin-15 mRNA in the gingiva and Selp mRNA in the spleen are present at higher levels. In the resistant mice no genes changed expression after P. gingivalis infection, while mRNA for interleukin-1, osteoprotegerin, and STAT6 all increased in the susceptible mice. CONCLUSIONS: Susceptibility and resistance are heritable traits. Strain differences in basal mRNA expression correlate with differences in susceptibility. Genes that change expression in response to infection also correlate with differences in susceptibility.

Genetic Control of the Immune Response in Pathogenesis.

BACKGROUND: Epidemiological studies have suggested that there is a genetic component to susceptibility to chronic periodontitis. Studies in humans and in animal models have suggested that some of the important components may be polymorphisms in key immunological genes. METHODS: This paper summarizes previously published data from a mouse model in which alveolar bone loss is induced by oral infection with Porphyromonas gingivalis. Mice of different inbred immune-normal strains were used, as well as the F1 heterozygotes from crosses between strains. In addition, tissue expression of an array of immunological genes was measured in the gingiva and spleen of these mice by quantitative reverse transcription-polymerase chain reaction (QPCR). RESULTS: Not all strains of mice are susceptible to bone loss. Intercross experiments demonstrate that susceptibility is an inherited trait. A subset of immunological genes tested showed differential basal expression in the gingiva or spleens (or both). Tumor necrosis factor and osteoprotegerin mRNAs are more highly expressed in the gingiva and interleukin-1 mRNA is more highly expressed in both the gingiva and the spleens of susceptible mice than resistant mice. In the resistant mice, interleukin-15 mRNA in the gingiva and Selp mRNA in the spleen are present at higher levels. In the resistant mice no genes changed expression after P. gingivalis infection, while mRNA for interleukin-1, osteoprotegerin, and STAT6 all increased in the susceptible mice. CONCLUSIONS: Susceptibility and resistance are heritable traits. Strain differences in basal mRNA expression correlate with differences in susceptibility. Genes that change expression in response to infection also correlate with differences in susceptibility.

Genetic susceptibility to chronic periodontal disease.

Evidence suggests that there is a significant genetic component to susceptibility and resistance to chronic periodontal disease. Data from both clinical studies and studies using animal models are reviewed here. Also outlined are the genomic methods that are now available for identifying susceptibility and resistance loci.

T cell knockout mice have diminished alveolar bone loss after oral infection with Porphyromonas gingivalis.

Periodontal diseases are chronic inflammatory diseases that can result in resorption of the alveolar bone of the jaw. We have developed a murine model in which alveolar bone loss is induced by oral infection with Porphyromonas gingivalis, an oral anaerobic bacterium associated with periodontal disease in humans. Here we compared a strain of immunocompetent mice (C57BL/6J) to the same strain of mice made T cell deficient by genetic deletion of the alpha chain of their T cell receptors (C57BL/6J-Tcra). T cell deficiency did not affect the ability of P. gingivalis to implant in the oral cavity. The two strains of mice had equal percentages of P. gingivalis among their cultivable anaerobes 7 weeks after infection. The same bacterial load led to much less bone resorption in the T cell deficient mice than in the immune normal mice, measured as either the number of sites with significant loss, or as the total amount of bone resorbed. T cell deficient mice lost bone at only three out of 14 measurement sites, compared with eight out of 14 sites in the wild-type mice. The total amount of bone lost was 70% less in the T cell deficient mice. T cell deficient mice had lower titers of P. gingivalis-specific IgG than the wild-type mice after oral infection did, but the same titers of specific IgA. Lower titers did not correlate with greater bone loss. Antigen-activated T lymphocytes are known to induce osteoclastogenesis; here we demonstrate that T cell deletion decreases the amount of alveolar bone loss induced by infection of the murine oral cavity.