Factors considered by new faculty in their decision to choose careers in academic dentistry

To determine the characteristics of new dental faculty and what factors influenced them to choose academic careers, a survey was sent to deans at all U.S. dental schools to be distributed to faculty with length of service of four years or less. Responses were received from 240 individuals. About half of the respondents had been in private practice for an average of eight years, and 20 percent had military experience averaging almost sixteen years. A majority had postgraduate training and 60 percent had specialty training. Nearly 32 percent of new faculty were female and 80 percent were U.S. citizens. Analyses of responses to survey items indicated that correlated factors in the survey fell into the following empirical categories: teaching and scholarship, income and indebtedness, research, work schedule, influence of mentors and role models, and long-term aspirations. In general, the respondents identified factors relating to teaching and scholarship to be the most important influences on their choice of academic careers, while concerns about income and indebtedness were the most important negative considerations in this regard. Other positive factors identified by the survey related to the influence of mentors and role models, long-term aspirations, and research. Age, private practice experience, and military experience were found to particularly influence the new faculty members\u27 responses to items concerning income and indebtedness, and citizenship influenced responses to factors relating to research. The data from this select group of dentists support the current view that inequities in income of dental faculty compared to private practitioners and student debt are important concerns in choosing academic careers. Importantly, the desire to teach and participate in scholarly activities are important attractions in academic careers. Mentoring activities and creation of opportunities for career development are crucial factors in developing interest in academics among graduate dentists

Anticardiolipin (aCL) in sera from periodontitis subjects activate Toll-like receptor 4 (TLR4).

Anticardiolipin antibodies (aCL) have been reported to be present in 15-20% of sera from subjects with periodontitis at concentrations exceeding those found in 95% of the healthy adult population. These antibodies, albeit at concentrations exceeding those generally found in periodontitis subjects, are typically present in patients with the antiphospholipid syndrome (APS), an autoimmune disease characterized by thrombosis and recurrent pregnancy loss. aCL from APS patients are proinflammatory and can activate trophoblasts, macrophages, and platelets via cell-surface interactions with their target antigen beta-2-glycoprotein-I (β2GPI). β2GPI is an anionic phospholipid-binding serum protein that can associate with toll-like receptors (TLR's) on the cell-surface, leading to cell activation following interaction with autoimmune aCL. We examined an expanded series of 629 sera from clinically characterized subjects for aCL content, and observed that 14-19% of these sera contained elevated (>95th %-tile) levels of aCL. We purified IgG from 16 subjects with elevated or normal levels of aCL and examined their ability to activate TLR2- or TLR4-transfected human embryonic kidney (HEK) cells, and observed that IgG from periodontitis patients with elevated aCL activated HEK-TLR4 cells, but not HEK-TLR2 cells. Prior removal of aCL by immunoabsorption significantly reduced the ability of IgG preparations from these sera to activate TLR4. Further experiments using a human first trimester trophoblastic cell line (HTR8 sv/neo) revealed that aCL from periodontitis patients stimulated IL-8 production, which was profoundly decreased if aCL was removed by immunoabsorption or if HTR8 sv/neo were pretreated with blocking anti-TLR4 antibodies. Thus, it appears that aCL from periodontitis patients can be proinflammatory, activating cells via TLR4. Since these antibodies are likely produced via molecular mimicry due to similarities between oral bacterial antigens and β2GPI, the data indicate that circulating serum aCL may induce or influence inflammatory responses at sites distant from the oral cavity

Opsonization of Actinobacillus actinomycetemcomitans by Immunoglobulin G Antibody Reactive with Phosphorylcholine

We used two strains of Actinobacillus actinomycetemcomitans, one bearing phosphorylcholine (PC) (strain D045D-40) and one devoid of PC antigens (strain DB03A-42), as well as a nonencapsulated strain of Streptococcus pneumoniae (strain 39937), to examine the opsonic properties of physiological concentrations (⩽30 μg/ml) of purified human anti-PC immunoglobulin G (IgG). Anti-PC bound to both A. actinomycetemcomitans DO45D-40 and S. pneumoniae 39937 and induced superoxide anion production by polymorphonuclear neutrophils; induction of the oxidative burst was inhibited by antibodies to either CD16 or CD32. Thus, anti-PC IgG at concentrations present in most human sera promotes the opsonization of PC-expressing strains of A. actinomycetemcomitans in the absence of complement, implying that anti-PC may be a protective antibody against such strains of bacteria

Delineation of the Role of Platelet-Activating Factor in the Immunoglobulin G2 Antibody Response

Localized aggressive periodontitis (LAgP) is a chronic inflammatory disease characterized by severe destruction of periodontal tissues surrounding the first molars and incisors. LAgP subjects produce large amounts of immunoglobulin G2 (IgG2) antibody against oral pathogens, and this response is inversely correlated with the severity of disease. We previously demonstrated that platelet-activating factor (PAF) is required for optimal IgG2 responses. The present investigation was designed to determine the mechanism of IgG2 induction by PAF. Exogenous PAF acetylhydrolase suppressed approximately 80% of pokeweed mitogen-stimulated IgG2 production, confirming that PAF is essential for optimal responses. PAF-activated leukocytes produced gamma interferon (IFN-γ), a Th1 cytokine that has been associated with IgG2 responses in previous studies. The monocyte-derived cytokines interleukin-12 (IL-12) and IL-18 are upstream of IFN-γ production, and IgG2 production was suppressed by neutralizing antibodies against these proteins. In addition, PAF induced monocyte-derived dendritic cells (DC) but not macrophages (MΦ) to secrete IL-12 and IL-18. This observation was interesting because monocyte differentiation in LAgP subjects is skewed to the DC phenotype. Although other investigators have implicated IFN-γ in IgG2 production, its precise role in this response is controversial. Our studies suggest that IFN-γ induces isotype switching to IgG2 but only in concert with the Th2 cytokine IL-4. Thus, it appears that the unique PAF metabolism of LAgP monocytes or DC promotes Th1 responses that are essential for optimal IgG2 antibody production. As IgG2 antibodies opsonize oral bacteria and promote their clearance and destruction, these alterations in PAF metabolism may be essential for limiting disease severity in LAgP patients