JL Ebersole

In February 2006, the US Supreme Court heard cases that may affect whether intermittent streams are jurisdictional waters under the Clean Water Act. In June 2006, however, the cases were remanded to the circuit court, leaving the status of intermittent streams uncertain once again. The presence of commercial species, such as coho salmon (Oncorhynchus kisutch), can be an important consideration when determining jurisdiction. These salmon spawn in the upper portions of Oregon coastal stream networks, where intermittent streams are common. In our study of a coastal Oregon watershed, we found that intermittent streams were an important source of coho salmon smolts. Residual pools in intermittent streams provided a means by which juvenile coho could survive during dry periods; smolts that overwintered in intermittent streams were larger than those from perennial streams. Movement of juvenile coho into intermittent tributaries from the mainstem was another way in which the fish exploited the habitat and illustrates the importance of maintaining accessibility for entire stream networks. Loss of intermittent stream habitat would have a negative effect on coho salmon populations in coastal drainages, including downstream navigable waters.

OBJECTIVE: The objective of this study was to determine the efficacy of a novel point-of-care immunoflow device (POCID) for detecting matrix metalloproteinase (MMP)-8 concentrations in oral fluids in comparison with a gold standard laboratory-based immunoassay. METHODS: Oral rinse fluid and whole expectorated saliva samples were collected from 41 participants clinically classified as periodontally healthy or diseased. Samples were analyzed for MMP-8 by Luminex immunoassay and POCID. Photographed POCID results were assessed by optical scan and visually by two examiners. Data were analyzed by Pearson's correlation and receiver-operating characteristics. RESULTS: MMP-8 was readily detected by the POCID, and concentrations correlated well with Luminex for both saliva and rinse fluids (r = 0.57-0.93). Thresholds that distinguished periodontitis from health were delineated from both the optical scans and visual reads of the POCID (sensitivity: 0.7-0.9, specificity: 0.5-0.7; P < 0.05). CONCLUSIONS: Performance of this POCID for detecting MMP-8 in oral rinse fluid or saliva was excellent. These findings help demonstrate the utility of salivary biomarkers for distinguishing periodontal disease from health using a rapid point-of-care approach.

OBJECTIVE(S): This report compares the virulence of selected strains of P. gingivalis, A. actinomycetemcomitans, C. rectus, F. nucleatum and T. denticola in a murine model as a measure of pathogenic potential of these oral microorganisms. The characteristics of the tissue destruction associated with these monoinfections were then related to a potential model for bacterial synergism in progressing periodontitis. DESIGN AND METHODS: All bacterial strains were grown to mid‐logarithmic to early stationary growth phase, harvested and used at various doses to challenge BALBlc normal and BALB/c dexamethasone (DEX) treated mice to mimic a neutrophil dysfunction. The characteristics of tissue destruction, and overt tissue destructive capacity of these species were examined as a function of challenge dose and time. OUTCOME MEASURES The mice were examined for an interval of approximately 15 days post‐challenge and the presencelabsence of lesions, localized or generalized nature of the lesion (including size in mm), and lethality of the infection were assessed. RESULTS: Comparison of the virulence of the various P. gingivalis strains related to lethality and lesion size associated with destruction of the connective tissue, indicated a virulence capacity of P. gingivalis strains 53977&gt;W50 = T22&gt;3079&gt;33277&gt;381. C. rectus elicited localized necrotic lesions which were limited to the epithelial layers of the skin. The size of the lesions also indicated a graded difference in virulence, such that C. rectus strains 234&gt;576&gt;&gt;33238. A . actinomycetemcornitans caused the formation of classic localized abscesses with a PMN infiltrate and inflammatory exudates. Although, each of the A. actinornyceterncomitans strains exhibited a similar virulence pattern in this murine model, A. actinomycetemcomitans serotype b representative strains were potentially more pathogenic with a virulence capacity of 3113D‐N = 3975A&gt;jP2&gt;Y4&gt;29523&gt;33384. Both C. rectus and A. actinomycetemcomitans strains showed clear evidence that recent clinical isolates were more virulent than laboratory strains. Challenge with F. nucleatum resulted in tissue destructive responses which were different from those observed with the other strains used in this study. A rapid onset of dose‐dependent lesion development, related to the formation of either closed abscesses or open lesions, was observed with F. nucleaturn . Tissue involvement was also greater at lower F. nucleaturn doses when compared to the other bacteria. F. nucleaturn challenge of DEX‐treated mice resulted in a shift to open lesions. T. denticola appeared to be more tissue invasive than the other species examined in this study. Challenge of mice with T. denticola resulted in involvement of multiple tissues, including epithelial and connective tissues, as well as appearing to invade muscle layers and deeper tissues. In addition to invading deeper tissues, the resulting lesions took considerably longer to resolve. In the DEX‐treated mice (neutrophil depleted), P. gingivalis, C. rectus , and A. actinomycetemcomitans were significantly more virulent. In contrast, while DEX treatment altered the characteristics of lesions caused by F. nucleatum , the extent of lesions produced by F. nucleatum and T. denticola was not substantially enhanced. CONCLUSIONS: The results obtained from this study suggest that different microorganisms have the ability to provide individual pathologies which may act in an additivelsynergistic fashion contributing to the tissue destruction noted in periodontitis.

A reduction in calorie intake [caloric restriction (CR)] appears to consistently decrease the biological rate of aging in a variety of organisms as well as protect against age-associated diseases including chronic inflammatory disorders such as cardiovascular disease and diabetes. Although the mechanisms behind this observation are not fully understood, identification of the main metabolic pathways affected by CR has generated interest in finding molecular targets that could be modulated by CR mimetics. This review describes the general concepts of CR and CR mimetics as well as discusses evidence related to their effects on inflammation and chronic inflammatory disorders. Additionally, emerging evidence related to the effects of CR on periodontal disease in non-human primates is presented. While the implementation of this type of dietary intervention appears to be challenging in our modern society where obesity is a major public health problem, CR mimetics could offer a promising alternative to control and perhaps prevent several chronic inflammatory disorders including periodontal disease.

As the highly active antiretroviral therapy (HAART) has transitioned human immunodeficiency virus (HIV) infection into a 'chronic disease' management strategy, there is growing evidence that infection with non-HIV pathogens in HIV+ patients may have important public health implications in undermining HAART success and acquired immunodeficiency syndrome progression. Several bacterial and host cell products during infections with non-HIV pathogens have shown the capacity to regulate HIV replication in latently infected cells. A high prevalence of oral infections caused by bacteria, viruses and fungi has been described in HIV+ patients, including periodontal disease. The oral cavity appears to be a site of HIV pathogenesis and potential reservoir for the disease as HIV RNA and DNA forms are present in saliva as well as in gingival crevicular fluid, and oral epithelial cells are susceptible to either cell free or cell-associated HIV infection. The clinical and biological bases of potential associations between chronic oral inflammatory disorders, such as periodontal disease, and exacerbation of HIV viraemia have received little attention. This review attempts to evaluate the current understanding of HIV reactivation as a result of co-infection and/or inflammation induced by non-HIV pathogens in HIV-infected patients, and presents a hypothetic model about the potential role of periodontitis as a global oral infection that potentially contributes to HIV recrudescence.