Biomarkers of periodontal inflammation in the Australian adult population

Background:  Several inflammatory biomarkers are implicated in the pathogenesis of periodontitis including interleukin-1β (IL-1β) and C-reactive protein (CRP). This study investigated the presence of these factors in gingival crevicular fluid (GCF) and their relationship to clinical and social determinants of periodontitis in the Australian population.
Methods:  Equal numbers of periodontitis cases and non-cases were sampled during oral epidemiologic examination in the National Survey of Adult Oral Health. GCF was sampled from four sites where probing pocket depth (PPD) and recession were recorded. From these, IL-1β and CRP were quantified by ELISA and the log amount of GCF IL-1β (pg) per person and the proportion of adults with detectable CRP was computed.
Results:  Periodontitis cases (n = 511) had significantly higher levels of IL-1β and CRP than non-cases (n = 562). PPD, clinical attachment loss, plaque and gingivitis indices were positively associated with elevated levels of both biomarkers. Levels of both were positively associated with age, low socio-economic position and non-Australian birth.
Conclusions:  The presence of IL-1β and CRP in GCF are associated with periodontal disease parameters within the Australian population. The levels of both biomarkers are influenced by age, education and eligibility for public dental care.     

In vitro chemosensitivity of head and neck cancer cell lines

Background

Systemic treatment of head and neck squamous cell carcinoma (HNSCC) includes a variety of antineoplastic drugs. However, drug-resistance interferes with the effectiveness of chemotherapy. Preclinical testing models are needed in order to develop approaches to overcome chemoresistance.

Methods

Ten human cell lines were obtained from HNSCC, including one with experimentally-induced cisplatin resistance. Inhibition of cell growth by seven chemotherapeutic agents (cisplatin, carboplatin, 5- fluorouracil, methotrexate, bleomycin, vincristin, and paclitaxel) was measured using metabolic MTT-uptake assay and correlated to clinically-achievable plasma concentrations.

Results

All drugs inhibited cell growth in a concentration-dependent manner with an IC50 comparable to that achievable in vivo. However, response curves for methotrexate were unsatisfactory and for paclitaxel, the solubilizer cremophor EL was toxic. Cross-resistance was observed between cisplatin and carboplatin.

Conclusion

Chemosensitivity of HNSCC cell lines can be determined using the MTT-uptake assay. For DNA-interfering cytostatics and vinca alkaloids this is a simple and reproducible procedure. Determined in vitro chemosensitivity serves as a baseline for further experimental approaches aiming to modulate chemoresistance in HNSCC with potential clinical significance.     

Coordination of glioblastoma cell motility by PKCι

Background  

Glioblastoma is one of the deadliest forms of cancer, in part because of its highly invasive nature. The tumor suppressor PTEN is frequently mutated in glioblastoma and is known to contribute to the invasive phenotype. However the downstream events that promote invasion are not fully understood. PTEN loss leads to activation of the atypical protein kinase C, PKCι. We have previously shown that PKCι is required for glioblastoma cell invasion, primarily by enhancing cell motility. Here we have used time-lapse videomicroscopy to more precisely define the role of PKCι in glioblastoma.     

Reflections on community-based population health intervention and evaluation for obesity and chronic disease prevention: the Healthy Alberta Communities project

Objectives  

To reflect upon a population health intervention for obesity and chronic disease prevention, with specific attention to the processes of change and developing, implementing and evaluating an intervention in a community–university–government partnership context.     

Osteoprotegerin: A novel biomarker for inflammatory bowel disease and gastrointestinal carcinoma

Osteoprotegerin (OPG) is a member of the tumor necrosis factor receptor superfamily of proteins. Although initial data illustrated the key role that OPG plays in bone turnover, numerous recent reports indicate that OPG is also an important factor in inflammatory pathways and tumor cell survival. OPG contributes directly to inflammatory processes and has been evaluated as a novel non‐invasive biomarker of gut inflammation. Furthermore, OPG affects cell turn‐over, differentiation, death, and survival via extracellular pathways, correlating with worse prognosis in inflammatory bowel diseases and several gastrointestinal carcinomas. It is now clear that OPG has multiple functions and characteristics. This review gives an overview of OPG, highlights its roles in different extracellular pathways, and outlines how OPG could be used as a novel non‐invasive biological marker in inflammatory bowel diseases and gastrointestinal carcinomas.