Substance P has been studied in relation to its distribution within gingival tissues as well as its effect on cultured human gingival fibroblasts. The tissue distribution was varied depending on the degree of inflammation present. In healthy tissues substance P was found in the connective tissues interspersed between the collagenous elements and was particularly prominent in the areas immediately subjacent to the epithelial rete pegs. In inflamed tissues, substance P was markedly increased particularly around the blood vessels as well as in close association with much of the inflammatory cell infiltrate. The effect of substance P on human gingival fibroblast proliferation was monitored by [3H]thymidine incorporation and indicated substance P to be mitogenic for these cells at low concentrations (1 × 10−9 M) and tended towards an inhibitory effect at higher concentrations (1 × 10−4 M). Substance P did not have any effect on the release of either total proteins or proteoglycans into the culture medium. However, exposure of the cells to substance P did cause a greater accumulation of both total protein and proteoglycan with the cell layer material. These findings suggest a potential role for substance P on gingival tissues and in particular their resident fibroblastic cells and can therefore be used as a basis for more detailed studies into the relationship between neuropeptide release associated with neurogenic inflammation and periodontal pathology. J Periodontol 1994; 65:1113–1121.
This article has an accompanying continuing medical education activity, also eligible for MOC credit, on page e67. Learning Objective-Upon completion of this activity, successful learners should be able to understand the prevalence of pancreatic cysts in clinical practice and determine the prognosis of asymptomatic pancreatic cysts. BACKGROUND & AIMS: The 2015 American Gastroenterological Association guidelines recommend discontinuation of surveillance of pancreatic cysts after 5 years, although there are limited data to support this recommendation. We aimed to determine the rate of pancreatic cancer development from neoplastic pancreatic cysts after 5 years of surveillance. METHODS: We performed a retrospective multicenter study, collecting data from 310 patients with asymptomatic suspected neoplastic pancreatic cysts, identified by endoscopic ultrasound from January 2002 to June 2010 at 4 medical centers in California. All patients were followed up for 5 years or more (median, 87 mo; range, 60-189 mo). Data were used to calculate the risk for pancreatic cancer and all-cause mortality. RESULTS: Three patients (1%) developed invasive pancreatic adenocarcinoma. Based on American Gastroenterological Association high-risk features (cyst size > 3 cm, dilated pancreatic duct, mural nodule), risks for cancer were 0%, 1%, and 15% for patients with 0, 1, or 2 high-risk features, respectively. Mortality from nonpancreatic causes was 8-fold higher than mortality from pancreatic cancer after more than 5 years of surveillance. CONCLUSIONS: There is a very low risk of malignant transformation of asymptomatic neoplastic pancreatic cysts after 5 years. Patients with pancreatic lesions and 0 or 1 high-risk feature have a less than 1% risk of developing pancreatic cancer, therefore discontinuation of surveillance can be considered for select patients. Patients with neoplastic pancreatic cysts with 2 high-risk features have a 15% risk of subsequent pancreatic cancer, therefore surgery or continued surveillance should be considered.
About 100 trillion microorganisms compose the microbiome of the gastrointestinal tract and are predominantly found within the colon. Until recently, few bacteria were thought to inhabit the normal healthy esophagus and stomach. However, contemporary studies using molecular techniques have contradicted these assumptions. In this review, we summarize the pertinent findings of these studies that demonstrate established, complex mixed-microbial communities within the foregut in both health and disease. These studies contribute to improved understanding of interactions between the host immunity and the microbiome that may ultimately allow for novel therapeutic targets.
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