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Biomedical subjects

G K Johnson

Publications and source records attributed to G K Johnson.

At least 37 records · Page 2Linked to original sources

Prostaglandin E2 and interleukin-1 concentrations in nicotine-exposed oral keratinocyte cultures.

Oral keratinocytes are the first cells in contact with tobacco components and are capable of producing various inflammatory mediators, including PGE2 and IL-1. The purpose of this study was to examine PGE2 and IL-1 concentrations in nicotine-exposed oral keratinocyte cultures. Gingival keratinocyte cultures were established from healthy gingival tissues obtained from 7 subjects. Cultures were divided into 4 groups exposed to serum free medium (control), 0.1 microM, 10 microM or 1 mM nicotine for 4, 24 or 48 h. Using enzyme-linked immunosorbent assays, PGE2 and IL-1 alpha were quantified in culture supernatants; IL-1 alpha and beta were also measured in lysed cells. A repeated measures analysis of variance was used to identify significant differences over time and treatment. Nicotine exposure did not significantly alter PGE2 levels at any given time period; however, PGE2 quantities declined significantly (p = 0.0001) over time. At both 24 and 48 h, IL-1 alpha concentrations in lysates from 1 mM nicotine-exposed cells were significantly (p < 0.01) greater than those for all other treatments. Interleukin-1 alpha quantities also declined significantly (p = 0.037) over time in the cultures. Interleukin-1 beta concentrations were elevated, albeit not significantly, in the 1 mM treated cells at 24 and 48 h. Cell viability, mass and counts were not affected by nicotine treatment; these parameters increased significantly (p < 0.005) over time. In summary, nicotine treatment significantly increased IL-1 alpha concentrations in cultured keratinocytes; however, PGE2 synthesis was not altered. Elevated IL-1 production by keratinocytes may have implications in tobacco-induced lesions, given the central role IL-1 plays in tissue response to injury.

Adult↗

Nicotine effects on PGE2 and IL-1 beta release by LPS-treated human monocytes.

Cigarette smoking is a major risk factor in the development and further progression of periodontitis. However, little is known regarding the pathogenesis of smoking-related periodontal diseases. The purpose of this study was to examine the effects of nicotine, alone and in combination with lipopolysaccharide (LPS), on monocyte secretion of bone-resorbing factors, PGE2 and IL-1 beta. Peripheral blood monocytes (PBM) were isolated by counterflow centrifugal elutriation from 15 healthy, non-smoking donors. PBM were incubated for 24 h in RPMI 1640 containing nicotine (0, 50 ng/ml, 1 microgram/ml, 10 micrograms/ml and 100 micrograms/ml) with or without 10 micrograms/ml Porphyromonas gingivalis LPS or Escherichia coli LPS. Culture supernatants were assayed for PGE2 and IL-1 beta by ELISA. None of the nicotine preparations resulted in significant PBM secretion of PGE2 and IL-1 beta above that of unstimulated cultures. However, PGE2 release was potentiated 1.7-fold by the combination of P. gingivalis LPS and 10 micrograms/ml nicotine relative to P. gingivalis LPS alone (p < 0.05, one-way ANOVA). Prostaglandin E2 release also was potentiated 3.5-fold by P. gingivalis LPS and 100 micrograms/ml nicotine relative to P. gingivalis LPS alone (p < 0.00001, one-way ANOVA) and 3.1-fold by E. coli LPS and 100 micrograms/ml nicotine relative to E. coli LPS alone (p < 0.00001, one-way ANOVA). IL-1 beta secretion was lower for either LPS plus 100 micrograms/ml nicotine relative to LPS alone, although not significantly. These data demonstrate upregulation of LPS-mediated monocyte secretion of PGE2 by nicotine and suggest a potential role for nicotine in periodontal disease pathogenesis.

Adult↗

Effect of smokeless tobacco extract on human gingival keratinocyte levels of prostaglandin E2 and interleukin-1.

Gingival recession and white mucosal lesions frequently occur at sites of smokeless tobacco (ST) placement. The etiology of these alterations is presumably related to the irritating effects of tobacco components. The purpose of this study was to examine the effect of an aqueous ST extract (STE) on gingival keratinocyte production of prostaglandin E2 (PGE2) and interleukin-1 (IL-1), mediators involved in periodontal destruction and keratinocyte proliferation. Keratinocyte cultures were established from healthy tissues discarded from 8 subjects undergoing crown lengthening procedures. Cells (passage 2-3) were seeded at 2.5 x 10(4) cells/well into 48 well tissue culture plates and maintained in serum-free media at 37 degrees C. On day 4 or 5, the wells were divided into 4 groups receiving either 10%, 5%, 2.5%, or 0% STE for time periods ranging from 30 to 240 minutes. PGE2 levels (pg/10(4) cells), as measured by enzyme immunoassay, were significantly (P < 0.05) increased in the 10% (215.66 +/- 34.58) and 5% STE (151.82 +/- 27.97) treated cultures compared to untreated cells (46.16 +/- 9.58). IL-1 alpha and IL-1 beta proteins were elevated (P < 0.05) in cell lysates (299.45 +/- 38.69 and 28.45 +/- 5.18, respectively) from 5% STE exposed cultures compared to control wells. At 10% STE, secreted IL-1 alpha was decreased (P < 0.05) relative to 2.5% STE. This may reflect a toxic effect, as 10% STE significantly (P < 0.05) depressed cell numbers and viability. Lower tobacco concentrations did not affect cell numbers or viability, but significantly (P < 0.05) increased PGE2 and IL-1 levels. Tobacco-induced synthesis of these mediators may play a role in the development of tobacco-related oral disease.

Adult↗

Levels of cigarette consumption and response to periodontal therapy.

Seventy-four patients with moderate to advanced periodontitis were classified by cigarette consumption at the initial exam: heavy smokers (HS) > or = 20 cigarettes/day (n = 31); light smokers (LS) < or = 19 cigarettes/day (n = 15); past smokers (PS) had a history of smoking but had quit by the initial exam (n = 10); and non-smokers (NS) had never smoked (n = 18). All patients were treated with four modalities of periodontal therapy followed by supportive periodontal treatment (SPT) for a period of up to 7 years. Clinical parameters including probing depth (PD), clinical attachment level (CAL), recession (REC), presence of bleeding on probing (BOP), and supragingival plaque (PL) were assessed at six sites around each tooth. Horizontal probing attachment level (HAL) was obtained at molar furcation sites. Data were collected initially, 4 weeks after non-surgical therapy, 10 weeks after surgical therapy, and yearly during SPT. HS and LS demonstrated less PD reduction and less CAL gain than PS and NS following active treatment and throughout SPT. Following active treatment, HAL changes were similar for all groups, but during 7 years of SPT, HS and LS experienced greater loss of HAL. There were no differences in BOP among the four groups. HS demonstrated a higher percentage of PL positive sites compared to the other groups. In summary, HS and LS responded less favorably to therapy than PS and NS. A past history of smoking was not deleterious to the response to therapy.

Adult↗

Treatment of pancreatic pseudocysts with ductal communication by transpapillary pancreatic duct endoprosthesis.

BACKGROUND: Endoscopic treatment of pancreatic pseudocysts via cystenterostomy has been recognized as a successful treatment option in carefully selected patients. Pancreatic transpapillary stenting as an alternative treatment option in patients with pancreatic pseudocysts directly communicating with the main duct has received little consideration. The aim of the current study was to assess the safety and utility of transpapillary pancreatic endoprosthesis in the treatment of communicating pseudocysts. METHODS: Twenty-one patients underwent placement of 33 transpapillary endoprostheses for the treatment of symptomatic pancreatic pseudocysts. All pseudocysts communicated with the main pancreatic duct and ranged in size from 3 to 9 cm (mean 6 cm). Eight patients had associated pancreatic duct strictures. RESULTS: Stent placement was successful in all cases: 13 directly into the pseudocyst, 8 beyond the stricture but not into the pseudocyst. Initial resolution of pseudocysts was seen in 17 patients, with 16 patients free of pseudocyst recurrence at mean follow-up of 37 months. All patients with associated strictures were treated successfully. Factors predictive of success included presence of strictures, size of pseudocyst greater than or equal to 6 cm, location in the body of the pancreas, and duration of pseudocyst less than 6 months. Complications included one episode of mild pancreatitis. CONCLUSIONS: Endoscopic treatment of symptomatic pancreatic pseudocysts with ductal communication by transpapillary pancreatic duct stenting is a safe, effective modality and should be considered a first line therapy.

Adult↗

A comparison of nonionic versus ionic contrast media: results of a prospective, multicenter study. Midwest Pancreaticobiliary Study Group.

BACKGROUND: Pancreatitis is one of the most common complications associated with ERCP. Multiple factors have been implicated for this potentially serious complication. Numerous suggestions for minimizing risks at ERCP have been offered, one of which is to use nonionic, low osmolarity contrast agents for pancreatic injection. Results of previous studies comparing different contrast media have been inconclusive. METHODS: To evaluate the role contrast material plays in the development of post-ERCP pancreatitis, the Midwest Pancreaticobiliary Group performed a prospective double-blind controlled study. A total of 1,979 consecutive ERCP patients were enrolled, and 1,659 patients with pancreatic duct injections were divided into subgroups according to the complexity of the ERCP. Post-ERCP pancreatitis was compared between similar groups. Patients were randomized to receive injections of nonionic, low osmolarity contrast or standard ionic contrast media. RESULTS: The overall incidence of post-procedural pancreatitis was 10.2%. Those with diagnostic ERCP had the lowest incidence at 5.6%. Therapeutic procedures (12.3%) and sphincter of Oddi manometry (15.2%) had higher rates. Those injected with standard (ionic) contrast had an incidence of 10.4% and after injection with lower osmolar (nonionic) contrast, there was a 10% post-procedural pancreatitis rate. CONCLUSIONS: Patients with more complex procedures develop pancreatitis more frequently. The use of low osmolar (nonionic) contrast media does not decrease the incidence of post-ERCP pancreatitis.

Cholangiopancreatography, Endoscopic Retrograde↗

The effects of smokeless tobacco on clinical parameters of inflammation and gingival crevicular fluid prostaglandin E2, interleukin-1 alpha, and interleukin-1 beta.

The purpose of this study was to examine the effect of smokeless tobacco (ST) on gingival inflammation as assessed clinically and biochemically by gingival crevicular fluid (GCF) levels of PGE2, IL-1 alpha, and IL-1 beta. These parameters were compared in ST users (n = 12) and control, non-tobacco using subjects (n = 8) matched for plaque and probing depth levels. Both GI and GCF PGE2 concentration were significantly (P < 0.05) elevated at ST placement sites compared to sites in control subjects. A short-term longitudinal trial spanning 7 days also was undertaken within ST users (n = 18) to study the dynamics of gingival inflammation when ST is moved to a new site. At day 0 habitual ST placement sites exhibited a significantly (P < 0.05) higher GI compared to non-tobacco placement sites. Following transfer of ST to a new placement site, 48 hour GI scores were increased (P < 0.05) at this region. Although GCF parameters were not significantly altered, over 80% of the subjects developed dramatic inflammatory reactions in the alveolar mucosa, ranging from erythema to ulceration, at the new site of placement. This observation of a more severe response in alveolar mucosa compared to gingiva may be related to the physical location of ST or differences in tissue characteristics.

Adult↗

The effects of scaling procedures on epithelial cell growth on titanium surfaces.

This study examined in vitro epithelial cell growth on titanium surfaces which had been instrumented by 3 types of periodontal curets. Commercially pure titanium discs were uniformly scaled using plastic, stainless steel, or gold-coated curets and then seeded with a microdot (50,000 cells per 10 microliters) of rat gingival epithelial cells. After 5 days of growth, epithelial cell surface area (mm2) coverage was measured on photographed specimens using a computer digitizing system. Scanning electron microscopic evaluation showed a denser central core of cellular growth on the stainless steel-treated surfaces as compared to the other surface treatments. Epithelial surface area coverage on the stainless steel, plastic, and control groups did not vary significantly among groups. However the gold-coated curet exposed surfaces supported significantly less epithelial growth than the stainless steel and control surfaces. A better understanding of in vitro epithelial cell responses to different titanium surface characteristics will assist in designing implant scaling procedures which allow maintenance of the implant perimucosal seal.

Animals↗

Prostaglandin E (PGE) and interleukin-1 beta (IL-1 beta) levels in gingival crevicular fluid during human orthodontic tooth movement.

The purpose of this study was to examine gingival crevicular fluid (GCF) levels of two potent bone resorbing mediators, prostaglandin E (PGE) and interleukin-1 beta (IL-1 beta), during human orthodontic tooth movement. The study included 10 patients, each having one treatment tooth undergoing orthodontic movement and a contralateral control tooth. The GCF was sampled at control sites and treatment (compression) sites before activation and a 1, 24, 48, and 168 hours. Prevention of plaque-induced inflammation allowed this study to focus on the dynamics of mechanically stimulated PGE and IL-1 beta GCF levels. The PGE and IL-1 beta levels were determined with radioimmunoassay. At 1 and 24 hours, mean GCF IL-1 beta levels were significantly elevated at treatment teeth (8.9 +/- 2.0 and 19.2 +/- 6.0 pg, respectively) compared with control teeth (2.0 +/- 1.1 pg, p = 0.0049, and 2.9 +/- 1.0 pg, p = 0.0209, respectively). The GCF levels of PGE for the treatment teeth were significantly higher at 24 and 48 hours (108.9 +/- 11.9 and 97.9 +/- 7.3 pg) than the control teeth (61.8 +/- 7.2 pg, p = 0.0071, and 70.8 +/- 7.4 pg, p = 0.0021, respectively). The GCF levels of PGE and IL-1 beta remained at baseline levels throughout the study for the control teeth, whereas significant elevations from baseline in GCF IL-1 beta (24 hours) and PGE levels (24 and 48 hours) were observed over time in the treatment teeth (p < or = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

The effect of smoking on the response to periodontal therapy.

This study evaluated the effect of smoking on the clinical response to non-surgical and surgical periodontal therapy. 74 adult subjects with moderate to advanced periodontitis were treated according to a split-mouth design involving the following treatment modalities: coronal scaling, root planing, modified Widman surgery, and flap with osseous resectional surgery. Clinical parameters assessed included probing depth, probing attachment level, horizontal attachment level in furcation sites, recession, presence of supragingival plaque and bleeding on probing. Data were collected: initially, 4 weeks following phase-I therapy, 10 weeks following phase-II therapy and on a yearly basis during 6 years of maintenance care. Data analysis demonstrated that smokers exhibited significantly less reduction of probing depth and less gain of probing attachment level when compared to non-smokers immediately following active therapy and during each of the 6 years of maintenance (p < 0.05). A greater loss of horizontal attachment level was evident in smokers at each yearly exam during maintenance therapy (p < 0.05). There were no differences between groups in recession changes. In general, these findings were true for the outcomes following all 4 modalities of therapy and were most pronounced in the deepest probing depth category (> or = 7 mm). Statistical analysis showed a tendency for smokers to have slightly more supragingival plaque and bleeding on probing. In summary, smokers responded less favorably than non-smokers to periodontal therapy which included 3-month maintenance follow-up.

Adult↗

Effects of nicotine and tobacco-specific nitrosamines on hamster cheek pouch and gastric mucosa.

Fifty-two hamsters were divided into 6 groups and their cheek pouches treated with either 0.01% NNN, 0.01% NNN and 6% nicotine, 0.01% NNK, 0.01% NNK and 6% nicotine, 6% nicotine, or sesame oil. After painting each pouch 3 times per week for 13 months, the animals were killed and specimens from the cheek pouch and forestomach examined. Cheek pouch epithelium showed more frequent histologic changes, including hyperplasia, hyperkeratosis and, in one animal, moderate dysplasia, when nicotine was combined with NNN than after treatment with NNN (or nicotine) alone. There was a higher frequency of hyperplasia with hyperkeratosis in the forestomach when nicotine was combined with NNK than following NNK, or nicotine treatment alone, and squamous cell papillomas were evident in animals treated with both NNK and nicotine. These results suggest that in mucosal tissues nicotine may enhance the effect of weak carcinogens such as the nitrosamines.

Animals↗

Prostaglandin E2 and interleukin-1 levels in smokeless tobacco-induced oral mucosal lesions.

Inflammatory mediators released as a result of smokeless tobacco (ST)-induced irritation may play a role in the development of oral mucosal lesions at habitual tobacco placement sites in ST users. The present study examined levels of interleukin-1 (IL-1) and prostaglandin E2 (PGE2) in ST-induced mucosal lesions and compared these to mediator levels in clinically normal mucosa. Soft tissue biopsies were obtained from white mucosal lesions at habitual placement sites and normal alveolar mucosal tissue at non-placement sites in 18 ST users. Fifteen non-tobacco using subjects also provided normal alveolar mucosal biopsies. IL-1 and PGE2 were recovered from the specimens, and mediator levels were determined by enzyme immunoassay. Prostaglandin E2 levels (pg/mg) were lower in both regions in the ST subjects, but values did not vary significantly between the regions with 2.77 +/- 0.72 and 2.86 +/- 0.99 at placement and non-placement sites, respectively, in ST users and 7.31 +/- 3.84 in non-tobacco users. Both IL-1 alpha and IL-1 beta (pg/mg) were significantly (p < 0.01) elevated in ST lesions (IL-1 alpha = 25.56 +/- 4.00; IL-1 beta = 7.76 +/- 1.68) compared to either non-placement sites in ST users (IL-1 alpha = 14.64 +/- 2.65; IL-1 beta = 1.63 +/- 0.72) or non-tobacco users (IL-1 alpha = 12.84 +/- 2.60; IL-1 beta = 2.04 +/- 0.75). In view of IL-1's role in keratinocyte proliferation and its inflammatory effects, this cytokine may contribute to mucosal and gingival alterations observed in ST users.

Adult↗

Smokeless tobacco effects on monocyte secretion of PGE2 and IL-1 beta.

The use of smokeless tobacco (ST) products is associated with mucosal lesions, gingival recession, and attachment loss at the site of tobacco placement. Monocytes/macrophages are primary producers of PGE2 and IL-1 beta, inflammatory mediators which are thought to play a role in the destruction of the periodontium. The purpose of this study was to determine the effect of ST alone and in combination with a major stimulator of inflammation, bacterial lipopolysaccharide (LPS), on monocyte secretion of these mediators. Peripheral blood monocytes (PBM) were isolated by counterflow centrifugal elutriation from 15 healthy donors who were non-ST users. PBM were incubated for 24 hours in RPMI 1640 containing various concentrations of ST (0%, 0.005%, 0.01%, 1%) with or without 10 micrograms/ml LPS (Porphyromonas gingivalis LPS or Escherichia coli LPS). Of the ST preparations, only 1% ST resulted in PBM mediator secretion (7.7 +/- 2.0 ng/ml for PGE2 and 1.3 +/- 0.2 ng/ml for IL-1 beta) above that of control (unstimulated) cultures. Furthermore, the combination of 1% ST and LPS resulted in a potentiation of PGE2 release (5-fold for E. coli LPS + 1% ST and 10-fold for P. gingivalis LPS + 1% ST; P < 0.0001, one-way ANOVA) relative to the LPS preparations alone. In contrast, PBM IL-1 beta release decreased more than 2-fold upon E. coli LPS and 1% ST exposure, relative to treatment with E. coli LPS alone (P < 0.0001, one-way ANOVA).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Functional requirements of a computer-based patient record system.

The installation of a computer-based patient record system represents a substantial capital investment, but the system can help provide higher quality health care at significantly lower cost. This article examines the functional requirements of such a system, as well as the steps required for implementation.

Cost Allocation↗

Measurement of blood flow in the skin and oral mucosa of the rhesus monkey (Macaca mulatta) using laser Doppler flowmetry.

1. It is generally assumed that oral blood flow is higher than that of skin, and invasive methods to measure blood flow support this view. 2. However, it was not known whether this finding would be confirmed by laser Doppler flowmetry, which is a noninvasive method to measure blood flow. 3. The purpose of this study was to compare blood flow in oral and skin regions of the rhesus monkey using laser Doppler flowmetry. 4. The results demonstrated that blood flow was significantly higher in oral regions as compared to facial skin (P < 0.05). 5. This finding is most likely related to the more abundant capillary supply in oral mucosa as compared to skin.

Animals↗

Measurement of blood flow to osseous tissue in dogs using the radiolabelled microsphere method.

1. The purpose of this study was to examine bone blood flow in various intra- and extra-oral sites. 2. The radiolabelled microsphere method was utilized to assess osseous blood flow in the following regions of 10 dogs: rib, long bone, and anterior and posterior regions of the maxilla and mandible. 3. Samples of cancellous and cortical bone were also obtained from each of these regions with the exception of the maxilla and the anterior mandible. 4. Mean blood flow ranged from 3.71 +/- 0.81 (SE) ml min.-1 100 g-1 in the mandibular posterior cortical bone to 22.7 +/- 4.66 ml min-1 100 g-1 in the cancellous rib samples. 5. Blood flow to the cancellous tissue of the rib was significantly greater (P < 0.05) than the other tissues with the exception of maxillary posterior bone and cortical rib. 6. Results from this study indicate that blood flow to the maxillary posterior bone is relatively high, but blood flow in other intraoral osseous sites is significantly less than that of cancellous rib bone.

Animals↗