Biomedical subjects

G K Johnson

Publications and source records attributed to G K Johnson.

At least 19 recordsLinked to original sources

PubMed2002

Subcellular localization of beta-catenin in malignant cell lines and squamous cell carcinomas of the oral cavity.

BACKGROUND: Beta-catenin, an E-cadherin-associated protein involved in cell-cell adhesion and signaling, has been hypothesized to translocate to the nucleus and activate transcription in several human cancers, including oral squamous cell carcinomas (OSCC). METHODS: In the present study, we analyzed the subcellular localization of beta-catenin in cultures of human oral normal and malignant (cell lines SCC15 and SCC25) keratinocytes and in 24 frozen samples of oral squamous cell carcinomas by a double-staining technique for nucleic acids and beta-catenin. Growth potential, as assessed by cell count at different time periods, was established for normal, SCC15 and SCC25 cell lines; oral squamous cell carcinomas were classified according to the histopathological and malignancy indexes. RESULTS: Beta-catenin localized at the plasma membrane in the normal and SCC15 cells, not in the SCC25 cells, where it localized mostly in the perinuclear and nuclear areas. In the growth assays, SCC25 cell lines proliferated faster than in normal and SCC15 cells over a period of 6 days (cell numbers were significantly different, P < 0.0001). Carcinoma sections showed a combination of membranous, cytoplasmic and, in few invading epithelial islands of two tumors, nuclear localization of beta-catenin. CONCLUSIONS: In oral squamous cell carcinomas, nuclear beta-catenin staining was observed only within invading islands of two carcinomas deep in the underlying connective tissue. On the basis of this study, we conclude that intranuclear beta-catenin does not appear to be a common finding in oral squamous cell carcinomas and that a clear association between intranuclear beta-catenin and histopathological and malignancy indexes in vivo could not be established.

Adolescent↗

PubMed2001

Discovery of new human beta-defensins using a genomics-based approach.

Epithelial beta-defensins are broad-spectrum cationic antimicrobial peptides that also act as chemokines for adaptive immune cells. In the human genome, all known defensin genes cluster to a <1 Mb region of chromosome 8p22-p23. To identify new defensin genes, the DNA sequence from a contig of large-insert genomic clones from the region containing human beta-defensin-2 (HBD-2) was analyzed for the presence of defensin genes. This sequence survey identified a novel beta-defensin, termed HBD-3. The HBD-3 gene contains two exons, is located 13 kb upstream from the HBD-2 gene, and it is transcribed in the same direction. A partial HBD-3 cDNA clone was amplified from cDNA derived from IL-1beta induced fetal lung tissue. The cDNA sequence encodes for a 67 amino acid peptide that is approximately 43% identical to HBD-2 and shares the beta-defensin six cysteine motif. By PCR analysis of two commercial cDNA panels, HBD-3 expression was detected in adult heart, skeletal muscle, placenta and in fetal thymus. From RT-PCR experiments, HBD-3 expression was observed in skin, esophagus, gingival keratinocytes, placenta and trachea. Furthermore, in fetal lung explants and gingival keratinocytes, HBD-3 mRNA expression was induced by IL-1beta. Additional sequence analysis identified the HE2 (human epididymis secretory protein) gene 17 kb upstream from the HBD-3 gene. One splice variant of this gene (HE2beta1) encodes a beta-defensin consensus cysteine motif, suggesting it represents a defensin gene product. HE2beta1 mRNA expression was detected in gingival keratinocytes and bronchial epithelia using RT-PCR analysis. The discovery of these novel beta-defensin genes may allow further understanding of the role of defensins in host immunity at mucosal surfaces.

Adult↗

PubMed2001

Periodontal disease in pregnancy complicated by type 1 diabetes mellitus.

BACKGROUND: Systemic disease and hormonal changes have been implicated as complicating factors for periodontal disease. Diabetes has been identified as a risk factor for periodontal disease, and diabetics can experience periodontal destruction at an earlier age than non-diabetic individuals. Increased hormone levels during pregnancy can contribute to increased gingival inflammation. The purpose of this study was to examine the association of type 1 diabetes mellitus (DM) on the periodontal status of pregnant women. METHODS: Thirty-three (13 diabetic and 20 non-diabetic) subjects, 20 to 39 weeks gestation, participated in this study. The mean age of the diabetics and non-diabetics was 28.5 +/- 7.1 (SD) and 27.0 +/- 7.3 years, respectively. The following parameters were assessed at Ramfjord's reference teeth: plaque index (PI), gingival inflammation (GI), probing depth (PD), gingival margin (GM) location, and clinical attachment level (CAL). RESULTS: Diabetic subjects had significantly (P<0.001) higher PI (1.48 +/- 0.69) and GI (1.77 +/- 0.44) scores than non-diabetics (PI = 0.63 +/- 0.38; GI = 0.93 +/- 0.48). Mean PD for diabetics (2.95 +/- 0.69 mm) was significantly different (P<0.024) from that of non-diabetics (2.44 +/- 0.32 mm). Although mean GM location was coronal to the cemento-enamel junction (CEJ) in both groups, gingival margins were at a more apical position (P<0.001) in the diabetics (-0.20 +/- 1.24 mm) compared to non-diabetics (-1.76 +/- 0.53 mm). Mean CAL values also varied significantly (P<0.001) between diabetics (2.60 +/- 1.54 mm) and non-diabetics (0.68 +/- 0.65 mm). Significant differences were seen for GI (P<0.001), PD (P=0.005), GM location (P<0.001), and CAL (P<0.001) when assessing the effect of diabetes and controlling for plaque. When assessing the effect of plaque and controlling for diabetes, the only significant difference was GI (P=0.001). CONCLUSIONS: The results of this study demonstrate that periodontal inflammation and destruction are increased in pregnant diabetics as compared to non-diabetic pregnant patients. These findings may have implications for diabetic control and, hence, maternal and fetal outcomes in pregnant diabetic patients.

Adult↗

PubMed2001

Treatment of periodontitis by local administration of minocycline microspheres: a controlled trial.

BACKGROUND: Periodontitis is an inflammatory condition of tooth-supporting tissues that is usually treated by mechanical removal of plaque and microorganisms that adhere to teeth. This treatment, known as scaling and root planing, is not optimally effective. Adjunctive therapy with locally delivered antimicrobials has resulted in improved clinical outcomes such as probing depth reduction. This article reports on the efficacy and safety of locally administered microencapsulated minocycline. METHODS: Seven hundred forty-eight (748) patients with moderate to advanced periodontitis were enrolled in a multi-center trial and randomized to 1 of 3 treatment arms: 1) scaling and root planing (SRP) alone; 2) SRP plus vehicle; or 3) SRP plus minocycline microspheres. The primary outcome measure was probing depth reduction at 9 months. Clinical assessments were performed at baseline and 1, 3, 6, and 9 months. RESULTS: Minocycline microspheres plus scaling and root planing provided substantially more probing depth reduction than either SRP alone or SRP plus vehicle. The difference reached statistical significance after the first month and was maintained throughout the trial. The improved outcome was observed to be independent of patients' smoking status, age, gender, or baseline disease level. There was no difference in the incidence of adverse effects among treatment groups. CONCLUSIONS: Scaling and root planing plus minocycline microspheres is more effective than scaling and root planing alone in reducing probing depths in periodontitis patients.

Administration, Topical↗

PubMed2001

Impact of tobacco use on periodontal status.

This article reviews the effects of smoked and smokeless tobacco on periodontal status, including the impact of smoking on periodontal therapy and potential mechanisms for the adverse effects of tobacco on the periodontium. Approximately half of periodontitis cases have been attributed to either current or former smoking. Both cigar and cigarette smokers have significantly greater loss of bone height than nonsmokers, and there is a trend for pipe smokers to have more bone loss than nonsmokers. Unlike smokers, who experience widespread periodontal destruction, the most prevalent effects of smokeless tobacco are localized to the site of placement, in the form of gingival recession and white mucosal lesions. Smoking has an adverse effect on all forms of periodontal therapy, and up to 90 percent of refractory periodontitis patients are smokers. The pathogenesis of smoking-related periodontal destruction has been attributed to alterations in the microflora and/or host response. Some data indicates that smoking may increase levels of certain periodontal pathogens, but there is more evidence that smoking has a negative effect on host response, such as neutrophil function and antibody production. An encouraging finding is that periodontal disease progression slows in patients who quit smoking and that these individuals have a similar response to periodontal therapy as nonsmokers. The facts presented in this paper will assist dental health professionals in treatment-planning decisions and provide them with important information to share with patients who use tobacco products.

Disease Susceptibility↗

PubMed1999

Clinical presentation and short-term outcome of endoscopic therapy of patients with symptomatic incomplete pancreas divisum.

BACKGROUND: The clinical significance of incomplete pancreas divisum (IPD) has not been fully described. In this study we report the clinical presentation and results of endoscopic treatment of the 32 (0.6%) patients with IPD seen at our center over a 10-year period. METHODS: The study population consisted of 24 women and 8 men (mean age 42 years, range 13 to 82 years). Ten (31%) patients presented with acute recurrent pancreatitis, 5 (16%) with chronic pancreatitis, and 3 (9%) with pancreatic type pain. Detailed history, laboratory tests, US, CT, and ERCP excluded other etiologies for their symptoms. The remaining 14 (44%) presented with biliary problems. The 18 symptomatic patients with IPD were treated as follows: 8 received dorsal duct stents, 3 underwent minor papilla endoscopic sphincterotomy and dorsal duct stent placement, 4 had minor papilla dilatation only, and 3 had ventral duct stents placed. RESULTS: Patients were then followed for recurrence of pancreatitis and pancreatic-type pain. Mean follow-up was 15.5 months (range 3 to 30 months). Six (60%) of the patients with acute recurrent pancreatitis and 4 (80%) with chronic pancreatitis benefitted from the endoscopic therapy. However, only 1 (33%) of the patients with pancreatic-type pain benefitted. CONCLUSION: The clinical presentation and response to endoscopic therapy of patients with ICP appeared to be similar to that of patients with complete pancreas divisum.

Abdominal Pain↗

PubMed1999

Differential DNA methylation of the p16 INK4A/CDKN2A promoter in human oral cancer cells and normal human oral keratinocytes.

The p16 INK4A tumor suppressor gene participates in establishing and maintaining the malignant phenotype of a variety of cancer cell lines and primary tumors. Recently it has been observed that p16 expression is lost in oral cavity cancer cell lines in the presence of a normal intact gene. To examine the role of DNA methylation as an explanation for these findings, we analyzed the DNA methylation patterns of the p16 INK4A promoter in DNA isolated from primary cultures of normal human oral keratinocytes and squamous cell carcinoma (SCC-15) oral cancer cells using bisulfite genomic sequencing. Our results demonstrated striking differences in the methylation status of the 5' CpG island of the p16 gene between normal and cancer cells. Normal human oral keratinocytes showed practically no methylation of the p16 INK4A promoter, while SCC-15 oral cancer cells showed almost complete methylation in this region. These data implicate DNA methylation as a mechanism for transcriptional silencing of the p16 INK4A gene in oral cancer cells.

Cyclin-Dependent Kinase Inhibitor p16↗

PubMed1999

Production of beta-defensin antimicrobial peptides by the oral mucosa and salivary glands.

beta-Defensins are cationic peptides with broad-spectrum antimicrobial activity that are produced by epithelia at mucosal surfaces. Two human beta-defensins, HBD-1 and HBD-2, were discovered in 1995 and 1997, respectively. However, little is known about the expression of HBD-1 or HBD-2 in tissues of the oral cavity and whether these proteins are secreted. In this study, we characterized the expression of HBD-1 and HBD-2 mRNAs within the major salivary glands, tongue, gingiva, and buccal mucosa and detected beta-defensin peptides in salivary secretions. Defensin mRNA expression was quantitated by RNase protection assays. HBD-1 mRNA expression was detected in the gingiva, parotid gland, buccal mucosa, and tongue. Expression of HBD-2 mRNA was detected only in the gingival mucosa and was most abundant in tissues with associated inflammation. To test whether beta-defensin expression was inducible, gingival keratinocyte cell cultures were treated with interleukin-1beta (IL-1beta) or bacterial lipopolysaccharide (LPS) for 24 h. HBD-2 expression increased approximately 16-fold with IL-1beta treatment and approximately 5-fold in the presence of LPS. Western immunoblotting, liquid chromatography, and mass spectrometry were used to identify the HBD-1 and HBD-2 peptides in human saliva. Human beta-defensins are expressed in oral tissues, and the proteins are secreted in saliva; HBD-1 expression was constitutive, while HBD-2 expression was induced by IL-1beta and LPS. Human beta-defensins may play an important role in the innate defenses against oral microorganisms.

3T3 Cells↗

PubMed1998

The role of surveillance endoscopic retrograde cholangiopancreatography in preventing episodic cholangitis in patients with recurrent common bile duct stones.

BACKGROUND AND STUDY AIMS: Approximately 2-7% of patients who have undergone previous removal of bile duct stones have recurrence often presenting as ascending cholangitis. The aim of this study was to identify the incidence, clinical presentation, and objective findings in this group of patients. Additionally, the effect of surveillance endoscopic retrograde cholangiopancreatography (ERCP) in preventing cholangitis, was studied. PATIENTS AND METHODS: Two thousand and ninety-six patients who underwent ERCP for cholelithiasis were studied with 45 of these patients being identified as having recurrent common bile duct stones. Of the 45, 13 had two or more recurrences without having any obvious predisposing factors. The mean age of the 13 patients was 57 years. The characteristics of 13 patients were reviewed, including sphincterotomy size, liver function tests, and contrast drainage time. RESULTS: All 13 patients with recurrent stones presented with ascending cholangitis. Stones were found to be soft, brown and accompanied by a large amount of sludge. The common bile duct in all 13 patients was noted to be dilated and had notable, widely patent sphincterotomes. There was significant delayed drainage in 77% of these patients. Yearly surveillance ERCPs were performed in the 13 patients, the incidence of acute cholangitis episodes per patient decreased from 2 to 0.6 with a four-year follow-up. CONCLUSION: In a subgroup of patients with multiple common bile duct stone recurrences, annual surveillance ERCP with stone removal decreases the incidence of recurrent episodes of ascending cholangitis as well as its associated morbidity and mortality.

Adult↗

PubMed1998

Development of smokeless tobacco-induced oral mucosal lesions.

This study examined clinical and inflammatory mediator parameters during the development of snuff-induced mucosal lesions. Nineteen smokeless tobacco (ST) users placed moist snuff at designated new placement sites over either a 2- or 7-day period. By day 2, the predominant clinical alteration was an erythematous reaction, and one-third of the subjects demonstrated white striations in combination with erythema or ulceration. By 7 days, 56% of the subjects displayed white striated lesions. Tissue concentrations (pg/mg) of IL-1beta were 4.6+/-1.6 at new placement sites as compared with 0.7+/-0.4 at control sites (P<0.05). PGE2 and IL-1alpha concentrations also were significantly higher (P<0.05) at new placement sites as compared with control sites (9.4+/-2.2 vs 4.1+/-0.7 and 6.2+/-1.3 vs 3.2+/-0.7, respectively). In view of the recognized role of PGE2 and IL-1 in immune and inflammatory functions, these mediators may play a role in the pathogenesis of clinical alterations at ST placement sites.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

PubMed1998

Histological alterations following short-term smokeless tobacco exposure in humans.

The purpose of this study was to investigate the histological changes following short-term smokeless tobacco application in humans. Sixteen smokeless tobacco-using subjects participated in this trial. Each subject had used at least 3 cans of snuff per week for the previous 2 yr and had an existing lesion at the site of habitual snuff placement. The experimental design included subject placement of moist snuff (University of Kentucky reference tobacco brand 1S3) at a new site in the mandibular arch. At either 2 or 7 d, biopsies were taken from the new lesions and from a non-placement site in the opposing arch. The volume density of inflammatory cells was determined by point counting. Keratin and epithelial thickness were evaluated by digitizing morphometry. Data were analyzed by repeated measures analysis of variance. In 7-d lesions, increased keratin thickness was observed at the new sites compared to the non-placement sites (p = 0.05). Increased volume density of fibroblasts (p = 0.027) and decreased volume densities of macrophages (p = 0.0083) and mast cells (p = 0.05) were observed at 2 d in new versus non-placement sites. Clinically, the new sites showed erythema, erythema plus ulceration, or white striations. This study demonstrated histological and clinical changes at new snuff placement sites in as few as 2-7 d, underscoring the rapidity of tissue alterations following snuff use.

Adult↗

PubMed1997

Evaluation of post-ERCP pancreatitis: potential causes noted during controlled study of differing contrast media. Midwest Pancreaticobiliary Study Group.

BACKGROUND: Possible sources of post-ERCP pancreatitis were evaluated during a prospective, randomized, controlled study comparing different contrast media. METHODS: A total of 1979 patients were randomized and subdivided into groups during the study. Patients were grouped for comparison depending on the type of procedure performed during ERCP. Diagnostic patients studied with pancreatograms (Group I) were compared with other groups, specifically, those not studied with pancreatograms (Group IV). All patients had subjective and objective estimates of the difficulty in cannulation of both ducts. The incidence of postprocedural pancreatitis was compared between and within each group. RESULTS: In Group I there was a progressively higher incidence of pancreatitis with increased numbers of pancreatic duct injections. Patients with the highest (19.5%) frequency of pancreatitis received 10 or more injections into the pancreatic duct. Group I cases with difficult common bile duct cannulations had a higher frequency of post-ERCP pancreatitis (9.5%), as compared with the entire group (5.6%). CONCLUSIONS: There was a higher incidence of pancreatitis associated with increased manipulation around the papillary orifice, especially with multiple pancreatic duct injections. There was also a slightly higher incidence of post-ERCP pancreatitis in cases with difficult common bile duct cannulation. Endoscopists are encouraged to evaluate and develop safer cannulation techniques that minimize the number of injections into the pancreatic duct and enhance selective cannulation.

Catheterization↗

PubMed1997

Effect of nicotine on arachidonic acid metabolites and epithelial parameters in rat oral mucosa.

This study examined the effects of nicotine on oral mucosal levels of eicosanoids and on histologic parameters, including keratinocyte proliferation. Surgically-created canals in the mandibular lips of 20 male Sprague Dawley rats received either nicotine or saline in a cotton pellet twice daily for six weeks. Thromboxane B2 (TxB2) levels were depressed (P < 0.05) in nicotine treated tissues compared to saline treatment (5.8 +/- 1.0 vs 13.4 +/- 2.1 pg/mg). Within the nicotine group, TxB2 concentrations were lower (P < 0.05) at the nicotine site compared to the posterior site (18.3 +/- 5.4 pg/mg). There was also a trend towards reduced 6-keto-PGF1 alpha in the nicotine-treated tissues compared to saline-exposed sites. These alterations in cyclooxygenase metabolites were not accompanied by changes in epithelial proliferation or histologic parameters. 12(S)-hydroxyeicosatetranoic acid (12-HETE) and leukotriene B4 (LTB4) were not affected by nicotine. Therefore, nicotine may not be directly responsible for the hyperplasia at habitual tobacco placement sites, but may contribute to alterations in cyclooxygenase products of arachidonic acid metabolism.

6-Ketoprostaglandin F1 alpha↗

PubMed1997

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↗

PubMed1996

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↗

PubMed1996

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↗

PubMed1996

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↗

PubMed1995

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↗