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M I Ryder

Publications and source records attributed to M I Ryder.

At least 19 recordsLinked to original sources
PubMed2004

Alteration of gene expression profiles of peripheral mononuclear blood cells by tobacco smoke: implications for periodontal diseases.

Alterations of the host response by tobacco smoke adversely affect the periodontium. In this study, we examined the effects of in vitro acute smoke exposure on changes in m-RNA expression of primary peripheral mononuclear blood cells through microarray analysis. Mononuclear blood cells were isolated from four healthy non-smokers and plated in culture wells. Half of the cells were then exposed to 5 min of tobacco smoke. Fluorescent c-DNA probes were prepared from the linearly amplified m-RNAs for each sample and hybridized to cDNA microarrays representing approximately 30000 human genes. Significant increases or decreases in m-RNA gene expression between non-smoke-exposed and smoke-exposed samples were identified by permutation t-test, as implemented by the Significance Analysis of Microarrays software package. After smoke exposure, the expression of 90 genes with known function was significantly elevated and the expression of 19 genes with known function was significantly depressed. In addition, 18 upregulated and 26 downregulated transcripts were expressed sequence tags with little information available on function. Approximately 20 of the significantly elevated genes had previously been reported in the literature to be associated with periodontal pathogenesis (fold changes in parentheses). These included plasminogen activator (4.4), Heat Shock Protein (Hsp) 40 kD (2.2), thrombomodulin (4.2), cytochrome c (1.8), COX-2 (2.6), interleukin-1a (1.4), chemokine ligand 1 (3.8), cathepsin L (2.0), and calgranulin A (2.1). In addition, several significantly elevated genes not previously reported in the literature may also play a role in periodontal pathogenesis, and thus warrant further investigation. These include Diphtheria toxin receptor (heparin-binding epidermal growth factor-like growth factor) (7.8), Hsp 10 kDa (1.7), Hsp 105 kD (2.1), Hsp 70 kDa (1.6), and mitogen activated protein kinase 3 (1.5). Among the significantly depressed genes that may play a protective or destructive role in periodontal pathogenesis were interferon gamma receptor 2 (0.58) and chemokine receptor 2 (0.24). Our results may be of use in the search for the molecular mechanisms for the adverse effects of tobacco smoke on the host response.

Adult↗
PubMed2002

Effects of tobacco smoke on the secretion of interleukin-1beta, tumor necrosis factor-alpha, and transforming growth factor-beta from peripheral blood mononuclear cells.

Alterations of the host response caused by short-term exposure to high levels of smoke during the act of smoking (acute smoke exposure) as well as long-term exposure to lower levels of tobacco substances in the bloodstream of smokers (chronic smoke exposure) may play a role in the pathogenesis of periodontal diseases in smokers. In this study, we examined the secretion of three cytokines [interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, and transforming growth factor (TGF)-beta] from mononuclear blood cells from current smokers and non-smokers exposed to in vitro tobacco smoke (which may be comparable to in vivo acute smoke exposure) and mononuclear blood cells from current smokers not exposed to further in vitro smoke (which may be comparable to chronic smoke exposure). Peripheral blood mononuclear cells were isolated from eight healthy current smokers and eight healthy non-smokers, plated in culture wells, exposed in vitro for 1-5 min to cigarette smoke in a smoke box system or not exposed (baseline controls), and then incubated without further smoke exposure for another 24 h. Supernatants from each well were then collected and assayed for the concentrations of the three cytokines by enzyme-linked immunosorbent assay (ELISA). At baseline, mean IL-1beta levels were higher in smokers than in non-smokers (mean: 10.6 vs. 5.9 pg/ml, anova: P < 0.05). In both smokers and non-smokers, secreted levels of IL-1beta increased from 0 to 5 min of in vitro smoke exposure (mean: 5.9-9.9 pg/ml, t-test: P < 0.05 for non-smokers only) with levels in smokers higher than in non-smokers (P > 0.05). Mean TNF-alpha levels increased from 0 to 2 min of smoke exposure and decreased from 2 to 5 min in smokers and non-smokers, with higher levels in non-smokers than smokers at all time-points (P > 0.05). Mean TGF-beta levels were higher in smokers than in non-smokers at all time-points (mean: 180.5 vs. 132.0 pg/ml, P < 0.05 at 5 min only) with no significant alteration of the pattern of secretion with cigarette smoke exposure. These observed alterations in the secretion of cytokines from mononuclear blood cells in smokers, relative to non-smokers, and with in vitro smoke exposure may play a role in the pathogenesis of periodontal diseases in smokers.

Adult↗
PubMed2001

An economic evaluation of a chlorhexidine chip for treating chronic periodontitis: the CHIP (chlorhexidine in periodontitis) study.

BACKGROUND: The authors previously suggested that an adjunctive, controlled-release chlorhexidine, or CHX, chip may reduce periodontal surgical needs at little additional cost. This article presents an economic analysis of the CHX chip in general dental practice. METHODS: In a one-year prospective clinical trial, 484 chronic periodontitis patients in 52 general practices across the United States were treated with either scaling and root planing, or SRP, plus any therapy prescribed by treating, unblinded dentists; or SRP plus other therapy as above but including the CHX chip. Economic data were collected from bills, case report forms and 12-month treatment recommendations from blinded periodontist evaluators. RESULTS: Total dental charges were higher for SRP + CHX chip patients vs. SRP patients when CHX chip costs were included (P = .027) but lower when CHX chip costs were excluded (P = .012). About one-half of the CHX chip acquisition cost was offset by savings in other charges. SRP + CHX chip patients were about 50 percent less likely to undergo surgical procedures than were SRP patients (P = .021). At the end of the trial, periodontist evaluators recommended similar additional procedures for both groups: SRP, about 46 percent; maintenance, about 37 percent; surgery, 56 percent for SRP alone and 63 percent for SRP + CHX chip. CONCLUSIONS: Adjunctive CHX chip use for general-practice patients with periodontitis increased costs but reduced surgeries over one year. At study's end, periodontists recommended similar additional surgical treatment for both groups. CLINICAL IMPLICATIONS: In general practice, routine use of the CHX chip suggests that costs will be partially offset by reduced surgery over at least one year.

Adult↗
PubMed2000

Periodontal management of HIV-infected patients.

Recognition and diagnosis of the general oral manifestations and specific periodontal manifestations of HIV infection will continue to be a major responsibility of the dental practitioner. The dental team needs to understand the underlying principles of care for the necrotizing and inflammatory periodontal changes associated with HIV. In addition, the practitioner must take into consideration how the presence of opportunistic infections in the periodontium such as Candida as well as the patient's level of immunosuppression may affect conventional approaches to the common forms of periodontal diseases. By combining local and systemic therapy aimed at both preventing and treating oral lesions and periodontal diseases, combined with new systemic antiviral and vaccine therapies, dental and medical practitioners may together help reduce both the dental morbidity and the overall patient morbidity in the HIV infected patient.

AIDS-Related Opportunistic Infections↗
PubMed1999

Effects of smoking on local delivery of controlled-release doxycycline as compared to scaling and root planing.

This paper examines the effects of smoking on the treatment outcomes of two nonsurgical therapies: (1) scaling and root planing alone (SRP) or (2) controlled-release of subgingivally delivered doxycycline hyclate in a polylactic acid based polymer gel. Subjects from 2 9-month multicenter studies were classified as nonsmokers (never smoked: 100 subjects), former smokers (137 subjects), and current smokers (> or = 10 cigarettes/day: 121 subjects). Clinical parameters were analyzed for treated sites with baseline probing depths > or = 5 mm and for a subset of treated sites with baseline probing depths of > or = 7 mm. Clinical parameters (plaque levels, clinical attachment levels, pocket depths, and bleeding on probing) were analyzed at baseline, 4, 6, and 9 months. In the doxycycline treated group in general, there were neither marked significant differences in clinical attachment gain nor differences in probing depth reduction among the 3 smoking groups. On the other hand, in the scaling and root planing treated group in general, there were significant differences in clinical attachment gain and pocket depth reduction, with non-smokers responding better than former smokers and current smokers at 6 and 9 months. These differences in clinical response between scaling and root planing alone versus controlled-release of locally-delivered doxycycline hyclate among these 3 smoking groups are discussed in relation to treatment implications for smokers.

Administration, Topical↗
PubMed1999

Cysteine protease inhibitory activity and levels of salivary cystatins in whole saliva of periodontally diseased patients.

The 3 human salivary cystatins S, SA and SN are multifunctional proteins that possess a cysteine protease inhibitory property, but their ability to act as such is very different (SN > SA >> S). One form, S, also appears to possess antibacterial properties towards the bacterium Porphyromonas gingivalis, often associated with periodontal diseases. In this study we measured the total cystatin inhibitory activity and the levels of each salivary cystatin in the whole saliva of 8 periodontally diseased patients and 2 groups of control subjects (n = 6 and n = 10). The total cystatin inhibitory activity and the total salivary cystatin concentration in the periodontally diseased patients were found to be lower than the controls (p < or = 0.005). The concentration of S was depleted to levels that would not allow it to be an effective antibacterial agent, and the concentration of SA, although depleted in some cases, was still present at sufficient levels to allow it to act as an effective physiological inhibitor of cathepsin L. The concentration of cystatin SN was also depleted in the periodontally diseased patients, but was still present in sufficient quantities to act as an effective physiological cysteine protease inhibitor of cathepsins H and L. In comparison, the concentration of all 3 salivary cystatins in the control subjects were sufficient to enable these proteins to be both effective physiological cysteine protease inhibitors and antibacterial agents.

Adult↗
PubMed1998

Alterations of neutrophil L-selectin and CD18 expression by tobacco smoke: implications for periodontal diseases.

Alterations in neutrophil functions by both chronic low levels of tobacco and by acute short-term higher levels of tobacco smoke, as encountered during the act of smoking, may play a role in the pathogenesis of periodontal diseases in smokers. Among the early migration events of neutrophil function is the alteration in surface expression of L-selectin and the CD11/18 integrins. In the present study we examined the effect of in vitro smoke exposure and nicotine alone on the expression of these 2 adhesion molecules in neutrophils from smokers and non-smokers. We also determined the physiological relevance of this in vitro system by assessing the levels of nicotine exposure in this in vitro system and comparing these levels to acute and chronic levels of nicotine in saliva and gingival crevicular fluid. Peripheral neutrophils were isolated from the blood of smokers (> 1 pack/d) and non-smokers and incubated in vitro with either cigarette smoke (0-5 min), 10(-7) M F-met-leu-phe, or nicotine alone at 1.62 mg/ml to 162 ng/ml (10(-2) M-10(-6) M). The neutrophils were then incubated with fluoresceine conjugated anti-Leu8 (L-selectin), anti-CD18 (CD18 integrin), or gamma-4 (non-specific control), fixed and analyzed by flow cytometry. With cigarette smoke exposure, there was an approximate 75% shedding of L-selectin in both smokers and non-smokers with no marked difference between groups at 1-5 min of smoke exposure. Cigarette smoke exposure resulted in a 15-20% increase in CD18 expression in both smokers and non-smokers. At all time points, there was slightly greater but statistically insignificant expression of CD18 integrin in non-smokers when compared to smokers. These patterns of CD18 increases and L-selectin shedding were similar in magnitude to incubations with 10(-7) M F-met-leu-phe. Acute smoke exposure resulted in elevation of nicotine in the smoke box to 529 ng/ml at 5 min, in saliva from 109.2 ng/ml before smoking to 1821.4 ng/ml after smoking, and in gingival crevicular fluid to 5961 ng/ml after smoking. No significant alterations in L-selectin or CD18 expression were noted with in vitro nicotine from 1.62 mg/ml to 162 ng/ml.

Adult↗
PubMed1998

Alterations of neutrophil oxidative burst by in vitro smoke exposure: implications for oral and systemic diseases.

Alterations of neutrophil functions by tobacco products may play a central role in the pathogenesis of periodontal diseases and several smoking-related systemic diseases. In the present study, we examined the in vitro effects of cigarette smoke on neutrophils at times and concentrations that may be encountered during smoke exposure. We measured the level of smoke exposure in the in vitro system by measuring the levels of nicotine and comparing these to levels in the oral cavity in smokers before and after smoking. We examined both the unstimulated and stimulated release of 2 oxidative burst products: superoxide (O-2) and hydrogen peroxide (H2O2). Salivary washings were collected from 7 smokers (> 1 pack/day) before smoking a cigarette. Immediately after they smoked a cigarette, a second set of washings was collected. In vitro exposure to smoke involved incubating aliquots of neutrophils in phosphate-buffered saline for 1 to 5 minutes. Nicotine and cotinine levels were quantitated using gas chromatography, with detection by electron impact mass spectrometry. Peripheral neutrophils were isolated from medically healthy non-smoking volunteers via a double-density gradient technique and incubated in vitro with whole cigarette smoke for 0 to 5 minutes. Phorbol myristate acetate (PMA; 10(-7) M) was used to stimulate half of the cell aliquots. Superoxide generation was assessed through the superoxide dismutase (SOD) inhibitable reduction of ferricytochrome c. H2O2 production was assessed through the H2O2-dependent breakdown of dichlorofluorescin diacetate to its fluorophore and measured by flow cytometry. There was a marked elevation in salivary nicotine concentration from before smoking (mean: 80.8 ng) to after smoking (mean 1,685 ng/mL). In the in vitro smoke box system, there was a time-related elevation in nicotine from 1 to 5 minutes (50-->136 ng/mL). In PMA-stimulated cells exposed to smoke, there was a time-related inhibition of both superoxide and H2O2 production. However, in unstimulated cells exposed to smoke, there was a time-related increase in the release of superoxide and H2O2. A novel finding in unstimulated cells exposed to smoke was that there appeared to be 2 distinct populations of cells--one of "high" H2O2 producers and one of "low" H2O2 producers. The proportion of high H2O2 producers increased relative to smoke exposure. The relative production of H2O2 in the unstimulated high producers was comparable to PMA-stimulated cells at 5 minutes. This release of superoxide and H2O2 in unstimulated cells exposed to smoke may alter the pathogenic processes both in periodontal diseases and other systemic diseases.

Analysis of Variance↗
PubMed1993

Epithelial cell kinetics with atelocollagen membranes: a study in rats.

A recent development in guided tissue regeneration procedures is the use of resorbable membranes, which eliminate the need for subsequent surgical removal. In this study we performed flap surgery in rats with (experimental) or without (control) implantation of one of the newer materials, atelocollagen. We observed the gingival epithelial cell kinetics using 3H-thymidine and examined the extent of gingival epithelium migration. Histological observations at day 1 on the experimental side demonstrated regenerated epithelium apposed to the collagen membrane with an intervening layer of necrotic tissues and/or fibrinous exudate. There was no observable proliferation of regenerated epithelium toward the root apex. On day 14, the regenerated epithelium migrated apically along the treated root surface in the control group. By contrast, on day 14 in the experimental group, the regenerated epithelium contacted the root surface at the cemento-enamel junction (CEJ). Apical to the CEJ, there was new cementum formation with inserting connective tissue fibers. Autoradiographs from day 1 experimental sides demonstrated labeled cells in the basal cell layers from oral, crevicular, and junctional epithelium. From day 1 to day 5, labeling indices of oral epithelium and regenerating crevicular epithelium on experimental sides were lower than on control sides. These histological and autoradiographic findings suggest that atelocollagen membrane inhibits apical migration of regenerating epithelium and accelerates connective tissue reattachment in part by inhibiting the mitotic function of basal epithelial cells in early stages of wound healing.

Animals↗
PubMed1993

Periodontal considerations in the patient with HIV.

The HIV-associated periodontal diseases present unique challenges to the dental practitioner. The presence and severity of HIV-associated gingivitis, HIV-associated periodontitis, and possibly necrotizing ulcerative gingivostomatitis, and other oral lesions may indicate the presence and staging of HIV infection. In general, a similar relationship does not appear to exist between adult periodontitis and HIV staging. There is a wide variation in recent reports on the epidemiology of HIV-associated diseases. These variations point to the need for a standard definition for HIV-associated periodontal diseases using both conventional periodontal evaluation criteria and criteria designed specifically for the characteristics of HIV-associated gingivitis and HIV-associated periodontitis. HIV staging, geographic location of the study, antiviral and antimicrobial therapies, and oral habits may also account for many of these differences. Both the HIV-associated gingivitis and periodontitis lesions have similar microbiologic profiles to adult periodontitis lesions for previously identified periodontopathic bacteria. In addition, these lesions may have a unique opportunistic microflora. The pathogenesis of HIV-associated periodontal diseases may be due to the microflora, the effects of HIV and other viral agents, or alterations in the host response. These factors should be taken into consideration in the treatment and prevention of these HIV-associated periodontal lesions.

CD4-CD8 Ratio↗
PubMed1990

Ammonia as a potential mediator of adult human periodontal infection: inhibition of neutrophil function.

Neutrophils (polymorphonuclear leucocytes) are the principal cell of the host defence system. Consequently, if periodontal pathogen-derived substances in the gingival crevice significantly inhibit their function, they could shift the bacterial-host balance in favour of the bacteria. The hypothesis that ammonia can inhibit neutrophil function was tested. Ammonia was specifically selected because periodontal pathogens produce substantial amounts of ammonia. The findings indicated that ammonia can inhibit neutrophil phagocytosis, degranulation and oxygen metabolism. Ammonia decreased the total number of phagocytosing polymorphonuclear neutrophils (66% of control) and also decreased degranulation (61% of control). Ammonia decreased oxygen metabolism of both resting and stimulated neutrophils (33 and 42% of control, respectively). These observations support the hypothesis that ammonia can inhibit the function of polymorphonuclear leukocytes. They suggest that the presence of ammonia in the gingival crevice may increase the risk of development of periodontal disease.

Adult↗
PubMed1990

Cytokeratin patterns in corneal, limbal, and conjunctival epithelium. An immunofluorescence study with PKK-1, 8.12, 8.60, and 4.62 anticytokeratin antibodies.

The authors examined immunofluorescently the specific cytokeratin staining patterns of corneal, limbal, and conjunctival epithelium with PKK-1, 8.12, 4.62, and 8.60 monoclonal anticytokeratin antibodies. Observations were made on unfixed frozen postmortem human tissue. The PKK-1 antibody stain was observed in all layers of corneal epithelium but only in suprabasal layers of limbal and conjunctival epithelium. By contrast, the 8.12 antibody stain was observed only in the superficial layer of corneal epithelium but through all layers of limbal and conjunctival epithelium. The 4.60 antibody stain was seen in focal areas of corneal and limbal epithelium and through all layers of conjunctival epithelium. The 8.60 antibody stain was not present in the three epithelia. These immunofluorescence studies showed unique cytokeratin patterns among layers in corneal, limbal, and conjunctival epithelium.

Adult↗
PubMed1990

In situ localization of cytoskeletal elements in the human trabecular meshwork and cornea.

The authors compared cytoskeletal elements of the in situ human trabecular-meshwork cell with in situ human corneal cells using indirect immunofluorescence staining for tubulin and intermediate filaments (vimentin, cytokeratin, and desmin) and NBD-phallacidin staining for f-actin using both fixed frozen and unfixed frozen sections from postmortem eyes. Both f-actin and tubulin were found throughout the cell body of trabecular-meshwork cells, keratocytes, corneal endothelium, and corneal epithelium. The f-actin staining pattern was concentrated at the cell periphery of these four cell types. Vimentin stain was intensely localized in focal areas of the trabecular-meshwork cell, keratocytes, and throughout the corneal endothelium. A general anticytokeratin antibody was intensely localized in corneal epithelium and endothelium. However, PKK-1 anticytokeratin antibody was seen only in superficial layers of corneal epithelium and not in corneal endothelium. The 4.62 anticytokeratin antibody was not observed in either corneal epithelium or endothelium. None of these three cytokeratin antibodies were seen in trabecular-meshwork cells or keratocytes. Desmin stain was not noted in any of these cell types. In general, cytoskeletal staining of unfixed frozen sections showed a similar staining pattern for f-actin and tubulin but a more uniform and intense staining pattern for vimentin and cytokeratin compared with fixed frozen material. The authors conclude that these cytoskeletal stains can differentiate human trabecular-meshwork cells from cells of the cornea in situ.

Actins↗
PubMed1988

Microtubule-granule relationships in motile human polymorphonuclear leukocytes.

We examined the relationship of microtubules to the granule organization in stimulated human polymorphonuclear leukocytes (PMNs). Electron microscopic (EM) observations of critical-point-dried PMNs revealed that only a portion of the granules appeared in close association to microtubules. These closely associated granules appeared to be attached to the microtubule via smaller-diameter filaments. The remaining granules appeared either attached to microtubules at a further distance, via smaller-diameter filaments such as actin, or unassociated with microtubules. EM observations of PMNs treated with either the microtubule promoter drug taxol or the microtubule depolymerization drugs nocodozole and colchicine revealed a redistribution of granules towards the nucleus. Granule clustering at the periphery of the cell was also noted with nocodozole and colchicine. With cytochalasin B, a uniform distribution of granules was noted. However, granule clustering was noted when PMNs were coincubated with cytochalasin B and colchicine. These results indicate that microtubules may have both a direct and indirect role (through other cytoskeletal elements) in the organization of PMN granules.

Alkaloids↗
PubMed1988

Quantitative assessment of cynomolgus monkey trabecular cell phagocytosis and adsorption.

A simple double fluorescence technique is described which allows quantification of cynomolgus monkey trabecular cell phagocytosis and adsorption. Within the first hour of exposure, significant adsorbance and minimal phagocytosis of polystyrene beads was observed. Peak internalization occurred at six hours after increasing linearly at a rate of 20% of maximum per hour; adsorbance was constant and minimal.

Adsorption↗
PubMed1988

The cytoskeleton of the cultured human trabecular cell. Characterization and drug responses.

To determine the organization of the three major cytoskeletal elements of cultured human trabecular meshwork cells (actin filaments, microtubules and intermediate filaments), we employed fluorescence microscopy and stereo-transmission electron microscopy of extracted, S-1 labeled and critical-point dried cells. Morphologic changes resulting from treatment with cytochalasin B, colchicine, taxol and nocodozole were also characterized. Compared with the cynomolgus monkey trabecular cell, morphologic differences in overall cell shape and orientation of both actin filaments and microtubules were noted. However, the responses to cytoskeletal active drugs were quite similar. Taxol, nocodozole and colchicine had a marked effect on microtubule organization, while nocodozole and colchicine had a marked effect on vimentin filament organization. None of these drugs produced marked changes in human trabecular cell shape. In contrast, treatment with the anti-actin drug cytochalasin B resulted in both a marked change in cell shape associated with organizational changes in all three cytoskeletal elements. These studies suggest a central role of actin filaments in determining overall cell shape and cytoskeletal organization in the cultured human trabecular cell.

Alkaloids↗
PubMed1988

Elevated phagocytosis, oxidative burst, and F-actin formation in PMNs from individuals with intraoral manifestations of HIV infection.

Alterations in polymorphonuclear leucocyte (PMN) function are frequently associated with intraoral disease. The purpose of this study was to evaluate if alterations exist in three early stimulatory events of PMN function in individuals with intraoral manifestations of human immunodeficiency virus (HIV) infection. Peripheral PMNs were isolated from nine HIV-seropositive male homosexuals with HIV-associated periodontitis and intraoral candidiasis and healthy HIV-seronegative age-matched heterosexuals (controls). Phagocytosis was assessed using fluorescent microspheres, oxidative burst was assessed via hydrolysis of 2',7'-dichlorofluorescein (FCDH) to 2',7'-dichlorofluorescein (FCDA) with PMA stimulation, and F-actin formation was assessed with NBD-phallacidin stain after stimulation with f-Met-Leu-Phe. Compared to controls, seven of nine HIV-seropositive patients demonstrated a significant increase in the percentage of phagocytic cells while seven of nine HIV-seropositive patients demonstrated a 5-59% increase in number of beads per cell. In the oxidative burst assay, seven of seven HIV-seropositive patients demonstrated a significant increase over controls in FCDA stain with PMA stimulation. In the F-actin assay, four of five HIV-seropositive patients demonstrated a significant increase over controls in NBD-phallacidin staining after f-Met-Leu-Phe stimulation.

Actins↗