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S Yilmaz

Publications and source records attributed to S Yilmaz.

At least 145 records · Page 8Linked to original sources
PubMed1994

Cytomegalovirus infection-enhanced allograft arteriosclerosis is prevented by DHPG prophylaxis in the rat.

BACKGROUND: Major risk factors for accelerated allograft arteriosclerosis include humoral and cellular immune response, hyperlipidemia, and viral infections. We demonstrated earlier that rat cytomegalovirus (RCMV) infection doubles smooth muscle cell proliferation and intimal thickening of rat aortic allografts. In this study, the effects of 9-(1,3-dihydroxy-2-propoxymethyl)guanine (DHPG) on RCMV-enhanced rat allograft arteriosclerosis are investigated. METHODS AND RESULTS: Aortic allografts from the DA to the WF rat strain were used. The recipients were inoculated with 10(5) plaque-forming units of RCMV 1 day after transplantation. Two groups of RCMV-infected rats were treated with DHPG with an initial dose of 20 mg/kg IP and a maintenance dose of 10 mg/kg IP twice a day for a period of 14 days. In the DHPG prophylaxis group (n = 22), the drug administration started 1 day before infection, and in the DHPG treatment group (n = 17), 7 days after infection. One group of infected rats was left untreated (n = 21). The grafts were removed 7 and 14 days and 1, 3, and 6 months after transplantation. In the DHPG prophylaxis group, no virus could be recovered by plaque assays. In the treatment group, 50% of rats were virus-positive at 1 month and 40% at 3 months. DHPG prophylaxis prevented the infiltration of inflammatory cells and their proliferation in the adventitia of RCMV-infected recipients (P < .01), with a 60% reduction in the interleukin-2 receptor expression (P < .05) and a 30% decrease in major histocompatibility complex class II expression (P = NS). DHPG prophylaxis did not significantly alter the levels of insulin-like growth factor-1, epidermal growth factor, platelet-derived growth factor-BB, transforming growth factor-beta 1, acidic fibroblast growth factor, and basic fibroblast growth factor messages in the allograft vascular wall. Early media necrosis was reduced. Arteriosclerotic alterations and proliferation of smooth muscle cells were both reduced 50% to 70% by DHPG prophylaxis (P < .05 at 3 months). The responses in the DHPG treatment group were quite similar but less impressive and statistically nonsignificant. CONCLUSIONS: We consider it likely that DHPG inhibits arteriosclerotic alterations primarily by reducing the infectious virus and thereby the inflammatory response in the allograft vascular wall; another possibility is a direct antiproliferative effect on smooth muscle cell replication. A dose-dependent inhibitory effect of DHPG on smooth muscle cell replication was recorded in an in vitro study.

Animals↗
PubMed1994

Chronic allograft rejection: an update.

The aetiology of chronic rejection is most likely multifactorial. The common feature in all organ allografts undergoing chronic rejection is persistent perivascular inflammation and a concentric generalised arteriosclerosis affecting all first and second order intramural arteries. A hypothesis is presented that low-grade damage to the endothelium induces the secretion of growth factors which, in turn, are responsible for smooth muscle cell replication and their influx into intima.

Animals↗
PubMed1994

Widening the zone of peri-implant attached gingiva.

The use of implant systems is a focus of interest nowadays, as an alternative method to classical dental prostheses used in partially or completely edentulous patients. Such an interest of both the patients and the clinicians seemed likely to be due to the opportunity of using fixed prostheses on these implants. However, besides its advantages, problems exist regarding the zone of attached gingiva around implants, for the vestibular depth has generally been decreased because of the excessive amount of alveolar bone resorption. The problem from the periodontal point of view is that the periodontal pockets around implants used as abutments may turn out to be pathologic pockets and an inadequate and nonfunctional vestibular depth will result. In this study, the conventional free soft tissue autograft technique was performed around 34 implants in 9 patients in whom 40 Brånemark implants in total were placed. The postoperative evaluations indicated that the decrease in the vestibular depth, due to the shrinkage of the keratinized tissue had a negative effect on this surgical procedure. The use of acrylic stents after surgery seemed to be a better solution and would give good clinical results.

Acrylic Resins↗
PubMed1994

The ultrastructural examination of gingival fibromatosis.

Hereditary gingival fibromatosis (GF) is a special type of fibrous overgrowth classified as non-inflammatory gingival enlargement. Microscopically, the connective tissue consists of coarse collagen bundles and fibroblasts. The ultrastructural examination of fibrous gingival hyperplasia reveals that fibroblasts phagocyte the mast cell granules and mast cells stimulate collagen synthesis which results in hyperplasia. In the ultrastructural examination of phenytoin-induced hyperplasia, fibroblasts, phagocytosing mast cell granules were also found. Based on these findings, the purpose of this study is to establish whether there is a relationship between fibroblasts and mast cells in GF. The gingival tissues of 5 patients with GF were examined ultrastructurally. In the connective tissue, well-defined bundles of collagen fibres were found together with fibroblasts and capillaries. There were mast cells around these capillaries which had collapsed lumens. The proximity of the mast cells and fibroblasts may indicate that mast cells play some role on collagen synthesis of fibroblasts.

Biopsy↗
PubMed1994

The evolution of clinical periodontal therapy.

Periodontal diseases are considered as old as the history of mankind, Magical, religious and herbal treatments were demonstrated in almost all of the early writings. However, methodical, carefully reasoned therapeutic approaches did not exist until the middle-ages and modern treatment with a scientific base and sophisticated instrumentation did not develop until the 18th century. Prior to the 1950s, diseases were mostly treated by root debridement and the extraction of the affected teeth. Until the 1970s, it was primarily the symptoms of periodontal diseases that were treated. The goal was radical elimination of the periodontal pocket (resective therapy). The means were gingivectomy, flap procedures and osseous surgery. The disadvantages were the massive sacrifice of periodontal tissues, lack of regeneration and clinically elongated teeth. These disadvantages, along with the realization of the importance of aetiologic agents, raised questions about the necessity of total pocket elimination, and the control of subgingival infection by a thorough scaling and root planing (nonsurgical therapy), with and without antibiotics, became a commonly used treatment during the 1980s. Comparative longitudinal studies, surgical versus nonsurgical, demonstrated that both surgical and nonsurgical therapy result in limited regeneration and healing with a long junctional epithelium. The most important aspects of today's modern concept of periodontal therapy are causal, regenerative, and specific for disease type and severity. Although the regeneration of the periodontium can be accomplished with the biological principles of guided tissue regeneration and graft materials, compared to conventional methods, the restoration of a completely normal periodontal status has not yet been achieved. We are about to reach our ultimate goals and presently, the more promising research directions for a substantial regeneration seems to lie in biological mediators. Although the future of periodontal therapy is bright, it is still of critical importance to have a preventive strategy to keep individuals healthy beforehand.

Gingival Diseases↗
PubMed1993

The impact of acute episodes of rejection on the generation of chronic rejection in rat renal allografts.

We have investigated the impact of the frequency of acute rejection episodes on the generation of chronic rejection in long-surviving rat renal allografts. A total of 33 renal transplantations was performed from DA to WF rats, receiving different cyclosporine-based immunosuppressive regimens. As a consequence, different numbers of acute rejection episodes were recorded in the recipients, all of which were successfully treated with cyclosporine. Upon sacrifice at 12 weeks posttransplantation, the frequency of acute rejection episodes was correlated with the major histological parameters of chronic rejection and with graft function. The intensity of the major histological parameters of chronic rejection, exemplified by vascular intimal proliferation and glomerular mesangial matrix increase, and the decline in graft function between the no-rejection vs. rejection groups, were directly proportional to the number of acute rejection episodes. Vascular intimal proliferation increased from 0.5 +/- 0.4 (arbitrary units) in the no-rejection group to 1.7 +/- 0.9 (P = 0.0093) after one rejection episode, to 2.2 +/- 0.3 (P = 0.0001) after two, and to 2.2 +/- 0.5 (P = 0.0014) after three or four rejection episodes. Glomerular mesangial matrix increased from 1.2 +/- 0.3 (arbitrary units) in the no-rejection group to 1.9 +/- 0.6 (P = 0.017) after one, to 2.2 +/- 0.5 (P = 0.0005) after two, and to 2.1 +/- 0.4 (P = 0.003) after three or four rejection episodes. Serum creatinine increased from 93 +/- 24 mumol/L in the no-rejection group to 196 +/- 92 mumol/L (P = 0.016) after one, to 238 +/- 38 mumol/L (P = 0.0001) after two, and to 308 +/- 85 mumol/L (P = 0.0016) after three or four rejection episodes. Prolongation of the preoperative ischemia time from 30-60 min correlated with an increase in the number of acute rejection episodes as well as an increase in chronic changes. To conclude, in the rat renal allograft model, acute allograft rejection carries a highly significant correlation with the development of chronic rejection.

Animals↗
PubMed1993

The effect of cyclosporin-A on the ultrastructure of gingival tissue in Behçet's disease.

Autoimmune processes are said to play an active role in aetiology of Behçet's disease (BD), which is also known as a multisystem disease. In the treatment of this autoimmune disease, cyclosporin A (CyA) is used. Gingival hyperplasia (GH) is one of the important side effects that have been observed in some of the patients. We aimed to evaluate the CyA-induced gingival hyperplasia in BD patients. There were 3 study groups, each having 5 patients. In the first group displaying GH, mast cells were located between epithelial cells and in the connective tissue. Mast cell granules were in crystalline form and electron-dense cored form. Fibroblasts and plasma cells were present in the connective tissue. The second group did not display GH and the mast cells were similar to those in the first group. The third group, was the control group, in which the mast cells were located between the epithelial cells and connective tissue. Mast cell granules were in electron-dense cored form. We concluded that the development of CyA-induced gingival hyperplasia is determined mainly by individual sensitivity to CyA, because although both test groups which received CyA showed an increased number and activity of fibroblasts, only one group of patients developed GH.

Adolescent↗
PubMed1993

A genetic and dermatoglyphic study on periodontitis.

Periodontal diseases encompass a wide range of disease manifestations and processes from the mildest inflammation of gingiva to the most advanced destructive periodontitis with loss of attachment, bone tissue and teeth. No entirely satisfactory identification and classification exist in periodontitis especially for high risk early onset periodontitis (EOP) cases, because of insufficient knowledge about the aetiological and host factors and their overlapping clinical and laboratory features. In this study, the dermatoglyphics, which is a genetic test method, suggesting the modes of inheritances of hereditary diseases, was performed on 36 EOP and 20 adult periodontitis (AP) patients and 20 periodontally healthy individuals. The diagnostic value of this genetic test method, which is the study of the quantitative and qualitative characteristics of patterns of ridged skin, and the role of heredity on periodontal diseases are discussed.

Adolescent↗
PubMed1992

Towards understanding the pathophysiology of chronic rejection.

Chronic allograft rejection is the major reason why allografts are lost. While only 2%-3% of all allografts are lost during the first year to irreversible acute rejection, approximately 6%-7% are lost during each subsequent year to chronic rejection. The major manifestation of chronic rejection in all organs is persistent perivascular inflammation and allograft arteriosclerosis. Bearing this in mind, we have developed a model to investigate the pathophysiology of allograft arteriosclerosis using aortic transplantations between inbred rat strains. The results obtained thus far indicate that several different inflammatory cascades are operative within the vascular wall during allograft arteriosclerosis. The relative importance of these different cascades, and particularly the role of growth factors as final effectors, has not yet been defined. Attempts to suppress allograft arteriosclerosis under experimental conditions have already met with some success: under conditions where no immunosuppression is provided we have been able to delay the process by at least 3 months, though we have not been able to block it indefinitely. It may be expected, however, that once the inflammatory cascades leading to smooth muscle cell replication in the allograft media and their influx into the intima are better defined, more specific approaches to the inhibition of allograft arteriosclerosis will be developed.

Animals↗
PubMed1992

Chronic rejection of rat renal allografts. II. The impact of prolonged ischemia time on transplant histology.

The effect of prolonged ischemia time on the generation of chronic rejection was investigated in long-surviving rat renal allografts. Three groups of rats were compared: allografts with a 30-min ischemia time, allografts with a 60-min ischemia time, and syngeneic grafts with a 60-min ischemia time. All transplants were initially immunosuppressed with 5 mg/kg/day of cyclosporine i.m. for 3 weeks postoperatively. The CsA trough levels were similar in the three rat groups. All groups demonstrated an initial rise and fall in serum creatinine; a simultaneous biopsy confirmed acute CsA toxicity. Thereafter the serum creatinine level remained on the normal control level both in the 30-min ischemia allografts and in the 60-min ischemia syngeneic grafts. After the initial decline, the serum creatinine level steadily increased in the 60-min ischemia allograft group and was 181 +/- 64 mumol/L at the end of the observation period, 12 weeks postoperatively, compared with 85 +/- 21 mumol/L in the 30-min ischemia allografts and 89 +/- 25 mumol/L in the 60-min ischemia syngeneic grafts. Quantitative histology that was performed upon autopsy demonstrated that the 60-min ischemia allografts showed persistent inflammation, inflammatory cell pyroninophilia, vascular arteriosclerosis and obliteration, and glomerular sclerosis, which were significantly stronger than in similarly immunosuppressed syngeneic transplants. Reduction of the ischemia time from 60 to 30 min significantly ameliorated the vascular and glomerular changes in the allografts but not the inflammatory alterations. This experimental study confirms previous clinical observations and demonstrates that prolonged ischemia contributes to chronic rejection in renal allografts. The results suggest that the effect of prolonged ischemia on chronic rejection is directed primarily to the parenchymal components of the graft, possibly to the graft vascular endothelium. As prolonged ischemia did not significantly affect the inflammation in the transplants, we conclude that the effect is not directed to the intensity of the host antigraft immune response.

Animals↗
PubMed1992

Clinical studies on juvenile, rapidly progressive and adult periodontitis before and after periodontal therapy (I).

The sample in the present study comprised 36 patients who were referred for treatment of periodontal disease. Twenty-four of them were early onset periodontitis (EOP) patients and 12 were adult periodontitis (AP) patients. Based upon the age, number of involved teeth and the location of diseased sites, the EOP patients were divided into two groups as juvenile periodontitis (JP) and rapidly progressive periodontitis (RPP). All the patients were individually examined both clinically and radiographically. At a baseline examination and 3 months after active therapy, the patients were evaluated for plaque, gingivitis, probing depths and probing attachment levels. Following instruction in proper oral hygiene measures, all of the patients were subjected to periodontal treatment. Treatment comprised scaling and root-planing, occlusal adjustment, tetracycline administration and periodontal surgery with osteoplasty. Results showed that age limits between JP and RPP cannot be drawn with certainty. The mean age for the JP group was 21.83 years and was 30.58 years for the RPP group. The number of involved teeth was found to increase with age. The first molars were the most frequently affected teeth followed by the incisors. Three months after active treatment, the response of periodontal tissues to therapy both in EOP and AP groups was almost identical.

Adolescent↗
PubMed1992

Diagnostic studies on juvenile, rapidly progressive and adult periodontitis before and after periodontal therapy (II).

The use of antibody levels may identify subjects developing destructive periodontitis or provide markers of disease type. Clinical parameters can be used to group cases but they are incapable of detecting differences in host-susceptibility and host immune response. The validity of radial immunodiffusion (RID) as a laboratory screening method in diagnosis based on antibody quantitation has been evaluated in 36 patients before and after periodontal therapy. It was concluded that the serum IgA, IgG, IgM and parotid IgA concentration profiles, measured with RID have little value in determining the subgroups of early onset periodontitis patients but they can be used to differentiate these groups from slowly progressing adult periodontitis patients.

Adolescent↗
PubMed1992

Chronic rejection of rat renal allograft. III. Ultrastructure of vascular and glomerular changes.

The main histological features for 'chronic' rejection of rat renal allograft are ongoing perivascular and interstitial inflammation, vascular intimal hyperplasia and glomerular sclerosis. In this communication we have investigated the ultrastructural features of renal parenchyma by comparing chronically rejecting rat renal allografts immunosuppressed initially with cyclosporine to similarly immunosuppressed syngeneic transplants. Electron microscopy confirmed that the primary arterial change was smooth muscle cell proliferation in media, thickening and focal destruction of the internal elastic lamina, and influx of smooth muscle cells and their proliferation in the intima, leading to a nearly complete occlusion of the lumen. In the glomeruli, the most prominent features were mesangial matrix increase, narrowing of capillary lumen, and basement membrane thickening with a double contour appearance in capillary walls. A thin membrane, similar to lamina densa, appeared beneath the endothelium in some segments. Mesangial interposition, formation of new basement membrane and mesangial widening due to increase of basement membrane-like material was nearly always present. As none of these vascular and glomerular changes were observed in similarly immunosuppressed syngeneic transplants, we consider these ultrastructural alterations characteristic for chronic rejection in a rat renal allograft.

Animals↗
PubMed1992

Chronic rejection of rat renal allograft. I. Histological differentiation between chronic rejection and cyclosporin nephrotoxicity.

Chronic allograft rejection is both a clinical and a histopathological diagnosis. Until recently, the histological definition of chronic renal allograft rejection was based on clinical diagnostic biopsies, where the evidence was partially obscured by recurrence of the original renal disease, and/or by administration of immunosuppressive drugs. In this communication, we present an experimental rat model for chronic renal allograft rejection, devoid of recurrence of the original disease. By comparing allografts to similarly immunosuppressed syngeneic transplants, we define which histological features should be attributed to chronic rejection and which to cyclosporin nephrotoxicity. Rat renal transplants were performed from DA (Ag-B4, RT1av1) to WF strain (Ag-B2, RT1u) or, for control, to DA strain, and immunosuppressed for 2 or 3 weeks with cyclosporin using a variety of different dosages. The animals were monitored weekly for serum creatinine levels and for blood cyclosporin concentrations, and core needle biopsies were performed on the grafts at regular intervals. At 3 months post-transplantation the animals were sacrificed and a complete histopathological evaluation was performed. Thirty-one histological variables were scored blindly by two investigators and separately for the graft interstitium, glomeruli, tubuli, and the graft vasculature. The following histological alterations were significantly more prominent in allografts than in similarly immunosuppressed syngeneic transplants: the intensity of interstitial inflammation, particularly the degree of pyroninophilia within the inflammatory cell population; the extent of glomerular mesangial matrix increase, basement membrane thickening, and glomerular sclerosis; the increase in the vascular intimal thickness affecting in particular the first and second order branches of the renal artery; and the obliteration of the graft vasculature. These alterations were considered as being primarily due to chronic rejection. In contrast, the extent of interstitial fibrosis and the extent of tubular changes, including tubular epithelial vacuolation, epithelial atrophy, and tubular basement membrane changes, were not significantly different in the allografts as compared to the syngeneic controls. These alterations were attributed primarily to cyclosporin nephrotoxicity. Serial monitoring of the grafts by needle biopsies clarified the sequence of events in the development of the chronic alterations in the transplant. The first event, as expected, was tubulointerstitial pyroninophilic inflammation, resembling that of acute episodes of rejection. This was significantly stronger and appeared earlier in allografts immunosuppressed for 2 rather than for 3 weeks. Vascular alterations developed next. The last to develop were the glomerular lesions.

Animals↗