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J J Jandinski

Publications and source records attributed to J J Jandinski.

18 recordsLinked to original sources
PubMed1995

Heparin fails to potentiate the effects of IL-1 beta-mediated bone resorption of fetal rat long bones in vitro.

Heparin has been identified as a potent modulator of bone resorption. Heparin induces osteoporosis during long-term administration and has been shown in vitro to enhance the effects of other bone resorbing factors, including parathyroid hormone. In this study, we examined the effects of heparin on the bone-resorbing activity of the inflammatory cytokine IL-1 beta. Resorption was determined by measuring release of previously incorporated 45Ca from fetal rat long bones cultured in medium supplemented with either 0.1% bovine serum albumin or 10% heat-inactivated fetal calf serum. Heparin, in the absence of serum, decreased basal resorption at 4 and 10 units/ml, and slightly increased resorption at 30 units/ml. Heparin had no effect on IL-1 beta-stimulated resorption. In the presence of serum, heparin induced a two-fold increase in resorption alone, however, when cocultured with IL-1 beta, heparin failed to further enhance IL-1 beta-stimulated resorption.

Animals↗
PubMed1994

Effects of plasminogen and interleukin-1 beta on bone resorption in vitro.

Inflammatory bone resorption, a characteristic feature of periodontal disease and rheumatoid arthritis, appears to be mediated by interleukin-1 beta (IL-1 beta). IL-1 beta has been shown to stimulate a wide range of proteolytic enzymes, including collagenases and plasminogen activators, in particular chondrocytes, synovial cells, and isolated osteoblasts. In this study, we have examined the hypothesis that IL-1 beta may stimulate bone loss by inducing the activity of plasminogen activators (PAs) in bone cultures. The latter would convert plasminogen to plasmin, which in turn can activate precursor procollagenase to collagenase. Active collagenase would then break down the bone collagen matrix. In the present study, release of 45Ca from fetal rat long bones in culture was studied in the presence of plasminogen and IL-1 beta. Plasminogen and IL-1 beta separately enhance resorption of fetal rat long bones in vitro. When plasminogen and IL-1 beta are added together at suboptimal levels, mainly additive effects are observed. The presence of heat-inactivated serum does not alter these results. These data tend to indicate that IL-1 beta is stimulating bone resorption through both PA-dependent and PA-independent pathways.

Animals↗
PubMed1991

Localization of interleukin-1 beta in human periodontal tissue.

Interleukin-1 beta (IL-1 beta) is the predominant form of IL-1 produced by macrophages. IL-1 beta possesses numerous and diverse biological activities. Several of these activities, including fibroblast proliferation, potentiation of the immune response, and stimulation of bone resorption may be of relevance to the pathogenesis of periodontal disease. This study was designed to examine the presence of IL-1 beta in human periodontal tissue. An antiserum directed against the N-terminal segment (117-131) of human IL-1 beta was used to detect IL-1 beta using immunofluorescent staining techniques. IL-1 beta positive staining cells were observed in both normal and diseased tissue and were limited to the lamina propria. Brightly staining cells were increased by almost 3-fold in periodontally diseased tissue when compared to normal tissue. Low intensity staining cells were equally distributed in the normal and diseased specimens. We propose that IL-1 beta and IL-1 beta produced by cells in periodontal tissues may be related to the pathological processes associated with periodontal disease.

Adult↗
PubMed1991

Tissue levels of bone resorptive cytokines in periodontal disease.

The levels of 3 bone resorptive cytokines, interleukin 1 alpha (IL-1 alpha), IL-1 beta, and tumor necrosis factor alpha (TNF alpha), were assessed in tissues from sites of periodontal disease. As determined by ELISA of tissue extracts, IL-1 beta and TNF alpha were detected in all diseased sites, whereas IL-1 alpha was present in 8/22 sites, IL-1 beta was present in highest concentration (mean +/- SEM: 11,695 +/- 2,888 pg/ml; 672 pM), followed by TNF alpha (434 +/- 135 pg/ml; 26 pM), and IL-1 alpha (342 +/- 160 pg/ml; 20 pM). The levels of all 3 mediators were significantly lower in clinically healthy tissues. There was a highly significant correlation between levels of IL-1 beta and TNF alpha (rs = 0.61, P less than 0.001), suggesting coordinated expression of these 2 mediators. The numbers of cells containing each mediator was also determined by indirect immunofluorescence on frozen tissue sections. Consistent with findings from tissue extracts, IL-1 beta-containing cells were present in approximately 5-fold higher numbers than TNF alpha-containing cells, and 40-fold higher numbers than IL-1-alpha-containing cells. Taken together with previous findings, these results indicate that IL-1 beta is likely to be an important mediator in the pathogenesis of periodontal disease.

Adult↗
PubMed1988

Osteoclast activating factor is now interleukin-1 beta: historical perspective and biological implications.

Interleukin-1 (IL-1) represents a family of polypeptides with widespread immunological and non-immunological activity. Recent studies show that osteoclast activating factor (OAF) is homologous to IL-1B. In this review, the biological properties, cell sources and actions of IL-1 are discussed. The numerous biological effects of IL-1 on various host systems suggest that elevated levels of the mediator may be an indicator of a pathological process. Since the IL-1 family plays an important role as a key mediator of the inflammatory, immunological and bone resorptive responses it is of considerable concern to dentists.

Animals↗
PubMed1981

Immunochemical evidence in two haplotypes for at least three D region-encoded molecules, D, L, and R.

Sequential immunoprecipitation analyses have defined a new transplantation antigen, designated R, which in addition to the 2 previously isolated D and L molecules is encoded in the D region. All 3 of these gene products are 45,000 m.w. glycoprotein, and each bears a unique combination of specificities as recognized by monoclonal and/or conventional anti-H-2 sera. Three D region products, D, L, and R, have now been isolated from soluble antigens of both the H-2d and H-2q haplotypes. The resulted reported here also indicate that the loss-mutant BALB/c-H-2dm2 fails to express both Ld and Rd antigens. Further chemical comparisons of the primary structure of R molecules with D and L molecules will now be necessary to determine whether R antigens are the products of a unique gene, as opposed to a glycosylation or conformational variant of D and/or L molecules. In either case, the discovery of 3 D region-encoded gene products in certain haplotypes raises new questions about the evolution and regulation of expression of H-2 loci.

Animals↗
PubMed1980

Role of self carriers in the immune response and tolerance. V. Reversal of trinitrophenyl-modified self suppression of the B-cell response by blocking of H-2 antigens.

Trinitrophenylated syngeneic spleen cells (TNP-SC) are potent tolerogens of the anti-TNP plaque-forming cell (PFC) response in vivo and in vitro. This unresponsive state requires T cells for both its induction and maintenance. Because H-2K/D-restricted cytotoxic T cells are also induced by exposure to TNP-SC, we determined the role(s) of histocompatibility antigens (K, I, and D) in the suppression of the PFC response by TNP-SC. We treated syngeneic TNP-modified stimulator cells with antiserum directed at K-, I-, or D-region determinants and found that blocking of H-2K or D antigens on TNP-SC transformed these tolerogens into immunogens capable of eliciting an anti-TNP PFC response in the absence of extrinsic immunogens like TNP-polymerized flagellin. In H-2k or H-2a(k/d) mice, only H-2Kk needs to be blocked on the stimulator cells, whereas H-2K or D recognition was apparent in B10.A(4R) mice. These observations indicate that suppression of the PFC response by TNP-SC shows the same restriction in recognition as does the cytotoxic T-cell response. Furthermore, our results suggest that TNP-I-A is recognized by the helper cells in this system as the intrinsic antigen. When both TNP-K and TNP-I-A are present and available on the same stimulator cell, suppression (via modified K recognition) is dominant over help.

Animals↗
PubMed1979

Role of self carriers in the immune response and tolerance. IV. Active T cell suppression in the maintenance of B cell tolerance to a "T-independent" antigen.

Previous studies indicated that T cells are required for tolerance induction by hapten-modified syngeneic spleen cells (TNP-SC) in vivo. The role of T cells in the maintenance of this unresponsive state has been examined herein. By three criteria--limiting dilution precursor analysis, removal of T cells by anti-Thy-1 + C, and direct mixing experiments--we show that T cells are required for the continued suppression of the B cell response to the T-independent antigen, TNP-POL. Suppressor cells can also be induced by TNP-teratoma cells, which lack detectable H-2 antigens. Both anti-Ly-1 + C and anti-Ly-2 + C treatment reversed suppression induced by TNP-SC. These results demonstrate that normal B cell reactivity is present in the spleens of mice rendered tolerant by haptenated self, but that Ly-1,2,3 or Ly-1 + Ly-2,3 suppressor T cells prevent their responsiveness.

Animals↗
PubMed1975

Cyanoacrylate as an adhesive for other medicaments: a study with triamcinalone on the healing of experimental oral ulcers.

This study was undertaken to determine whether cyanoacrylate can be used to adhere other medicaments to oral ulcers in the hope of promoting healing. Triamcinalone was chosen since it is used presently in pastes in the oral cavity. Sixty rats were dived into three equal groups. In each animal under anesthesia with ether, bilateral equivalent ulcers, 2 mm in depth and diameter, were made with the tip of a rongeur on the midlateral aspect of the tongue. The right side served as a control. The left side was experimental and received the following: group I--isobutyl-2-cyanoacrylate only; group II--powdered triamcinalone acetonide; group III--triamcinalone covered with cyanoacrylate. All materials were reapplied every 24 hours for 4 days. Two animals from each group (6) were sacrificed at 1, 4, and 8 hours and 1, 2, 3, 5, 14, and 21 days. The results indicate that a powdered medicament can be held in place on oral ulcers for at least 24 hours. The ulcers with cyanoacrylate revealed less edema and cellular response for up to 24 hours. Healing of the ulcers was neither promoted nor delayed in any group.

Animals↗
PubMedDate not supplied

Oral soft tissue manifestations and CD4 lymphocyte counts in HIV-infected children.

This study investigated the prevalence of oral soft tissue lesions in children infected with HIV and the relationship of CD4 lymphocyte levels with the prevalence of those lesions. Sixty HIV-positive children enrolled in the Children's Hospital AIDS Program (age 5.8 +/- 3 years) were selected for study. Only five subjects (8%) had healthy gingiva and a low mean plaque index (22%). The remainder had gingivitis or periodontitis with relatively high plaque indices (47, 55, and 94%, respectively). A declining CD4 lymphocyte count (1357 to 35) was associated with an increasing severity of gingival disease.

AIDS-Related Opportunistic Infections↗
PubMedDate not supplied

Detection and measurement of inflammatory cytokines in implant crevicular fluid: a pilot study.

Peri-implantitis has been shown to possess clinical characteristics similar to those of periodontitis. This pilot study was conducted to determine levels of inflammatory cytokines in crevicular fluid from healthy implants and those implants affected by peri-implantitis. Fifty implants from 13 patients were examined. A clinical examination was performed, and gingival crevicular fluid samples were collected and analyzed for cytokines. Implants were categorized clinically as healthy, early peri-implantitis, or advanced peri-implantitis. Interleukin-1 beta was detected in the crevicular fluid of implants in all three groups (healthy = 59.47 +/- 15.55 pg/site; early peri-implantitis = 460.77 +/- 35.67 pg/site; and advanced peri-implantitis = 191.10 +/- 21.60 pg/site [mean +/- SEM]). These results indicate that interleukin-1 beta is present in implant gingival crevicular fluid and may be modulating attachment loss in implants suffering from peri-implantitis. Thus, interleukin-1 beta may be used to monitor disease progression.

Alveolar Bone Loss↗
PubMedDate not supplied

Detection of prostaglandin E2 and matrix metalloproteinases in implant crevicular fluid.

Studies show that implants exhibiting peri-implantitis contain elevated levels of the cytokine interleukin-1 beta in the gingival crevicular fluid (GCF). This study further evaluated possible mechanisms of osseous loss in peri-implantitis by examining GCF samples for the presence of prostaglandin E2 (PGE2) and proteolytic enzymes, specifically matrix metalloproteinases (MMPs). Results indicated that levels of PGE2 in healthy sites were not significantly different from those at diseased sites. MMP species migrated at 92 kd and 66 kd. No qualitative difference in bands was seen between healthy implants and those diagnosed with early peri-implantitis. Results suggested that PGE2 and MMP levels are not useful biologic markers for distinguishing between healthy and diseased implants.

Alveolar Bone Loss↗