Biomedical subjects

A M Iacopino

Publications and source records attributed to A M Iacopino.

At least 19 recordsLinked to original sources

PubMed2001

Effect of recombinant human bone morphogenetic protein-2 on bone regeneration and osseointegration of dental implants.

Recombinant human bone morphogenetic protein-2 (rhBMP-2) induced bone regeneration and osseointegration was evaluated in bony defects created within the hollow chamber of endosseous dental implants in 14 foxhound dogs. Bilateral extractions of mandibular premolars were performed and surgical implantation of 104 hollow cylinder implants followed after 8 weeks of healing. Experimental implants had their hollow chamber filled with 20 microg of rhBMP-2 delivered with a bovine collagen carrier, whereas the control implants had their apical chamber left empty. Dogs were followed for 2, 4, 8 and 12 weeks. Histomorphometric evaluation and immunohistochemical analysis were performed. Minimal bone was regenerated at 2 weeks for both groups. At 4 weeks, bone fill averaged 23.48% for the rhBMP-2 and 5.98% for the control group (P<0.05). At 8 weeks, mean bone fill was 20.94% and 7.75% for the rhBMP-2 and the controls, respectively (P<0.05). At 12 weeks, mean bone fill was 31.39% and 24.31% for the rhBMP-2 and control implants, respectively (P>0.05). Bone-implant contact (BIC) increased for both groups over time and at 8 weeks the rhBMP-2 BIC value was 18.65% and for the control 7.22% (P<0.05). At 12 weeks, the BIC was 43.78% and 21.05% for the rhBMP-2 and the control group, respectively (P<0.05). Immunohistochemical staining for type II collagen was positive only for parts of the collagen carrier and formation of cartilaginous intermediate was not observed in any of the specimens. The results suggest that, in confined defects adjacent to dental implants, rhBMP-2 can induce bone regeneration in close apposition to the implant surface.

Animals↗

PubMed2001

The effect of FIV infection on CD4+ and CD8+ counts in periradicular lesions.

AIM: The purpose of this study was to elucidate whether a decrease/increase in T-cell populations is present in the development of periradicular disease in the immunocompromised feline model. METHODOLOGY: Eight cats were immunosuppressed with steroids prior to infection with feline immunodeficiency virus (FIV). Another eight cats, age and sex matched littermates, were monitored and tested at equivalent periods of time and served as uninoculated, seronegative controls. Periradicular lesions were induced using local bacterial inoculations into the pulp of the canine teeth and assessed after one- and four-week periods, corresponding to the acute and chronic stages of the periradicular disease. Block sections were obtained and specimens were prepared for H & E and immunohistochemical staining for CD4+ and CD8+ receptors. Cells were quantified using a computer imaging system and data analysed using generalized estimating equation (GEE) regression models. RESULTS: Significantly lower CD4+ counts and CD4+/ CD8+ ratios were observed at all time periods in the periradicular region of the FIV group (P = 0.0006). No significant difference in CD8+ counts was observed between the two groups. In both groups there was a significant difference in the CD4+ counts between one week and baseline, and 1 week and 4 weeks. There was no significant difference between baseline and 4 weeks for either group. CONCLUSION: FIV infection reflected decreased CD4+ counts at the periradicular level, however, inflammation and progression of the lesion, appeared to be comparable to the non-immunocompromised controls.

Animals↗

PubMed2001

Interleukin-1beta production in periradicular lesions in a human immunodeficiency virus/acquired immune deficiency syndrome model compared with a noninfected host.

This study elucidates the role of interleukin-1 (IL-1) in developing periradicular lesions in immunocompetent and immunocompromised (human immunodeficiency virus/acquired immune deficiency syndrome) hosts. Eight cats were immunosuppressed with steroids before infection with feline immunodeficiency virus (FIV). Eight uninoculated cats served as controls. Periradicular lesions were induced around the canine teeth. At 1 and 4 wk periradicular exudate was sampled via the root canals. IL-1beta levels were measured with ELISA. Data were analyzed using the Mann-Whitney U test and the Wilcoxon signed rank test. Statistically significant differences existed in cytokine levels between the FIV and non-FIV groups (p < 0.001). Cytokines were below detectable levels in the FIV group. A significant decrease in IL-1beta levels at 4 wk compared with 1 wk occurred in the non-FIV group (p < 0.05). In conclusion decreased IL-1beta production was obtained in the FIV group. In the non-FIV group decreases in IL-1beta levels were encountered at the chronic stage of the periradicular lesion compared with the acute stage.

Acute Disease↗

PubMed2001

Periodontitis and diabetes interrelationships: role of inflammation.

Diabetes mellitus is a systemic disease with several major complications affecting both the quality and length of life. One of these complications is periodontal disease (periodontitis). Periodontitis is much more than a localized oral infection. Recent data indicate that periodontitis may cause changes in systemic physiology. The interrelationships between periodontitis and diabetes provide an example of systemic disease predisposing to oral infection, and once that infection is established, the oral infection exacerbates systemic disease. In this case, it may also be possible for the oral infection to predispose to systemic disease. In order to understand the cellular/molecular mechanisms responsible for such a cyclical association, one must identify common physiological changes associated with diabetes and periodontitis that produce a synergy when the conditions coexist. A potential mechanistic link involves the broad axis of inflammation, specifically immune cell phenotype, serum lipid levels, and tissue homeostasis. Diabetes-induced changes in immune cell function produce an inflammatory immune cell phenotype (upregulation of proinflammatory cytokines from monocytes/polymorphonuclear leukocytes and downregulation of growth factors from macrophages). This predisposes to chronic inflammation, progressive tissue breakdown, and diminished tissue repair capacity. Periodontal tissues frequently manifest these changes because they are constantly wounded by substances emanating from bacterial biofilms. Diabetic patients are prone to elevated low density lipoprotein cholesterol and triglycerides (LDL/TRG) even when blood glucose levels are well controlled. This is significant, as recent studies demonstrate that hyperlipidemia may be one of the factors associated with diabetes-induced immune cell alterations. Recent human studies have established a relationship between high serum lipid levels and periodontitis. Some evidence now suggests that periodontitis itself may lead to elevated LDL/TRG. Periodontitis-induced bacteremia/endotoxemia has been shown to cause elevations of serum proinflammatory cytokines such as interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha), which have been demonstrated to produce alterations in lipid metabolism leading to hyperlipidemia. Within this context, periodontitis may contribute to elevated proinflammatory cytokines/serum lipids and potentially to systemic disease arising from chronic hyperlipidemia and/or increased inflammatory mediators. These cytokines can produce an insulin resistance syndrome similar to that observed in diabetes and initiate destruction of pancreatic beta cells leading to development of diabetes. Thus, there is potential for periodontitis to exacerbate diabetes-induced hyperlipidemia, immune cell alterations, and diminished tissue repair capacity. It may also be possible for chronic periodontitis to induce diabetes.

Bacteremia↗

PubMed2000

Phenytoin and cyclosporin A suppress the expression of MMP-1, TIMP-1, and cathepsin L, but not cathepsin B in cultured gingival fibroblasts.

BACKGROUND: Fibroblasts are known not only to synthesize and secrete extracellular matrix proteins, but also to degrade them for connective tissue remodeling. Drug-induced gingival overgrowth is characterized by a massive accumulation of extracellular matrix components in gingival connective tissues. Although some previous reports suggested that causative drugs stimulated the fibroblast proliferation, the results are not conclusive yet. In this study, we hypothesized that drug-induced gingival overgrowth could be a consequence of impaired ability of matrix degradation rather than an enhanced proliferation of gingival fibroblasts induced by these drugs. METHODS: Normal human gingival fibroblasts were cultured with or without either 20 microg/ml of phenytoin or 200 ng/ml of cyclosporin A. Total RNA and cellular proteins were collected every day for RT-PCR analyses and for measuring lysosomal enzyme activity. In addition, an immunohistochemical study was performed to detect lysosomal enzymes in cells from enlarged gingiva of the patients with phenytoin-induced gingival overgrowth. RESULTS: RT-PCR analyses revealed that these drugs suppressed the expression of MMP-1, TIMP-1, and cathepsin L, but not that of cathepsin B in a time-dependent manner. Then, we measured the activity of lysosomal enzymes and cathepsin B and L. The results indicated that although cathepsin B activity was not observed to be impaired, regardless of the drugs used in these cells, both total and active forms of combined activity of cathepsins B and L were suppressed in a time-dependent manner. CONCLUSIONS: The results indicate that, besides suggested effects of these drugs on gingival fibroblasts and/or on accumulated cells in the gingival tissues, extracellular matrix-degrading ability, particularly that by cathepsin L, is also suppressed by cyclosporin A and phenytoin in gingival fibroblasts, and that lysosomal enzyme plays an important role in the pathogenesis of drug-induced gingival hyperplasia.

Anticonvulsants↗

PubMed2000

Pathophysiological relationships between periodontitis and systemic disease: recent concepts involving serum lipids.

Periodontitis has been traditionally regarded as a chronic inflammatory oral infection. However, recent studies indicate that this oral disease may have profound effects on systemic health. The search for cellular/molecular mechanisms linking periodontitis to changes in systemic health and systemic physiology has resulted in the evolution of a new area of lipid research establishing linkages between existing multidisciplinary biomedical literature, recent observations concerning the effects of serum lipids on immune cell phenotype/function, and a heightened interest in systemic responses to chronic localized infections. There appears to be more than a casual relationship between serum lipid levels and systemic health (particularly cardiovascular disease, diabetes, tissue repair capacity, and immune cell function), susceptibility to periodontitis, and serum levels of pro-inflammatory cytokines. In terms of the potential relationship between periodontitis and systemic disease, it is possible that periodontitis-induced changes in immune cell function cause metabolic dysregulation of lipid metabolism through mechanisms involving proinflammatory cytokines. Sustained elevations of serum lipids and/or pro-inflammatory cytokines may have a serious negative impact on systemic health. The purpose of this paper is to present the background, supporting data, and hypotheses related to this concept. As active participants in this emerging and exciting area of investigation, we hope to stimulate interest and awareness among biomedical scientists and practitioners.

Cytokines↗

PubMed2000

Rethinking knowledge and pedagogy in dental education.

Dentistry as a profession has often been considered both art and science. Traditional dental education has attempted to address both; however, in many places only the science of dentistry is emphasized. The move toward competency-based curricula in dental education requires an expansion of what constitutes meaningful knowledge in the curriculum and what pedagogies best support that curriculum. The scientific and technical knowledge considered foundational to clinical practice is not sufficient to teach competencies associated with the art of dentistry. Habermas, a social scientist, offers a way of looking beyond technical knowledge to consider two other forms of knowledge: practical and emancipatory. Pedagogy that supports development of practical and emancipatory knowledge includes problem-based learning and case methods, heuristics, reflective practica, journals, storytelling, and performance-based assessment methods. These important teaching strategies are being integrated into various dental curricula including a new competency-based dental curriculum at Marquette University's School of Dentistry. It will be critical for dental educators to continue developing these methods to provide efficient and effective education for future practitioners in both the art and science of dentistry.

Clinical Clerkship↗

PubMed1999

Phytoestrogens alter hypothalamic calbindin-D28k levels during prenatal development.

Calbindin-D28K (CALB) in the medial basal hypothalamic (MBH) and preoptic area (POA) of male and female fetuses from pregnant rats fed different phytoestrogens diets during gestation was examined by Western analysis. In animals fed a phytoestrogen containing diet (Phyto-200), males displayed significantly higher CALB levels compared to females. Whereas, in animals fed a phytoestrogen-free diet (Phyto-free), females exhibited significantly higher CALB levels compared to Phyto-200 female values. The present data have far reaching implications where phytoestrogen content in diets apparently influence MBH-POA CALB levels prenatally. The altered CALB levels may in turn modify sexually dimorphic brain structures during neuronal development by buffering Ca2+ that is associated with programmed cell death.

Animals↗

PubMed1999

In vitro alteration of macrophage phenotype and function by serum lipids.

Diabetes (type I and type II) affects approximately 13 million people in the United States. Delayed and incomplete healing of wounds can be a major problem for diabetic patients. Macrophages are an important cell in the complex process of wound repair representing the major source of cytokines throughout the wound-healing process. Cytokines mediate many of the cellular responses critical to timely wound repair. It has been suggested that diabetes impairs wound healing through disruption of local cytokine production. Our previous in vivo studies in rats demonstrated that diabetes-induced and diet-induced hyperlipidemia cause changes in macrophage phenotype and function (Iacopino 1995; Doxey et al. 1998), suggesting that alterations in macrophage cytokine profiles represent the cellular/molecular mechanism responsible for delayed wound healing. The purpose of this study was to investigate how monocyte maturation/differentiation and cytokine production were altered by serum lipids in an in vitro system using human cells. Commercially prepared purified human monocytes were cultured and exposed to serum lipids. Phenotypic analysis of differentiated macrophages was then performed by flow cytometry and fluorescent microscopy using surface antigens specific for various macrophage subsets. Selected cytokines in conditioned medium were assayed using commercial human enzyme-linked immunosorbent assay (ELISA) kits. We demonstrate that serum lipids cause an increase in monocytic differentiation leading to an inflammatory macrophage phenotype rather than a reparative/proliferative phenotype. We also show that serum lipids cause a generalized decrease in macrophage cytokine production using interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), platelet-derived growth factor (PDGF), and transforming growth factor beta 1 (TGF-beta 1) as marker cytokines. Our present in vitro results using human cells confirm our previous in vivo studies in the rat and support the hypothesis that diabetes-induced hyperlipidemia alters the monocyte differentiation process resulting in changes of macrophage subsets and cytokine release at the wound site, ultimately impairing the wound-healing process.

Animals↗

PubMed1999

Response of periradicular tissues to growth factors introduced into the surgical site in the root-end filling material.

AIM: The objective of this study was to evaluate the healing of the periradicular tissues when exogenous growth factors were delivered to the respected root-end. The healing response was compared with that when Diaket was used as a control. METHODOLOGY: Non-surgical root canal treatment was performed on mandibular teeth in mongrel dogs. Surgical treatment followed and included root-end resection and root-end cavity preparation. Insulin-like growth factor in combination with platelet-derived growth factor, or fibroblast growth factor alone, were then placed in the root-end preparations on a polylactic acid carrier (Atrisorb) with or without the incorporation of the carrier tetracalcium phosphate. The healing was evaluated at 60 days with regard to presence of inflammatory response, bone regeneration, periodontal ligament formation and cementum formation. RESULTS: Osseous regeneration in the excisional would and periodontal formation were significantly greater when Diaket was used as the root-end filling material. Likewise, cementum deposition occurred significantly more frequently in the Diaket group (P < 0.05). The polylactic carrier Atrisorb remained in the surgical sites for the duration of the study. CONCLUSIONS: The use of specific growth factors, FGF and a combination of IGF/PDGF, delivered to the prepared root end in a collagen carrier did not initiate the desired periradicular tissue response of regeneration. Diaket, as used in this study, did stimulate a periradicular tissue response compatible with regeneration.

Analysis of Variance↗

PubMed1999

Heightened gingival inflammation and attachment loss in type 2 diabetics with hyperlipidemia.

BACKGROUND: Our previous studies in diabetic (DB) rats suggest that hyperlipidemia may cause a dysregulation of the cellular and local cytokine response to periodontitis (AP). The objective of the present study was to determine if diabetes has a similar dysregulatory effect on the gingival response to AP in humans. METHODS: Peripheral blood, as well as gingival tissue (GT) and gingival crevicular fluid (GCF), was obtained from a total of 35 patients who were categorized into the following groups based on level of diabetic (type 2) control and presence or absence of adult periodontitis (AP): group 1, systemically and periodontally healthy (n = 6); group 2, systemically healthy with adult periodontitis (n = 7); group 3, well-controlled diabetes and periodontally healthy (n = 6); group 4, well-controlled diabetes with adult periodontitis (n = 5); group 5, poorly controlled diabetes and periodontally healthy (n = 5); group 6, poorly controlled diabetes and adult periodontitis (n = 6). All subjects were given a thorough periodontal examination, including probing depths (PD), clinical attachment levels (CAL), gingival index (GI), plaque index (PI), and vertical bitewing radiographs. Blood studies included levels of glycated hemoglobin (HbA1c), triglycerides (TG), cholesterol (CHL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL). The levels of interleukin-1 beta (IL-1beta) in GCF and GT, interleukin-6 (IL-6), and platelet-derived growth factor AB (PDGF-AB) in GT from patients in each experimental group were analyzed by enzyme-linked immunosorbent assay (ELISA). RESULTS: Our results indicate that all clinical indices except PI were significantly elevated in the poorly controlled and well-controlled diabetics, compared to systemically healthy patients, but only in the subjects without preexisiting AP (Tukey's multiple comparisons, P <0.05). Pairwise linear regression analysis revealed significant (P <0.01) positive associations between periodontal inflammation (PD, CAL, PI, GI) and levels of GCF IL-1beta, GT IL- 1beta GT IL-6, but not GT PDGF; moreover, GT IL-6 levels were significantly associated (P<0.05) with GT IL-1beta. As TG levels increased in the non-AP patients (group 1 < group 3 < group 5), there was a trend, not significant, for increased GCF IL-1beta levels and increased gingival inflammation. Interestingly, periodontitis resulted in increased PDGF-AB levels in the gingiva of systemically healthy and well-controlled diabetes patients, but this increase was obtunded in poorly controlled diabetes patients. CONCLUSIONS: This confirms our earlier work in the diabetic rat model. These studies indicate that decreased metabolic control in type 2 diabetics results in increased serum triglycerides and has a negative influence on all clinical measures of periodontal health, particularly in patients without preexisting periodontitis. Levels of the cytokine IL- 1beta showed a trend for increasing as diabetic control diminished. In contrast, levels of the growth factor PDGF, which normally increase in periodontitis, decreased in poorly controlled diabetics with periodontitis. These studies suggest a possible dysregulation of the normal cytokine/growth factor signaling axis in poorly controlled type 2 diabetics that may contribute to periodontal breakdown/diminished repair.

Adult↗

PubMed1999

Association between periodontitis and hyperlipidemia: cause or effect?

BACKGROUND: Epidemiological studies suggest a relationship between periodontitis and coronary artery disease, but the mechanism has not been established. Recent studies in animals indicate that low dose endotoxin, as in a gram-negative infection, can induce hyperlipidemia and myeloid cell hyperactivity. The association between periodontitis, systemic exposure to Porphyromonas gingivalis, lipopolysaccharides (LPS), and hyperlipidemia has not been examined in humans. METHODS: Sera were obtained from 26 adult periodontitis patients and 25 healthy control (C) subjects selected from patients and staff. Serum antibodies against Porphyromonas gingivalis and its LPS were analyzed by enzyme-linked immunosorbent assay (ELISA) and Western blotting, respectively. Serum triglycerides (TG) and cholesterol (CHOL) were assayed by a commercial laboratory. The associations between AP and blood levels of TG, CHOL, and anti-P. gingivalis whole cells and LPS were examined by logistic regression analysis. Peripheral blood polymorphonuclear leukocytes (PMNs) from 6 healthy fasted donors were incubated with purified TG (0.1 mg/ml) for 2 hours at 37 degrees C, stimulated with 100 ng/ml P. gingivalis LPS, and the release of IL-1beta measured by ELISA. RESULTS: The presence of periodontitis was significantly associated with age (odds ratio = 3.5, P = 0.04), elevated TG levels (odds ratio = 8.6, P = 0.0009), elevated CHOL levels (odds ratio = 7, P = 0.004), elevated ELISA titer (odds ratio = 35, P = 0.003) and reactivity with P. gingivalis LPS (odds ratio = 41, P = 0.001). PMNs from all 6 healthy patients released modest levels of IL-1beta (10 to 60 pg/ml) when stimulated with 100 ng/ml P. gingivalis LPS. Addition of TG resulted in a significant increase (P <0.05) in IL- 1beta secreted that ranged from 7 to 150% over LPS alone. No IL-1beta was elicited by TG or vehicle alone. CONCLUSIONS: The results of this study indicate the presence of a significant relationship between periodontitis, hyperlipidemia, and serum antibodies against P. gingivalis LPS that warrants further examination in a larger patient population. Furthermore, these studies indicate that elevated triglycerides are able to modulate IL-1beta production by PMNs stimulated with P. gingivalis LPS.

Adult↗

PubMed1999

Cyclosporine A-induced gingival overgrowth: a comprehensive review.

Cyclosporine A, an extremely effective immunosuppressant, is also associated with various untoward effects, including gingival overgrowth. Despite intense clinical and laboratory investigation, the cellular-molecular mechanism through which cyclosporine A simultaneously acts as a selective immunosuppressant while it elicits a connective tissue reaction in the gingiva remains poorly understood. In recent years, cellular and molecular biologic techniques have elucidated a variety of growth factors that control connective tissue homeostasis. Two growth factors known to be major elements in wound repair and connective tissue homeostasis are platelet-derived growth factor and transforming growth factor-beta 1. Increased gingival levels of these factors may be responsible for promoting fibroblastic proliferation and fibroblastic production of extracellular matrix constituents in overgrown gingival tissues. Expression of these factors has recently been shown to be upregulated in these tissues. The results of these recent studies may provide a foundation for understanding the molecular mechanism involved in the pathogenesis of cyclosporine A-induced gingival overgrowth.

Cyclosporine↗

PubMed1998

Diabetes-induced impairment of macrophage cytokine release in a rat model: potential role of serum lipids.

Animals↗

PubMed1998

Calbindin-D28k buffers intracellular calcium and promotes resistance to degeneration in PC12 cells.

The calcium-binding protein calbindin-D28k (CB) has been hypothesized to function, in part, as a neuroprotective protein. CB is localized within nerve cells that are often less vulnerable to degeneration in patients with Alzheimer's disease and Parkinson's disease, and cells containing CB can buffer intracellular calcium concentrations ([Ca2+]i). The present study was designed to directly test the hypothesis that CB can protect cells from degeneration by reducing [Ca2+]i. PC12 cells, transfected to express different levels of CB, were found to be significantly less vulnerable to degeneration caused by serum withdrawal, glutamate, and the neurotoxin 1-methyl-4-phenylpyridinium (MPP+). However, CB did not protect cells from degeneration caused by the calcium ionophore A23187. CB-transfected cells exhibited reduced elevations in [Ca2+]i following treatment with bradykinin, or ATP compared to non-CB-containing cells. These data indicate that CB can protect cells from degeneration caused by certain conditions, and it reduces elevations in [Ca2+]i caused by influx from extracellular sources.

1-Methyl-4-phenylpyridinium↗

PubMed1998

Diabetes prevents periodontitis-induced increases in gingival platelet derived growth factor-B and interleukin 1-beta in a rat model.

Periodontitis is a chronic inflammatory disease characterized by a progression that is very much dependent on host response. The gingiva can be considered to be in a constant state of wounding (pathologic wounding by bacterial plaque) and a constant state of maintenance/repair. In this context, any metabolic disturbance in the host which compromises tissue repair/wound healing will exacerbate the progression of periodontitis. Diabetes presents an interesting example because two major complications of diabetes are delayed wound healing and periodontitis. Our previous studies indicate that delayed wound healing and periodontitis may be manifestations of a general systemic deficit in diabetes involving alteration of macrophage cytokine gene expression. The present study was designed to determine whether: 1) diabetes-induced metabolic alterations affect gingival cytokine levels; and 2) diabetes-induced metabolic alterations modify the gingival cytokine profile in periodontitis. Sprague-Dawley rats (N=12/group) were injected with streptozotocin (65 mg/kg) into the tail vein to induce diabetes (defined by blood glucose levels > 250 mg/dl) or received the injection vehicle or no treatment as controls. Periodontitis was induced in additional groups of diabetic and control rats by gavage with Porphyromonas gingivalis A7436. After 90 days, serum glucose was analyzed to document diabetes; alveolar bone level was measured to document severity of periodontitis; gingiva was harvested circumferentially from the first and second molars; and cytokines in gingival homogenates were assayed by ELISA using commercial kits. Cytokine levels were expressed as mean+/-SEM pg/microg protein. Diabetes alone did not alter the gingival cytokine profile for platelet-derived growth factor B (PDGF-B), interleukin 1-beta (IL-1beta), transforming growth factor-beta (TGF-beta), and tumor necrosis factor-alpha (TNF-alpha). Periodontitis alone demonstrated a significant increase (P < 0.05) in levels of PDGF-B and IL-1beta. Diabetes superimposed on periodontitis prevented these increases. Thus, diabetes-induced metabolic alterations do not affect gingival cytokine levels per se; however, they do alter the normal host response to periodontitis through blockage of periodontitis-induced increases in PDGF-B and IL-1beta.

Alveolar Bone Loss↗

PubMed1998

In vitro evaluation of complex carbohydrate denture adhesive formulations.

OBJECTIVE: Acemannan, a complex mannose carbohydrate derived from the aloe vera plant, has an inherent stickiness/viscosity. Prototype Acemannan denture adhesive formulations were evaluated for pH changes, cytotoxicity to human gingival fibroblasts and adhesive strength in both dry and wet conditions. METHOD AND MATERIALS: The denture adhesive formulations consisted of five combinations of Acemannan with varying concentrations of preservatives and two other formulations without preservatives. The pH of each formulation was measured over 24 hours. Assessment of cytotoxicity was accomplished using the in vitro, tetrazolium-based colorimetric assay on cultures of human gingival fibroblasts after exposure to the adhesive formulations for up to 24 hours. The adhesive strength was evaluated with a universal testing machine under initial dry conditions and after immersion in a constant-temperature water bath for up to 20 minutes. RESULTS: Formulations 1 and 2 achieved and maintained pH values above 6.0 (the critical pH for hydroxyapatite dissolution) approximately 6 hours into the study. None of the prototypes demonstrated an initial pH above the critical pH. Formulations 1, 2, 3, and 5 exhibited significant cytotoxicity to human gingival fibroblasts over 24 hours. Formulations 4, 20:1, and 150:1 demonstrated minimal cytotoxicity. Formulation 1 exhibited the poorest adhesive strength, while the most viscous formulation (prototype 150:1) was by far the best performer. Generally, adhesive bond strengths for all prototypes were quite high and relatively stable over time in a wet environment. CONCLUSION: To achieve the ideal adhesive in terms of strength, pH, and cytotoxicity, Acemannan formulation 150:1 should be adjusted to contain the preservative concentration of formulation 4 and have an initial pH value of 6.0 or higher.

Adhesiveness↗

PubMed1997

Type II collagen and TGF-betas in developing and aging porcine mandibular condylar cartilage: immunohistochemical studies.

Transforming growth factor-betas (TGF-betas) have been associated with the development and maintenance of articular cartilage. However, no studies have addressed their role in the postnatal development of mandibular condylar cartilage. This investigation represents the first immunohistochemical characterization of TGF-beta isoforms and type II collagen in porcine mandibular condylar cartilage from various age groups. Furthermore, it is the first description of possible age-related changes in the expression of these proteins during postnatal development of this tissue. Condylar cartilage was dissected from freshly harvested temporomandibular joints of newborn, 6-, 12-, 24-, and 36-month-old farm swine. TGF-beta1, TGF-beta2, TGF-beta3, and type II collagen were localized via standard immunohistochemical procedures. An immunoblot technique was employed to compare the relative amount of each protein present in the various age groups. Immunoreactivity was detected in mandibular condylar cartilage for all three isoforms of TGF-beta and for Type II collagen. All age groups demonstrated some evidence of immunostaining, primarily in the cytoplasm of cells from most zones of the cartilage. Immunoblot results indicated that TGF-beta isoforms had individualized patterns of expression. When newborn protein levels were taken as the baseline, TGF-beta1 demonstrated a significant increase at ages 24 and 36 months. TGF-beta2 significantly increased at 6, 12, 24, and 36 months (peak levels at 24 months; similar levels at 6, 12, and 36 months), whereas TGF-beta3 remained stable at all ages. Type II collagen demonstrated increases that paralleled the increased levels of TGF-beta1 and TGF-beta2 at 24 and 36 months.

Aging↗