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PubMed2004

Connective tissue metabolism and gingival overgrowth.

Gingival overgrowth occurs mainly as a result of certain anti-seizure, immunosuppressive, or antihypertensive drug therapies. Excess gingival tissues impede oral function and are disfiguring. Effective oral hygiene is compromised in the presence of gingival overgrowth, and it is now recognized that this may have negative implications for the systemic health of affected patients. Recent studies indicate that cytokine balances are abnormal in drug-induced forms of gingival overgrowth. Data supporting molecular and cellular characteristics that distinguish different forms of gingival overgrowth are summarized, and aspects of gingival fibroblast extracellular matrix metabolism that are unique to gingival tissues and cells are reviewed. Abnormal cytokine balances derived principally from lymphocytes and macrophages, and unique aspects of gingival extracellular matrix metabolism, are elements of a working model presented to facilitate our gaining a better understanding of mechanisms and of the tissue specificity of gingival overgrowth.

Animals↗

PubMed2004

Trial of metronidazole vs. azithromycin for treatment of cyclosporine-induced gingival overgrowth.

Gingival overgrowth usually characterized by increased cellular growth of gingival fibroblasts appears to be multifactorial. In patients receiving CyA for more than 3 months, the incidence can approach 70% and can be attributed to pharmaceutical immunosuppression. Case reports have reported regression of overgrowth with both metronidazole and azithromycin. The goal of this study was to determine the efficacy of metronidazole and azithromycin in reducing CyA-induced gingival overgrowth. Twenty-five patients were included in this double-blinded randomized study. All patients were receiving CyA as medically indicated and diagnosed with gingival overgrowth by a dentist. Patients were randomized to receive either 5-days of azithromycin or 7-days of metronidazole given at baseline only. The extent of gingival overgrowth was measured at 0, 2, 4, 6, 12, and 24 wk. Fourteen patients at CCF and 11 patients at CCHMC were studied. Repeated measures anova was performed to assess differences within and between groups. Gingival overgrowth at baseline was not statistically different between groups. The mean degree of gingival overgrowth after treatment was different across all time intervals (p = 0.0049) showing azithromycin to be more effective than metronidazole. Therapy with azithromycin offers an effective alternative to the management of CyA-induced gingival overgrowth.

Adolescent↗

PubMedDate not supplied

[The causes of gingival overgrowth].

Gingival overgrowth includes a series of diseases with many clinical appearances. The pathological mechanisms being obscure there were used many terms for defining it. Thus, "gingival hyperplasia" and "gingival hypertrophy" were the definitions used to define this pathology. Therefore, the term of "gingival overgrowth" replaced in last decades the above two terms. This article have the goal of trying a classification of the entities forming the large family of gingival overgrowth.

Dentures↗

PubMed1996

The pathogenesis of drug-induced gingival overgrowth.

Gingival overgrowth is a well-documented unwanted effect, associated with phenytoin, cyclosporin, and the calcium channel blockers. The pathogenesis of drug-induced gingival overgrowth is uncertain, and there appears to be no unifying hypothesis that links together the 3 commonly implicated drugs. In this review, we consider a multifactorial model which expands on the interaction between drug and/or metabolite, with the gingival fibroblasts. Factors which impact upon this model include age, genetic predisposition, pharmacokinetic variables, plaque-induced inflammatory and immunological changes and activation of growth factors. Of these, genetic factors which give rise to fibroblast heterogeneity, gingival inflammation, and pharmacokinetic variables appear to be significant in the expression of gingival overgrowth. A more thorough understanding of the pathogenesis of this unwanted effect will hopefully elucidate appropriate mechanisms for its control.

Adult↗

PubMedDate not supplied

Calcium channel blocker induced gingival overgrowth.

Gingival overgrowth occurs with phenytoin, cyclosporin, and calcium antagonists. It can be disfiguring and painful. The prevalence of gingival overgrowth with the use of calcium antagonists may be as high as 38%. The prevalence with nifedipine may be greater than with other calcium blockers. Overgrowth occurs 3.3-times more commonly in men than in women. Plaque control is necessary. Some patients may require gingival surgery.

Calcium Channel Blockers↗

PubMed2003

Preservation of the negative image of tooth enamel with dental impression material enhances morphometric measurements of gingival overgrowth.

Gingival overgrowth is a common health problem caused by genetic and environmental risk factors. Animal models for quantitative histological studies are needed to uncover genetic predisposition and dose-response data that might put individuals at increased risk for gingival disease. Gingival height, thickness, inflammation, and the degree of encroachment of gingiva over the tooth, are clinical measures of overgrowth; most of these parameters can be measured histologically, but in order to quantify gingival coverage of the tooth, the image of the crown must be present. Tooth and bone typically require decalcification for histology; thus, the tooth crown, a critical landmark, is lost. We describe a method for imaging the crown histologically, using impression materials applied to dissected mouse mandibles. Four dental alginates, three polyvinyl siloxanes, and one polyether and gelatin were used. The impression-material/mandibular tissue blocks were processed routinely. Polyvinyl siloxanes were incompatible with embedding resin; alginates, polyether and gelatin could be fixed, decalcified, embedded, and sectioned. Alginates and gelatin could be stained. Success in imaging the tooth crown varied with the preparation, but the alginates, polyether, and gelatin permitted a useful degree of measurement of exposed crown and enamel thickness, along with other morphometric parameters such as thickness of the dentin, lateral mandibular ramus, rete pegs, height of the gingiva, and volume density of vessels and inflammatory cells in the lamina propria. In conclusion, this new application for impression materials allows gingival coverage of tooth crown, as well as numerous other parameters to be measured for comparison with clinical data.

Alginates↗

PubMed2006

Expression of transforming growth factor-beta receptor II mRNA in cyclosporine-induced gingival overgrowth.

Gingival overgrowth (GO), characterized by increased cellular and extracellular matrix components in gingival tissue, is a frequent side effect of cyclosporine (CsA). In previous studies, elevated levels of transforming growth factor-beta (TGF-beta) have been detected in GO tissue, which led to the conclusion that TGF-beta plays a major part in the pathogenesis. TGF-beta activity is mediated by three receptors; TGF-beta receptor II (TGF-beta RII), the most important, has been immunohistochemically detected in GO and normal gingival tissue. The aim of this study was to clarify whether TGF-beta RII is overexpressed in CsA-induced GO. The expression of TGF-beta RII mRNA in GO tissue of patients on CsA (n = 10, 5 women, aged 42.5 +/- 14.9 years) with renal transplantation (transplant duration 3.6 +/- 0.96 years) was compared with that in healthy gingiva of control subjects (n = 10, 5 women, aged 42.5 +/- 7.6 years). Semiquantitative reverse transcribed-polymerase chain reactions (RT-PCR) were applied with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as an internal standard. TGF-beta RII mRNA was readily detected in the GO tissue of patients on CsA. The level of TGF-beta RII mRNA relative to GAPDH in GO cases was not significantly higher than the relative TGF-beta mRNA level in normal gingiva (0.60 +/- 0.16 vs 0.52 +/- 0.19; P = .575). The precise mechanism of CsA-induced GO remains uncertain. According to our results, TGF-beta RII was not upregulated in CsA-induced GO, and may have no important role in this disorder. However, the involvement of TGF-beta in the molecular pathology of GO may be mediated via TGF-beta RI or RIII.

Adult↗

PubMed2006

Platelet-derived growth factor (PDGF) isoform and PDGF receptor expression in drug-induced gingival overgrowth and hereditary gingival fibrosis.

OBJECTIVE: To investigate possible associations between platelet-derived growth factor (PDGF), PDGF receptor expression and macrophages in drug-induced and hereditary gingival overgrowth. MATERIALS AND METHODS: Tissues from patients with drug-induced gingival overgrowth (DIGO) (n = 10) and hereditary gingival fibrosis (n = 10) were studied and compared with 'control' gingiva (n = 10). Expression of PDGF and its alpha and beta receptors was investigated immunohistochemically and by RT-PCR. Macrophages were identified by immunostaining for CD68. RESULTS: PDGF isoforms and receptors were detected in most cells within all specimens. There were no differences in the numbers of macrophages, or fibroblasts expressing PDGF or receptors, between groups. The level of PDGF expression by fibroblasts, determined by absorbance measurements, was similar between groups for PDGF A. Significantly lower levels of total PDGF and the receptors were detected in drug-induced overgrowth compared to those in hereditary fibrosis (P < 0.004) and control specimens (P < 0.034). All specimens expressed mRNA for PDGF A, PDGF B and alpha and beta receptors. CONCLUSIONS: These data do not support a pivotal role for macrophage-derived PDGF B in the pathogenesis of DIGO. They suggest that fibroblasts in drug-induced lesions have a lowered capacity to produce, and respond to, PDGF, a property not shared by fibroblasts associated with hereditary fibrosis.

Adolescent↗

PubMed2003

Gene expression of extracellular matrix proteoglycans in human cyclosporin-induced gingival overgrowth.

BACKGROUND: Gingival overgrowth is one of the side effects associated with the systemic use of cyclosporin A (CsA). In vitro studies on the extracellular matrix of gingival tissues have demonstrated an altered composition, particularly an accumulation of proteoglycans and collagen. We investigated the gene expression of extracellular matrix proteoglycans in CsA-induced gingival tissue alterations. METHODS: mRNA expression of the proteoglycans perlecan, decorin, biglycan, and versican was analyzed by reverse transcription polymerase chain reaction (RT-PCR) in gingival samples obtained from 12 individuals, six with CsA-induced gingival overgrowth (CsA group) and six with a normal gingiva (control group). The RT-PCR products were subjected to 1% agarose gel electrophoresis containing ethidium bromide and analyzed qualitatively and semiquantitatively by densitometry. Density values were normalized by determining the expression of the housekeeping gene beta-actin in the same sample. Groups were compared by the Student's t test. RESULTS: Perlecan expression showed a marked increase (54%) in the CsA group compared to the control group (P < 0.01), while no significant differences were observed for the other proteoglycans. CONCLUSION: CsA-induced gingival overgrowth seems to be associated with increased expression of perlecan, a typical basement membrane proteoglycan, but not decorin, biglycan, or versican.

Adult↗

PubMed1993

The prevalence and severity of cyclosporin and nifedipine-induced gingival overgrowth.

The gingival health of 32 renal transplant patients who were medicated with cyclosporin was compared with a similar cohort of 23 renal transplant patients medicated with both cyclosporin and nifedipine. Both groups of patients had been taking the above medication for at least 3 months. Plaque scores, gingival inflammation and probing depths were similar for both groups. Patients medicated with the combination of nifedipine and cyclosporin had a significantly higher gingival overgrowth score (p = 0.046) when compared with the group receiving cyclosporin alone. The incidence of clinically significant overgrowth (i.e., overgrowth > 30% which would require surgical intervention) was similar in both groups. Gingival overgrowth was not related to cyclosporin dosage. It is concluded that patients taking cyclosporin or cyclosporin and nifedipine experience gingival overgrowth and that the severity of the overgrowth is greater in patients taking the combined therapy. The levels of plaque and gingival inflammation appear to be associated with this phenomenon.

Adult↗

PubMed1999

Cyclosporin A regulates interleukin-1beta and interleukin-6 expression in gingiva: implications for gingival overgrowth.

BACKGROUND: Gingival overgrowth is a common side effect following the administration of cyclosporin A (CsA); however, the cellular mechanisms remain poorly understood. CsA's immunosuppressant properties involve the regulation of synthesis and cellular response to cytokines. A CsA-induced alteration in the cytokine profile within gingival tissue could provide a mechanism for gingival hyperplasia. The aim of this study was to investigate the effects of CsA on the production of 2 cytokines - interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) - by both gingival fibroblasts and peripheral blood mononuclear cells (PBMC). METHODS: Cells were stimulated for 24 hours in the presence of CsA over a concentration range of 100 to 2,000 ng/ml and the resultant cytokine production determined by ELISA. In addition, levels of both cytokines within normal, inflamed, and overgrown gingival tissue were determined. RESULTS: CsA inhibited IL-6 production by gingival fibroblasts in a dose-dependent manner. In contrast, at a concentration of 2,000 ng/ml, CsA stimulated IL-6 production by PBMC (P <0.05). Fibroblasts derived from overgrown gingiva produced significantly higher levels of IL-6 than their normal counterparts (P <0.05). CsA inhibited IL-1beta production by PBMC over the whole concentration range (P <0.05). IL-1beta was not found in measurable quantities in any of the fibroblast cultures. Levels of IL-6 extracted from overgrown gingival tissue were significantly higher than in inflamed or normal tissue. In contrast IL-1beta levels in overgrown tissue were not statistically significantly greater than those in inflamed tissue. CONCLUSIONS: These results show that CsA does regulate cytokine expression in gingival tissue. This effect may play an important role in the pathogenesis of CsA-induced gingival overgrowth.

Adult↗

PubMed2006

Plasma and gingival crevicular fluid phenytoin concentrations as risk factors for gingival overgrowth.

BACKGROUND: Gingival enlargement is one of the side effects associated with the administration of phenytoin. The mechanism by which phenytoin induces gingival enlargement is not well understood. This study was conducted to investigate the relationship between plasma and gingival crevicular fluid (GCF) phenytoin concentrations and the degree of gingival overgrowth in patients with similar gingival and plaque indices and also to determine the risk factors for gingival enlargement. METHODS: Eighteen patients taking phenytoin in regular doses > or =6 months prior to the investigation participated in the study. Gingival enlargement was evaluated with two indices to score vertical and horizontal overgrowth. The gingival index (GI), plaque index (PI), gingival bleeding time index (GBTI), probing depth (PD), and clinical attachment level (CAL) were also evaluated. GCF and plasma phenytoin concentrations were determined by using high-performance liquid chromatography (HPLC). RESULTS: There was no significant difference between responders and non-responders for PD, CAL, PI, GI, and GBTI. Phenytoin was detected in all of the GCF and plasma samples using the HPLC analysis method. The mean concentration of phenytoin in GCF was significantly greater than the concentration of phenytoin in plasma. No significant difference was observed for the concentration of GCF phenytoin between responders and non-responders. However, the concentration of plasma phenytoin was significantly higher in responders than non-responders. CONCLUSION: This study showed that plasma phenytoin level appeared to be a risk factor for phenytoin-induced gingival overgrowth.

Adult↗

PubMed1992

The incidence and severity of nifedipine-induced gingival overgrowth.

The gingival health of 19 patients with cardiovascular problems who were medicated with nifedipine was compared with a similar cohort treated with atenolol and a control group of healthy patients. In the nifedipine and atenolol groups, patients had been taking their respective medication for a minimum period of 6 months. Plaque scores were similar for all three groups. However, patients medicated with nifedipine had a significantly higher gingival index (P less than 0.005), gingival overgrowth scores (P less than 0.02) and probing sites greater than 3 mm (P less than 0.005) when compared with the atenolol and control groups. 4 patients in the nifedipine group experienced clinically significant gingival overgrowth which required surgical excision. Gingival changes in the nifedipine patients were not related to drug dosage or plaque scores. It is concluded that nifedipine therapy results in significant gingival changes, an effect which may be mediated by the drug's action on calcium transport.

Atenolol↗

PubMed1993

Nifedipine-induced gingival overgrowth in the presence or absence of gingival inflammation in rats.

One adverse effect of nifedipine, a long-acting vasodilator, is gingival overgrowth. Preexisting gingival inflammation and/or dental plaque has been suggested to be responsible for the progression of this side effect, but the precise mechanism is uncertain because of a lack of suitable animal models. A study was therefore done to establish an experimental model of gingival overgrowth in rats and to investigate the possible involvement of gingival inflammation and/or dental plaque in its development. Specific pathogen-free Fischer rats (male, 14 days old) were used. Gingival inflammation and dental plaque accumulation were induced by infection with Streptococcus mutans MT8148R. The nifedipine-treated rats (experimental group) were fed a caries-inducing diet containing nifedipine either with or without infection, while the nifedipine-untreated rats (control group) were fed the same diet, similarly with or without the infection. Marked gingival overgrowth was induced in the mandibular molar region of nifedipine-treated rats regardless of S. mutans infection, although the infection resulted in a further increase in the degree of gingival overgrowth. Histological examination of the gingival overgrowth revealed the presence of redundant subepithelial connective tissue in the treated rats, and inflammatory cell infiltration was apparent only in the tissue of the S. mutans-infected rats regardless of the nifedipine administration. These findings suggest that nifedipine induces gingival overgrowth in rats either in the presence or absence of gingival inflammation and/or dental plaque, although these factors can augment the effect of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

PubMed1995

Common and less common gingival overgrowth conditions.

Gingival enlargement is caused by some local and systemic pathologic conditions. Clinical manifestations vary and depend on the underlying defects. Diagnosis of these abnormalities and their relationship to underlying systemic conditions is essential prior to establishment of any treatment. Several gingival overgrowth conditions resulting from various causes are included in this review. Some conditions are rare and appear with clinical features interesting to both dentists and dermatologists. A brief review of causes, pathogenesis, and differential diagnosis is presented.

Diagnosis, Differential↗

PubMed1987

Cyclosporin-induced gingival overgrowth: correlation with dental plaque scores, gingivitis scores, and cyclosporin levels in serum and saliva.

Gingival overgrowth, dental plaque, and gingivitis were assessed by means of standardized semiquantitative indices in thirty renal transplant patients undergoing immunosuppression with cyclosporin-A (Cy-A). Radioimmunoassay techniques were used to determine Cy-A in serum samples and in parotid, submandibular, and whole saliva samples from each patient. A significant positive correlation was found between gingival overgrowth scores and both dental plaque and gingivitis scores. A significant positive correlation was found between whole-saliva Cy-A and both plaque and gingival overgrowth scores. No such correlation was found when parotid Cy-A or submandibular Cy-A was considered. This was attributed to differences in saliva-collection methods, and a possible role of dental plaque as a local reservoir of Cy-A is proposed.

Adult↗

PubMed2001

Connective tissue growth factor in drug-induced gingival overgrowth.

BACKGROUND: Drug-induced gingival overgrowth is a known side effect of certain chemotherapeutic agents used for the treatment of systemic disorders. The pathogenesis and mechanisms responsible for this condition are not fully understood. This study assesses for the presence and localization of connective tissue growth factor (CTGF) in drug-induced gingival overgrowth tissues. CTGF immunostaining was compared with sections stained with transforming growth factor (TGF)-beta1 and CD31 antibodies in order to investigate possible pathogenic mechanisms. METHODS: Gingival overgrowth samples were obtained from patients undergoing therapy with phenytoin (n = 9), nifedipine (n = 4), cyclosporin A (n = 5), and control tissues from systemically healthy donors (n = 9). Tissue sections were subjected to peroxidase immunohistochemistry and were stained with CTGF and TGF-beta1 polyclonal primary antibodies. Possible relationships between CTGF staining and angiogenesis were also studied using an anti-CD31 antibody as a marker for endothelial cells. Staining was analyzed by computer-assisted quantitative and semiquantitative methodology at 5 defined sites in all samples based on the location of specific landmarks including epithelium and underlying connective tissues. RESULTS: Cellular and extracellular CTGF content in phenytoin gingival overgrowth tissues was significantly (P<0.05) higher compared to the other gingival overgrowth tissues and the controls. Higher CTGF staining in phenytoin gingival overgrowth tissues was accompanied by an increased abundance of fibroblasts and connective tissue fibers. No strong association of CTGF staining with TGF-beta1 or CD31 staining was found. CONCLUSIONS: The data from the present study show significantly higher CTGF staining in phenytoin-induced gingival overgrowth tissues compared to controls, cyclosporin A-, or nifedipine-induced gingival overgrowth. Moreover, semiquantitative analyses of histologic samples support the concept that the phenytoin overgrowth tissues are fibrotic. These associations suggest a possible role for CTGF in promoting development of fibrotic lesions in phenytoin-induced gingival overgrowth.

Adult↗

PubMed2006

Increased expression of vascular endothelial growth factor in cyclosporin A-induced gingival overgrowth in rats.

BACKGROUND: Gingival overgrowth is a side effect associated with cyclosporin A (CsA) therapy. The lesion is characterized by increased epithelial thickness, enlargement of connective tissue, and increased vascularization. The aim of this experimental study was to examine the role of vascular endothelial growth factor (VEGF) in the pathogenesis of CsA-induced gingival overgrowth. METHODS: Twenty male Wistar rats were divided into two groups of 10 animals each. For the development of gingival overgrowth, one group received CsA therapy subcutaneously in a daily dose of 10 mg/kg for 60 days, and the other group was used as a control. At the end of the experimental period, rats were subsequently decapitated, and the mandibles with the surrounding gingiva and soft tissue were removed. Half of each sample was used for histomorphometric analysis, and the other half was used for biochemical analysis. Histomorphometric analysis included the measurements of the number and diameter of blood vessel profiles under a microscope, and biochemical analysis included the assessment of VEGF concentration by enzyme-linked immunosorbent assay (ELISA). RESULTS: The histomorphometric findings showed that the number of blood vessel profiles increased in the CsA group compared to the control group (P <0.001), although the increase in the diameter of blood vessel profiles was not significant (P >0.05). The biochemical findings showed that in vivo VEGF expression was higher in the CsA group compared to the control group (P <0.001). CONCLUSION: The results of this study suggest that increased VEGF expression may be associated with the pathogenesis of CsA-induced gingival overgrowth.

Animals↗