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PubMed1993

Reverse smoking as a risk factor for palatal cancer: a cross-sectional study in rural Andhra Pradesh, India.

A cross-sectional study of reverse smoking and its association with pre-malignant and malignant lesions of the palate was conducted in the north coastal areas of Andhra Pradesh, India. A total of 480 randomly selected persons were interviewed. Information about smoking status, diet and access to mass media was obtained in each case and an examination of the oral cavity was performed. Reverse smoking of chutta was practised by 33% of the total rural population. The prevalence rate of all palatal lesions was 55%. The prevalence rates of the separate lesions: leukoplakia palatii, palatal keratosis and palatal cancer, were 9.8%, 18.1% and 1.9%, respectively. The presence of these (pre-)malignant lesions was strongly associated with reverse smoking and also associated with conventional chutta smoking. Reverse smoking induced significantly more lesions than conventional chutta smoking, and was a major determinant of subsequent palatal cancer: all 9 newly diagnosed palatal cancers were observed within the group of reverse smokers. There was an inverse relationship between the incidence of palatal lesions and vitamin A intake. The study of access to mass media indicated that the most favourable medium for promoting a prevention campaign would be the cinema.

Age Factors↗
PubMed1975

Inhibitory effect of corticoids on the proliferative pattern in mouse palatal processes.

The formation of the secondary palate in mice is accompanied by intensive mitotic activity, which is mainly concentrated at the medial edges of the palatal processes. In control H-Velaz randombred fetuses the mitotic activity culminated approximately 24 h before palatal-shelf horizontalization, so that the period of intensive cell proliferation coincided with the period when cleft palate could be induced by cortisone administration. Effects of teratogenic doses of corticoids, injected directly into amniotic sac of embryos on day 13 (0.3 mg hydrocortisone) or im to pregnant females on day 12 (7.5 mg cortisone acetate), on the proliferative peak in palatal processes were studied using intraamniotic injection of colchicine. Counts of colchicine-blocked mitoses in histological serial sections revealed both a significant decrease in overall mitotic density and a posterior shift of the proliferative peak in the palatal processes of fetuses treated with doses of corticoids producing cleft palate.

Adrenal Cortex Hormones↗
PubMed1977

6-Aminonicotinamide-induced cleft palate in the mouse: the nature of the difference between the A/J and C57Bl/6J strains in frequency of response and its genetic basis.

Cleft palate induction by 6-aminonicotinamide (6-AN) was examined in the A/J and C57BL/6J strains of mice to determine the nature of the strain difference in frequency of cleft-palate response. Probit analysis of the cleft-palate response to dose of different genotypes revealed a family of linear and parallel dose-response curves. The genotypes differ only in dosage tolerance (log ED50) to 6-AN that is required for the cleft-palate response. No evidence for a maternal cytoplasmic effect on 6-AN-induced cleft palate was found under the conditions of the present study. When the difference is dosage tolerance to 6-AN between A/J and C57BL/6J was examined with a single dose and measured by differences in frequency of induced cleft palate on a probit scale, there was some departure from genetic additivity. There was an indication off dominance deviation of the F1 embryos in the direction of C57BL/6J.A3-locus, epistatic model is proposed to account for the difference in embryonic tolerance ot 6-AN-induced cleft palate. There was a suggestion of association with the brown (b) locus.

6-Aminonicotinamide↗
PubMed1980

A glucocorticoid receptor in fetal mouse: its relationship to cleft palate formation.

Fetal mouse tissue was investigated for a glucocorticoid binding receptor which might be responsible for cleft palate formation. Fetal mouse heads contain a soluble component which binds the glucocorticoid triamcinolone acetonide in vitro with high affinity. This binding component is present in small finite amounts. Other glucocorticoids compete with triamcinolone acetonide for the binding site in a manner consistent with their potency ranking as cleft palate teratogens. Several mineralocorticoids and progestins also compete when administered in vitro but not when administered in vivo. Triamcinolone acetonide binding was determined in three mouse strains, A/J, C3H, and C57BL, which are listed in decreasing order of cleft palate susceptibility to cortisone. No positive correlation was found between cortisone cleft palate susceptibility and either triamcinolone acetonide binding affinity or binding amount in fetuses from these strains. Cleft palate dose response curves for triamcinolone acetonide were determined in these strains, but they were not parallel to each other as they were for cortisone. This suggests that triamcinolone acetonide may cause cleft palate by different mechanisms in these strains. Thus, fetal mouse tissue contains an apparent glucocorticoid receptors, but its relationship to cleft palate formation in mice is not clear.

Animals↗
PubMed1983

Abnormal head posture associated with induction of cleft palate by methylmercury in C57BL/6J mice.

Maternal treatment with methylmercury (MeHg) has been shown to induce a high frequency of cleft palate and produce growth retardation in rat and mouse fetuses, but the relation between these effects is unknown. The objective of this study was to determine if mandibular growth retardation was a factor that contributed to induction of cleft palate in C57BL/6J mice. Two doses of MeHg (10 mg/kg maternal body weight) were given subcutaneously on days 10 and 11 of gestation, and the fetuses were morphometrically studied on days 14, 15, and 18. Full clefts of the secondary palate were present in approximately half of the treated day 15 and 18 fetuses; therefore, the cleft palate (CP) and noncleft palate (NCP) groups were analyzed separately to facilitate identification of morphologic changes associated with the clefting. The results showed that, compared with controls, the day 14 MeHg-treated fetuses had significantly smaller placental weights, but only half of the fetuses had delayed palatal shelf elevation, reduced body weight, and delayed morphological development. However on day 15, the CP and the NCP groups had similar reductions in body weight and placental weight. A striking downward and forward positioning of the head was present in the MeHg-treated fetuses with the CP group more severely affected than the NCP group. Significant differences between the three groups (control, NCP, and CP) were present with mean head-to-body angles of 67 degrees, 60 degrees and 51 degrees, respectively. The absence of normal head lifting resulted in a relative mandibular retrognathia that when combined with a decrease in mandibular length produced alterations in spatial relations that were most severe in the CP fetuses. The results suggest that after exposure to MeHg, palatal closure is affected by altered tongue posture associated with the abnormal head positioning and shortening of the mandible that develop following placental and embryonic growth retardation.

Animals↗
PubMed1986

Caffeine effects on cyclic AMP levels in the mouse embryonic limb and palate in vitro.

Caffeine is a teratogen that causes limb and palate malformations in rodents. Since the ability to raise cyclic nucleotide levels is a known biological action of caffeine, cyclic AMP levels were measured in CD-1 mouse embryonic forelimb from whole embryo culture and embryonic limb and palate cells grown in primary culture following treatment with various concentrations of caffeine (0, 1, 3, or 10 mM). In forelimb buds from whole embryo culture, a dose-dependent response was observed. Caffeine at 1 mM concentration stimulated cyclic AMP levels to 151% of control value at 60 min. Even greater stimulation of cyclic AMP occurred at higher caffeine concentrations. A dose-dependent response was seen in both limb and palate cell culture. In limb cell culture, all caffeine concentrations significantly stimulated cyclic AMP after 10 min compared to control. In palate cell culture, there was a twofold increase in cyclic AMP at the 1-mM caffeine concentration. At higher caffeine concentrations, cyclic AMP was significantly increased after 60 min. In addition, stimulation of cyclic AMP in cultured limb and palate cells by isoproterenol, a beta-adrenergic agonist, was used as a positive control. Isoproterenol stimulated a 2.5-fold greater response in the palate cells than in the limb bud cells at isoproterenol levels of 10(-5) or 10(-4) M. The increase of cyclic AMP may be influential in the process of abnormal limb or palate development.

Animals↗
PubMed1989

Growth of the secondary palate in the hamster following hydrocortisone treatment: shelf area, cell number, and DNA synthesis.

The contribution made by mesenchymal cells during the later stages of palatal development was examined in control and hydrocortisone-treated hamster embryos. Cross-sectional area of the palatal shelf was measured, and the numbers of both epithelial and mesenchymal cells were counted. DNA synthesis was measured by 3H-thymidine incorporation and was used as an index of growth by cell proliferation. The observations in controls indicated that, unlike development during the initial 24 hr, the later period of vertical palate development, followed by reorientation of shelves and their closure, was characterized by a steady level of mesenchymal cell number and palatal shelf area. An absence of corresponding growth in the epithelial cell number suggests that the cells may accommodate the growth either by increasing their size and/or by stretching along the basal lamina. Hydrocortisone treatment did not alter the growth pattern of cell numbers or shelf area. However, it prevented the fusion between the opposing shelves, perhaps by affecting the cytodifferentiation of the palatal tissues. Although a continuous increase in the number of mesenchymal cells during the latter half of vertical shelf development, i.e., between days 11:00 and 12:00 of gestation, is not required for reorientation and fusion of the shelves, it is not clear from the data from the present study whether a critical number of cells and/or cell density is essential for reorientation and fusion of the palate. It was suggested that, for normal palatal development, information on cell cycle and positioning of mesenchymal cells within the shelf during the vertical development may be crucial for further understanding of subsequent events of palatogenesis.

Animals↗
PubMed1992

Embryonic palatal responses to teratogens in serum-free organ culture.

This study examines development of rat, mouse, and human embryonic palates in submerged, serum-free organ culture. The concentration-response profiles for retinoic acid (RA), triamcinolone (TRI), hydrocortisone (HC), dexamethasone (DEX), and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) were examined and the mechanisms of clefting in vitro were compared to observed in vivo responses. Craniofacial regions were dissected on gestational day (GD) 12 for mice and GD 14 for rat, and cultured for 3-4 days in Bigger's BGJb medium in flasks flushed with 50% O2, 45% N2, 5% CO2. Growth and fusion of secondary palates were scored under a dissecting microscope. In serum-free control medium, mouse and rat palatal fusion occurred within the 4-day culture period. Supplementing with fetal bovine serum (FBS) in excess of 1% interfered with growth and fusion in control medium. RA significantly inhibited fusion of mouse and rat palates at 5 x 10(-9) and 1 x 10(-10) M, respectively, with RA-induced clefting related to abnormal proliferation and differentiation of medial epithelia. In contrast, glucocorticoid-induced clefting was due to concentration-dependent inhibition of shelf growth. TRI significantly inhibited fusion at 4 x 10(-5) M, and 1 x 10(-4) M DEX or HC, inhibited fusion of 19 and 42% of shelves, respectively. The response rate for DEX in the presence of 1% FBS was increased (42% unfused). TCDD clefting was due to altered medial epithelial differentiation and 1 x 10(-8) M TCDD affected 36% of CD-1 mouse, 23% of C57BL/6N mouse, and 47% of F344 rat palates. When the medium was supplemented with 1% FBS, selenium, transferrin, and additional glutamine, the response of C57BL/6N embryos increased to 75%. This rate is similar to that reported for Trowell's-type cultures with IMEM:F12 medium and 1% FBS. The increased responsiveness to DEX or TCDD in the presence of serum suggests that an unknown factor in serum may be required for full activity. Three human embryonic palatal explants (GD 52 or 53) were cultured for 3-6 days and fused during culture. The present study demonstrates that serum-free organ culture supports development of mouse, rat, and human palatal explants. The present study demonstrates the capacity of this organ culture system to model palatogenesis for several species, and to distinguish between various mechanisms of clefting as presented through selected model compounds. This model should be useful for exploring mechanisms of activity at a cellular and molecular level.

Abnormalities, Drug-Induced↗
PubMed2007

A novel technique for visualization of the normal and cleft fetal secondary palate: angled insonation and three-dimensional ultrasound.

OBJECTIVE: To evaluate the effectiveness of a novel approach to the visualization of the fetal secondary palate using three-dimensional (3D) ultrasound. METHODS: Sonographic examinations were performed in normal fetuses and in one fetus with cleft lip and palate. To avoid acoustic shadowing from the alveolar ridge, the secondary palate was insonated at a 45 degrees angle in the sagittal plane, and 3D ultrasound was used to reconstruct axial and coronal planes. RESULTS: The secondary palate was successfully visualized in 10 of 15 normal fetuses, both in the axial and coronal planes. In the fetus with cleft lip and palate the lesion of the secondary palate was clearly demonstrated, particularly in the coronal plane. CONCLUSION: Angled insonation and 3D ultrasound allow clear visualization of normal and cleft secondary palate.

Cleft Lip↗
PubMed1997

Basic fibroblast growth factor induces apoptosis in myofibroblastic cells isolated from rat palatal mucosa.

The effect of basic fibroblast growth factor (bFGF) on apoptosis in normal rat palatal fibroblasts and rat palatal scar fibroblasts was examined by the TUNEL method in order to clarify the mechanism of apoptosis induction in myofibroblasts during the scar formation process. A percentage of scar fibroblasts undergoing apoptosis was significantly higher than that of palatal fibroblasts when they were treated with bFGF succeeding to serum starvation. Palatal fibroblasts, phenotypically modulated into myofibroblasts by the pretreatment with transforming growth factor-beta 1 (TGF-beta 1), similarly showed a higher level of apoptosis induction by bFGF-treatment. TGF-beta 1 elevated protein and mRNA level of FGF receptor (FGFR) in palatal fibroblasts. Tyrosine autophosphorylation of FGFR upon stimulation by bFGF was significantly higher in scar fibroblasts than in normal palatal fibroblasts. These findings suggested that bFGF may be a potential stimulator of apoptosis in myofibroblasts during palatal scar formation and that FGFR may be responsible for this process.

Animals↗
PubMed1994

Cytochemical identification of programmed cell death in the fusing fetal mouse palate by specific labelling of DNA fragmentation.

The process of palate fusion was examined in 13- and 14-day-old mouse fetuses by using in situ staining for nuclear DNA fragmentation (TUNEL method) and immunofluorescent staining for keratin, with special reference to the disruption of the midline epithelial seam. TUNEL-positive cells were found in the disappearing midline seam and the oral and nasal epithelial triangles at some late stages of palate fusion, but not in the palatal shelves prior to contact or in the intact midline epithelial seam. It seems that DNA fragmentation or apoptosis is required for the midline epithelial seam to disrupt, but may not be necessary for initial contact of palatal shelves or for the epithelial fusion of opposing palatal shelves. A similar sign of apoptotic cell death was observed in the disappearing epithelial seam between the fusing nasal septum and dorsal palate. We have demonstrated that apoptotic programmed cell death does occur at some stages of palate fusion, although the present results do not exclude the possibility of epithelial-mesenchymal transformation and the oral and nasal migration of midline epithelial cells.

Animals↗
PubMed2002

Vascularization of the palate in maxillary osteotomies: anatomical study.

Le Fort 1 maxillary osteotomy carries a risk of injury to the descending palatine arteries which vascularize the bulk of the mucosa of the bony palate. Some authors believe that injury to these arteries in the greater palatine canal is intrinsic to the procedure without any consequence for the trophicity of the mucosa or bony palate. In order to assess the risk of injury to the descending palatine arteries during such surgery, and to demonstrate the supplementary vascularization which would avoid ischemia of the palate, we carried out a study of the vascularization of the palate on 11 fresh cadavers. We used intra-arterial injection of colored latex and dissection of the vessels running to the palate. The study was done without osteotomy in the first subject, after a Le Fort 1 osteotomy in the five following subjects and after a Le Fort 1 osteotomy and ligation of the two descending palatine arteries in the last five subjects. Our results show that injury of the descending palatine arteries is not intrinsic to the procedure in spite of mobilization of the palatine plateau. When the descending palatine arteries are ligated there is diminution in coloration of the mucosa of the bony palate but there is substitution by the arteries vascularizing the soft palate, essentially the ascending palatine artery and the pharyngeal branch arising from the ascending pharyngeal artery. However, this substitute vascularization has individual variations.

Histocytological Preparation Techniques↗
PubMed2004

Pattern of tongue pressure on hard palate during swallowing.

Contact of the tongue against the hard palate plays an important role in swallowing. This study aimed to clarify the pattern of contact between the tongue and hard palate by analyzing tongue pressure produced in swallowing 15 ml of water by healthy subjects wearing an experimental palatal plate with seven pressure sensors. Tongue pressure was generated initially by close contact with the anteriomedian part of the hard palate, then with the circumferential part, and finally softly with the posteriomedian part. Tongue pressure reached a peak quickly, then decreased gradually before disappearing almost simultaneously at each measured part of the hard palate. Magnitude and duration were significantly larger in the anteriomedian part compared to the other six parts measured, and was significantly smaller in the posteriomedian part. No laterality was found in tongue pressure produced at the circumferential parts of the hard palate. Our findings indicate that the order of tongue contact against each part of the hard palate as well as duration and magnitude of tongue pressure are coordinated precisely during swallowing. These findings could aid assessment of the tongue movement of dysphagic patients during rehabilitation.

Deglutition↗
PubMed1984

The effects of dexamethasone on palate mesenchymal cell phospholipase activity.

Corticosteroids will induce cleft palate in mice. One suggested mechanism for this effect is through inhibition of phospholipase activity. This hypothesis was tested by measuring the effects of dexamethasone, a synthetic corticosteroid, on phospholipase activity in cultures of palate mesenchymal cells. Palate mesenchymal cells were prelabeled with [3H]arachidonic acid. The cells were subsequently treated with various concentrations of dexamethasone. Concurrently, cultures of M-MSV-transformed 3T3 cells were prepared identically. After treatment, phospholipase activity was stimulated by the addition of serum or epidermal growth factor (EGF), and radioactivity released into the medium was taken as a measure of phospholipase activity. Dexamethasone (1 X 10(-5) or 1 X 10(-4) M) could inhibit serum-stimulated phospholipase activity in transformed 3T3 cells after 1 to 24 hr of treatment. However, no inhibition of activity was measured in palate mesenchymal cells following this period of treatment. Not until 120 hr of treatment with dexamethasone (1 X 10(-4) M) was any significant inhibition of serum-stimulated phospholipase activity observed in palate mesenchymal cells. When EGF was used to stimulate phospholipase activity, dexamethasone (1 X 10(-5) M) caused an increase in phospholipase activity in palate mesenchymal cells. These observations suggested that phospholipase in transformed 3T3 cells was sensitive to inhibition by dexamethasone. However, palate mesenchymal cell phospholipase is only minimally sensitive to dexamethasone, and in certain instances can be enhanced. These results cannot support the hypothesis that corticosteroids mediate their teratogenic effect via inhibition of phospholipase activity.

Animals↗
PubMed1985

Toxic interaction of specific polychlorinated biphenyls and 2,3,7,8-tetrachlorodibenzo-p-dioxin: increased incidence of cleft palate in mice.

The induction of cleft palate in C57BL/6N mice is an extremely reproducible and sensitive indicator of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) toxicity. This endpoint was used to look for potential interactions between two polychlorinated biphenyl (PCB) congeners and TCDD. Both 2,3,4,5,3',4'-hexachlorobiphenyl (HCB) and 2,4,5,2',4',5'-HCB are of relatively low toxic potency, but their biological properties differ. Pregnant mice were treated with TCDD and either HCB on gestation Days 10 through 13, and the fetuses examined for the presence of cleft palate and renal abnormalities on gestation Day 18. At a dose of TCDD which caused a low level of cleft palate, moderate hydronephrosis was observed. No renal or palatal anomalies were detected after 2,4,5,2',4',5'-HCB treatment, and the combination of this isomer with TCDD had no effect on the incidence of TCDD-induced cleft palate. 2,3,4,5,3',4'-HCB caused mild renal toxicity, but no cleft palate. However, treatment of pregnant mice with a combination of TCDD and 2,3,4,5,3',4'-HCB resulted in a 10-fold increase in the incidence of cleft palate. Thus, the toxicity of compounds such as TCDD may be enhanced by compounds of relatively low acute toxicity such as selected PCBs. The widespread environmental occurrence of such combinations suggests a need for further evaluation of the mechanism of this interaction.

Abnormalities, Drug-Induced↗
PubMed1989

2,3,7,8-Tetrachlorodibenzo-p-dioxin alters embryonic palatal medial epithelial cell differentiation in vitro.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is teratogenic in mice, inducing cleft palate and hydronephrosis. After exposure in vivo, TCDD specifically alters differentiation of embryonic palatal medial epithelial cells. In this study, the palatal epithelial cell response to TCDD is determined in vitro. C57BL/6N palatal shelves were placed in organ culture on gestation day (GD) 12 in Richter's improved modified Eagle's medium:Ham's F12 medium (1:1) with 1% fetal bovine serum for 3 or 4 days. Medium contained 0.1% dimethylsulfoxide and TCDD at 0, 10(-13), 10(-12), 10(-11), 10(-10), and 10(-9) M, with some doses at 5 x 10(-11), 7.5 x 10(-11), and 5 x 10(-12) M. Epithelial cell responses to TCDD occurred over a narrow range of concentrations, with maximal response at 5 x 10(-11) M. Cytotoxicity was detected at 1 x 10(-10) M. At a stage when control medial cells ceased proliferation and EGF receptors were not detected immunohistochemically. TCDD-exposed medial cells incorporated [3H]thymidine and high levels of epidermal growth factor receptors were detected. TCDD prevented programmed cell death of medial peridermal cells, and induced a shift in the differentiation of medial cells toward an oral-like phenotype. The responses to TCDD observed after exposure in vitro were indistinguishable from previously reported effects observed after exposure in vivo. In the present study, the distribution of TCDD in the fetus after exposure in vivo was examined. The levels of exposure to TCDD are similar for in vitro and in vivo exposure routes. The levels of TCDD in 1 x 10(-11) to 1 x 10(-10) M solutions (3 to 32 pg/ml) were comparable to levels observed in fetal tissues after in vivo exposure on GD 11 to 30 microns/kg [3H]TCDD, where the palatal shelf contained 1.4 to 3.5. pg TCDD, representing 0.0003% of the total dose. In vivo, TCDD was detected in the GD 11 embryo 3 hr postexposure and the TCDD was equally distributed between the embryonic head and body. At 72 hr postexposure, 0.035% of the total dose was in fetal tissues, and 1% of the TCDD in the fetus was found in the palatal shelf. The present study shows that the palatal epithelium responds to TCDD in vitro in a manner comparable to that observed after in vivo exposure, and that the response occurs at a concentration comparable to in vivo levels in the fetus. The availability of an in vitro system will facilitate studies of TCDD toxicity that are difficult or impossible to perform in vivo, such as comparisons of TCDD effects between species, including human tissues.

Animals↗
PubMed2005

Speech and swallowing following radial forearm flap reconstruction of major soft palate defects.

Velopharyngeal function is often compromised by the resection and reconstruction of oropharyngeal and palatal tumours. While free tissue transfer has improved the outcomes of head and neck reconstruction. In general, palatal reconstruction remains a challenge. Velopharyngeal function was analysed in eight patients following microsurgical reconstruction of defects of between 50 and 100% of the soft palate. The radial forearm fasciocutaneous free flap was used in all cases. The outcome of reconstruction was analysed by patient questionnaire and with standardised tests of speech and swallowing function. Velopharyngeal function post-operatively ranged from poor to near normal. Poor function appeared due to the loss of active elevation and contracture of the reconstructed palate producing failure of velopharyngeal closure during swallowing and speech. The results emphasise the limitations of reconstruction of a dynamic structure such as the soft palate with the static fold of skin and soft tissue produced by a fasciocutaneous flap. The relatively poor results obtained suggest that an anatomical approach to soft palate reconstruction is inadequate and reduction of the calibre of the velopharyngeal aperture is required to compensate for the lack of mobility in the reconstructed palate.

Carcinoma, Squamous Cell↗
PubMed1999

Interferon-gamma inhibits the myofibroblastic phenotype of rat palatal fibroblasts induced by transforming growth factor-beta1 in vitro.

Interferon-gamma (IFN-gamma), a multifunctional cytokine, has been noted as a potential therapeutic agent for various fibrotic disorders, including excessive scar tissue formation. We previously reported that transforming growth factor-beta1 (TGF-beta1) induced the myofibroblastic phenotype in palatal fibroblasts derived from palatal mucosa, and that such effects might have a close link to palatal scar formation. In the present study, we examined the effects of IFN-gamma on TGF-beta1-pretreated palatal fibroblasts for the purpose of clarifying the suppressive potency against myofibroblastic phenotype expression in vitro. IFN-gamma significantly altered the spindle morphology of TGF-beta1-pretreated palatal fibroblasts into the polygonal one that was similar to the non-treated palatal fibroblasts. This change was parallel with a decrease in the expression of alpha-smooth muscle actin protein, a marker for myofibroblast, as determined by immunoblot analysis. Northern blot analysis showed that IFN-gamma inhibited proalpha2(I) collagen mRNA expression that was stimulated by TGF-beta1 pretreatment for 24 h. Furthermore, IFN-gamma decreased the cell contractility enhanced by TGF-beta1 pretreatment for 24 h in a three-dimensional collagen gel culture system. These results suggest that IFN-gamma may have negative effects with regard to controlling the myofibroblastic phenotype induced by TGF-beta1 in palatal fibroblasts.

Actins↗