Gingival Fibromatosis Research Articles

Antifibrotic Potential of MiR-335-3p in Hereditary Gingival Fibromatosis

Hereditary gingival fibromatosis (HGF) is a highly genetically heterogeneous disease, and current therapeutic method is limited to surgical resection with a high recurrence rate. MicroRNAs (miRNAs) are able to fine-tune large-scale target genes. Here we established a simple but effective computational strategy based on available miRNA target prediction algorithms to pinpoint the most potent miRNA that could negatively regulate a group of functional genes. Based on this rationale, miR-335-3p was top ranked by putatively targeting 85 verified profibrotic genes and 79 upregulated genes in HGF patients. Experimentally, downregulation of miR-355-3p was demonstrated in HGF-derived gingival fibroblasts as well as in transforming growth factor β–stimulated normal human gingival fibroblasts (NHGFs) compared to normal control. Ectopic miR-335-3p attenuated, whereas knockdown of miR-335-3p promoted, the fibrogenic activity of human gingival fibroblasts. Mechanically, miR-335-3p directly targeted SOS1, SMAD2/3, and CTNNB1 by canonical and noncanonical base paring. In particular, different portfolios of fibrotic markers were suppressed by silencing SOS1, SMAD2/3, or CTNNB1, respectively. Thus, our study first proposes a novel miRNA screening approach targeting a functionally related gene set and identifies miR-335-3p as a novel target for HGF treatment. Mechanically, miR-335-3p suppresses the fibrogenic activity of human gingival fibroblasts by repressing multiple core molecules in profibrotic networks. Our strategy provides a new paradigm in the treatment for HGF as well as other diseases.

Genetic and developmental disorders of the oral mucosa: Epidemiology; molecular mechanisms; diagnostic criteria; management.

A large number of disorders may affect the oral cavity, including genetic diseases, infections, cancers, blood diseases, skin diseases, endocrine and metabolic disorders, autoimmune and rheumatologic diseases, local lesions, to name a few. Oral mucosa shows a considerable variation in its normal structure and a wide range of conditions may affect it. Such conditions are often harmless or minor and could be primary or secondary to systemic disease. Several of them are quite rare and, hence, the diagnosis is not easy. Clinically, lesions may appear as ulcers, discoloration of the oral mucosa and alterations in size and configuration of oral anatomy. Genetic disorders have specific manifestations and can be caused by a derangement of one or more components of the tissue. Many of them follow the skin or systemic signs of the underlying genetic disease, but in a few cases oral signs could be the first manifestation of the disorder. Among them genodermatoses are prominent. They are inherited disorders characterized by a multisystem involvement. This review describes chondro-ectodermal dysplasia, dyskeratosis congenita, Ehlers-Danlos syndrome, hereditary benign intraepithelial dyskeratosis, keratosis follicularis, lipoid proteinosis, multiple hamartoma syndrome, pachyonychia congenita, Peutz-Jeghers syndrome, tuberous sclerosis and white sponge nevus. Other genetic disorders not included in the genodermatosis group and reported in the present review are: acanthosis nigricans, angio-osteo-hypertrophic syndrome, encephalotrigeminal angiomatosis, familial adenomatous polyposis, focal dermal hypoplasia, focal palmoplantar and oral mucosa hyperkeratosis syndrome, gingival fibromatosis, Maffucci's syndrome, neurofibromatosis (type 1) and oro-facial-digital syndrome (type 1). Disorders during embryonic development might lead to a wide range of abnormalities in the oral cavity; some of them are quite common but of negligible concern, whereas others are rare but serious, affecting not only the oral mucosa, but also other structures of the oral cavity (ie palate, tongue and gingiva). Fordyce's granules, leukoedema, cysts of the oral mucosa in newborns, retrocuspid papilla, geographic tongue, fissured tongue, median rhomboid glossitis, hairy tongue, lingual varices and lingual thyroid nodule are described. This review may help dentists, dental hygienists, but also general internists and pediatricians to diagnose different disorders of the oral mucosa, to understand the pathogenesis and to schedule a treatment plan.

SUN-286 Growth Hormone Deficiency and Gingival Fibromatosis Due to Missense Mutation of KCNQ1

Background: Multiple genes have been implicated in the genetic etiology of growth hormone deficiency (GHD) including genes that contribute to hypothalamus and pituitary development. Mutations of these genes can be associated with additional pituitary hormone deficiencies and developmental abnormalities. KCNQ1 gene encodes the alpha subunit of the voltage-gated ion channel Kv7.1, which has been previously implicated in cardiac arrhythmia syndromes. In 2017, two missense mutations, c.347G>T p.(Arg116Leu) or c.1106C>T p.(Pro369Leu), in KCNQ1 were reported for the first time in three unrelated families causing GHD and maternally inherited gingival fibromatosis (GF) (1). Members of these families displayed variable phenotypes including GHD, multiple pituitary hormone deficiencies, small pituitary on MRI, GF, craniofacial dysmorphic features, and short QT syndrome. Many had hypogonadotropic hypogonadism. Clinical Case: 9 year old male was referred to pediatric endocrinology for short stature and slow growth. He maintained height around 6%ile (Z=-1.55) until the age of 9 years with subsequent slowing to 0.95%ile (Z=-2.34). He had history of significant gingival hyperplasia requiring 5 surgical interventions in the past. He has done well developmentally. No history of cardiac arrhythmia. Physical exam showed coarse facial features and normal pre-pubertal genitalia. Family history was negative for short stature, arrhythmia, gingival hyperplasia, or coarse facial features. Studies showed delayed bone age of 6 years, low IGF-1 of 57 ng/ml, max growth hormone level of only 3 ng/ml on Arginine-Glucagon tolerance test, and normal other pituitary hormones. EKG and MRI of brain and pituitary were normal. Given his coarse facial features and gingival problem, he had a detailed work up for lysosomal storage disorders with negative results. Whole exome sequencing showed a missense variant in the maternal KCNQ1 gene denoted as c.1106C>T p.(Pro369Leu). Neither of his parents were found to have this KCNQ1 variant. He was started on growth hormone therapy with appropriate catchup growth. He was noticed 9 months later to have pubertal changes with testicular volume of 4-5 ml, LH 1.1 mIU/ml, and testosterone level of 98 ng/dl. Conclusion: To our knowledge, this is the first case of GHD and GF due to KCNQ1 mutation to be reported in the United States. Our patient had many unique features in contrast to previous report including lack of identified parental mutation, lack of clinical features in the family and early puberty indicating that there is still more to learn about clinical spectrum of KCNQ1 mutations in children. Reference: (1) Two missense mutations in KCNQ1 cause pituitary hormone deficiency and maternally inherited gingival fibromatosis. J.Tommiska et al, Nat Commun. 2017 Nov 3;8(1):1289.

Exomic and transcriptomic alterations of hereditary gingival fibromatosis.

Hereditary gingival fibromatosis (HGF) is a rare oral disease characterized by either localized or generalized gradual, benign, non-hemorrhagic enlargement of gingivae. Although several genetic causes of HGF are known, the genetic etiology of HGF as a non-syndromic and idiopathic entity remains uncertain. We performed exome and RNA-seq of idiopathic HGF patients and controls, and then devised a computational framework that specifies exomic/transcriptomic alterations interconnected by a regulatory network to unravel genetic etiology of HGF. Moreover, given the lack of animal model or large-scale cohort data of HGF, we developed a strategy to cross-check their clinical relevance through in silico gene-phenotype mapping with biomedical literature mining and semantic analysis of disease phenotype similarities. Exomic variants and differentially expressed genes of HGF were connected by members of TGF-β/SMAD signaling pathway and craniofacial development processes, accounting for the molecular mechanism of fibroblast overgrowth mimicking HGF. Our cross-check supports that genes derived from the regulatory network analysis have pathogenic roles in fibromatosis-related diseases. The computational approach of connecting exomic and transcriptomic alterations through regulatory networks is applicable in the clinical interpretation of genetic variants in HGF patients.

Idiopathic gingival fibromatosis

Gingival fibromatosis (GF) is a heterogenous group of disorders characterized by progressive enlargement of the gingiva caused by an increase in submucosal connective tissue elements. Many cases are iatrogenic; some are inherited while others are idiopathic. We describe a case of ten year old girl brought from the department of pedodontics to periodontics with the chief complaint of gradual and progressive enlargement of both upper and lower gingival tissues from the age of 2 years. Gingivectomy was performed quadrant-wise under local anesthesia to restore the patient’s esthetics and functional/ masticatory needs. Key Words: Gingiva, Fibromatosis, Gingivectomy

Zimmerman-Laband Syndrome Oral Manifestations A Case Report

Zimmerman-Laband syndrome was reported by Zimmerman in the year 1928 which is a rare inherited autosomal dominant disease characterized by generalized enlargement of the attached and marginal gingiva, abnormalities of nose, ear, deformities of nails, joint hyperextensibility, hepatosplenomegaly, skeletal abnormalities and occasional mental retardation. Idiopathic gingival enlargement is usually evident after the eruption of the permanent teeth. Both sexes are equally affected. Genetic loci for autosomal dominant modes of gingival fibromatosis is localized to chromosome 2p21p22 (HGF-1) and chromosome 5q12-q22 (HGF-2). This syndrome is not a life threatening disorder. Hereditary gingival enlargement is associated with syndromes like Rutherford syndrome, Zimmerman-Laband syndrome, Murray-Puretic-Drescher syndrome, Cross syndrome and Ramon’s syndrome. The most important feature of this syndrome is gingival enlargement appearing early in childhood. Idiopathic gingival enlargement is usually evident after the eruption of the permanent teeth. Surgical correction of gingival fibromatosis is recommended, although there is no information on the permanence of the results of this treatment. We present a case of a 14 year old female patient with Zimmerman-Laband syndrome. Gingivectomy was carried out in the upper and lower anterior region there by exposing the impacted teeth.

Dermatoglyphics–An Indicator for Periodontal Disease? A Cross-Sectional Study

BACKGROUND: Dermatoglyphics is the dermal ridge configuration of digits, palms and soles. These patterns are genetically determined and are unique for each individual. It can be considered as a window of congenital and intrauterine abnormalities. In dentistry, it has been studied to predict disorders such as dental caries, malocclusions, congenital abnormalities such as gingival fibromatosis and periodontitis. The aim of the current study was to evaluate the dermatoglyphic patterns and correlate it with healthy individuals, aggressive periodontitis and chronic periodontitis patients. AIM: To evaluate the dermatoglyphic patterns and correlate it with healthy individuals, aggressive periodontitis and chronic periodontitis patients. MATERIALS AND METHODS: The study population consisted of 3 groups. Group 1 consisted of healthy individuals (n=15), group 2 consisted of patients with chronic periodontitis (n=15) and group 3 consisted of patients with aggressive periodontitis (n=15). Finger prints were obtained and analysed. SPSS v20 was used for statistical analysis. RESULTS: On comparing the pattern of individual fingers, the present study shows that there are increased whorls seen in the middle finger of chronic periodontitis patients and increased loops in aggressive periodontitis patients when compared to healthy subjects, however it was not statistically significant(p=0.897). Overall comparison of the dermatoglyphic patterns does not reveal any difference among the 3 groups. No significant difference was seen comparing chronic periodontitis with aggressive periodontitis group.

Zimmermann-Laband syndrome: Clinical and cytogenetic study in two related patients.

BackgroundZimmermann–Laband Syndrome (ZLS) is an extremely rare autosomal dominant congenital disorder. It is a craniofacial malformation syndrome with predominant intraoral involvement consisting of gingival fibromatosis diffusion in early development. The molecular basis of ZLS is still unknown. Although familial aggregation with different inheritance patterns is detected in ZLS patients, most of the cases are sporadic.Material and MethodsWe report on two sibling patients with clinical manifestations of ZLS. Blood samples of both patients were obtained in EDTA-tubes followed by performing cytogenetic study using Cyto2.7M array. Analysis of the copy number was performed using the Chromosome Analysis Suite Software (version 1.0.1, annotation file na 30, Affymetrix) and interpreted with recourse to the UCSC genome browser (http://genome.ucsc.edu/; Human Mar. 2006NCBI Build 36.1/hg18 assembly).ResultsThe array analysis revealed overlapping regions of chromosomal aberrations in both patients. We detected a 258-kb deletion at 3q13.13, a 89-kb duplication at 1q25.2 as well as two 67-kb duplications at 1p12 and 19q12. These altered regions do not contain any known genes and protein-coding sequences.ConclusionsIn conclusion, the findings of this report revealed new chromosomal aberrations, including a deletion at 3q13.13 and duplications at 1q25.2, 1p12 and 19q12, in the two patients with ZLS. Such findings indicate that whole genome screening for genomic rearrangements is fruitful in typical and atypical patients with ZLS. Key words:Zimmermann-Laband syndrome, cytogenetic array, whole genome screening, chromosomal aberration, gingival fibromatosis.

Laser versus conventional surgery in management of hereditary gingival fibromatosis - Case series

Purpose: The goal of the presente article is to help the clinican to compare the clinical outcome of gingivectomy with laser versus conventional surgery. Case report: A 15 yrs old male patient reported with generalized hereditary gingival enlargement with clinical aspect of gingiva covering one third of dental crowns. No exposure to drugs like phenytoin, cyclosporine or calcium channel blockers such as nifedipine. There was no other medical history such as bone deformities or mentally retardation. Family history reveals hereditary gingival enlargement. On examination of patient “A” siblings also showed similar characteristic gingival features. Based on these facts differential diagnosis was made between “drug induced gingival enlargement” and “hereditary gingival fibromatosis” and confirmed with histopathological findings. Conclusions: Patients were subjected to 2 modalities of treatment in a split mouth; laser and conventional gingivectomy. Patient was more comfortable (was measured on a scale from 1 to 10 using visual analog scale) during and after treatment and healing was also faster and recurrence was delayed in laser technique.

HEREDITARY GINGIVAL FIBROMATOSIS

Hereditary gingival fibromatosis also referred to as idiopathic gingival hyperplasia,elephantiasis gingivae etc; is a rare hereditary localized or generalized condition, whichrepresents as swelling of gingivae of varied degrees with no apparent cause. Swelling is usuallyfirm, pink and usually no signs of inflammation if oral hygiene is up to fair. Condition may occursolitary or in a syndrome. Recent findings report a defect in the Son of seven less-1 gene onchromose 2p21-p22(HGF1) as a possible cause. This case report presents a severe HGF case,importance of earlier management ( as it may unable the patient to close their mouth), possiblegravitational role in enlargement of swellings and its proper remedy.

Enamel renal syndrome: A novel homozygous FAM20A founder mutation in 5 new Brazilian families

Enamel renal syndrome (ERS) is a rare autosomal recessive disorder not fully characterized. Here we investigated ERS characteristics in 11 patients from 5 Brazilian families through clinical examination, imaging, renal ultrasonography, laboratory tests and DNA sequencing. The patients' age ranged from 6 to 25 years-old, and the presence of hypoplastic amelogenesis imperfecta, microdontia, intra-pulpal calcification, impacted posterior teeth with hyperplastic pericoronal follicles, gingival fibromatosis, ectopic calcifications on gingival and pericoronal tissues, and nephrocalcinosis were common findings to all patients. Only 4 patients showed abnormal laboratory tests (vitamin D, parathyroid hormone, phosphate, calcium). Intellectual disability and renal cysts were present in 2 patients each. Biallelic loss of function mutation in FAM20A gene, characterized by one base pair deletion in exon 11, resulting in a frameshift replacing a glutamine at codon 483 for a lysine and terminating at position 24 [NG_029809.1: c.1447delG; p.(Glu483Lysfs*24)], was detected in all patients, strongly suggesting a founder effect. Our results reinforce the distinct orofacial features of ERS, which are the clue for kidney examination and genetic testing. Early diagnosis is essential to minimize the deleterious effects related to ERS. Here we report the largest series of patients with ERS in a same population, and describe, for the first time, a founder mutation for FAM20A.

Fibroblasts from recurrent fibrotic overgrowths reveal high rate of proliferation in vitro - findings from the study of hereditary and idiopathic gingival fibromatosis

ABSTRACTPurpose: Investigate the content of fibrotic fibrils in gingival tissue and the proliferation of fibroblasts collected from recurrent and non-recurrent hereditary gingival fibromatosis (HGF) and idiopathic gingival fibromatosis (IGF).Methods: Gingival biopsies were collected from HGF (n = 3) and IGF (n = 3) donors with recurrent and non-recurrent gingival overgrowths and from a control group (Ctrl, n = 3). Hematoxylin staining was performed to evaluate the histomorphology of gingival tissue. Heidenhain’s AZAN trichrome staining served for visualization of fibrotic fibrils in gingiva. Quantitative analysis of the content of fibrotic fibrils in gingival tissue was performed using a polarized light microscope. Proliferation was evaluated at 24 h, 48 h, and 72 h in fibroblast cultures using a cell proliferation ELISA assay based on 5-bromo-2ʹ-deoxyuridine (BrdU).Results: Numerous blood vessels and fibroblasts were observed in recurrent overgrowths, whereas moderate blood vessels and moderate to scanty fibroblasts were detected in non-recurrent overgrowths. Heidenhain’s staining revealed numerous collagen fibers in both recurrent and non-recurrent overgrowths. Quantitative analysis in a polarizing microscope showed significant accumulation of fibrotic fibrils exclusively in the overgrowths with the recurrence. In all time-points, increased proliferation of cells from all recurrent overgrowths was observed, but not from overgrowths which do not reoccur.Conclusions: The study revealed that recurrent gingival overgrowths consist of highly fibrotic and dense connective tissue with numerous blood vessels and abundant fibroblasts. We also demonstrated that unlike fibroblasts derived from overgrowths, which did not present recurrence, fibroblasts derived from highly fibrotic and recurrent overgrowths maintain high rate of proliferation in vitro.

Hereditary Gingival Fibromatosis: a Case Report with Seven-Year Follow-up.

IntroductionHereditary gingival fibromatosis (HGF) is a rare disease characterized by gingival enlargement, normal color with benign and firm consistency. This growth may be exacerbated by use of drugs and plaque build-up. The treatment for this clinical condition is surgical excision of the enlarged gingival tissue or the extraction of all teeth.Case ReportA 20-year-old Brazilian female handicapped patient with a chief complaint of exaggerated gingival enlargement who had been prescribed Carbamazepine and Gardenal was referred to our center. According to the clinical presentation and family history, the final diagnosis of gingival enlargement was HGF. Full dental treatment was performed, including basic periodontal treatment, restorations, sealants, and gingivoplasty with internal bevel. Special care was taken to ensure that there was no change in patient’s anticonvulsant medication. The patient has been monitored for seven years without signs of recurrence of gingival hyperplasia due to constant professional and home control of plaque.

Towards the targeted management of hereditary gingival fibromatosis

Although hereditary gingival fibromatosis is a rare condition, it leaves unrestroable psychological, esthetical as well as functional problems to the affected patients. The purpose of the current research is to find a non-surgical pharmacological mechanism that could provide a control of the active phase of such disease helping individual to continue their lives.

Ultrastructural Evaluation and Comparison of Connective Tissue in Hereditary Gingival Fibromatosis and Normal Gingiva

Ultrastructural Evaluation and Comparison of Connective Tissue in Hereditary Gingival Fibromatosis and Normal Gingiva

TIMP-1 association with collagen type I overproduction in hereditary gingival fibromatosis.

To investigate the processes associated with the excessive production of collagen I in hereditary gingival fibromatosis (HGF). Three HGF subjects and five controls were enrolled in the study. Histomorphological and immunohistological analyses were performed on gingival tissues. The expression of heat-shock protein 47 (HSP47), collagen I, transforming growth factor-β1 (TGF-β1), connective tissue growth factor (CTGF), matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) by gingival fibroblasts isolated from HGF and controls was analysed using qRT-PCR, Western blotting and ELISA. Considerable accumulation of fibrotic fibrils and increased synthesis of HSP47 were noted in HGF gingival tissues. The synthesis of collagen I, HSP47, TGF-β1, CTGF and TIMP-1 was significantly elevated in HGF gingival fibroblasts compared with controls, while the production of MMP-1 was decreased. We report that fibrosis in HGF gingival tissues is associated with increased synthesis of HSP47. This finding was confirmed by an in vitro study, where excessive production of collagen I was associated with increased synthesis of HSP47, TGF-β1 and CTGF by HGF gingival fibroblasts. Moreover, the shift in the TIMP-1/MMP-1 ratio identifies increased synthesis of TIMP-1 as one of the processes associated with collagen I overproduction in HGF fibroblasts.

PC296: Recurrent idiopathic gingival fibromatosis associated with generalized aggressive periodontitis: a case report

PC296: Recurrent idiopathic gingival fibromatosis associated with generalized aggressive periodontitis: a case report

The Role of KCNQ1 Mutations and Maternal Beta Blocker Use During Pregnancy in the Growth of Children With Long QT Syndrome.

Two missense mutations in KCNQ1, an imprinted gene that encodes the alpha subunit of the voltage-gated potassium channel Kv7.1, cause autosomal dominant growth hormone deficiency and maternally inherited gingival fibromatosis. We evaluated endocrine features, birth size, and subsequent somatic growth of patients with long QT syndrome 1 (LQT1) due to loss-of-function mutations in KCNQ1. Medical records of 104 patients with LQT1 in a single tertiary care center between 1995 and 2015 were retrospectively reviewed. Clinical and endocrine data of the LQT1 patients were included in the analyses. At birth, patients with a maternally inherited mutation (n = 52) were shorter than those with paternal inheritance of the mutation (n = 29) (birth length, -0.70 ± 1.1 SDS vs. -0.2 ± 1.0 SDS, P < 0.05). Further analyses showed, however, that only newborns (n = 19) of mothers who had received beta blockers during pregnancy were shorter and lighter at birth than those with paternal inheritance of the mutation (n = 29) (-0.89 ± 1.0 SDS vs. -0.20 ± 1.0 SDS, P < 0.05; and 3,173 ± 469 vs. 3,515 ± 466 g, P < 0.05). Maternal beta blocker treatment during the pregnancy was also associated with lower cord blood TSH levels (P = 0.011) and significant catch-up growth during the first year of life (Δ0.08 SDS/month, P = 0.004). Later, childhood growth of the patients was unremarkable. Loss-of-function mutations in KCNQ1 are not associated with abnormalities in growth, whereas maternal beta blocker use during pregnancy seems to modify prenatal growth of LQT1 patients-a phenomenon followed by catch-up growth after birth.

Screening for germline KCNQ1 and KCNE2 mutations in a set of somatotropinoma patients.

ObjectiveRecently, mutations in KCNQ1, a potassium channel gene usually linked to long QT syndrome, were reported to cause maternally inherited gingival fibromatosis and growth hormone deficiency (GHD). Expression of the mutated KCNQ1 with the auxiliary potassium channel subunit KCNE2 was shown to reduce pituitary hormone secretion in functional experiments. Here, we investigated if germline mutations in KCNQ1 and KCNE2 were present in patients with somatotropinomas, which represent a model of growth hormone excess.Design and methods KCNQ1 and KCNE2 were screened for germline mutations in 53 patients with acromegaly by Sanger sequencing. Effects of the variants were predicted by in silico tools.ResultsOnly deep intronic and synonymous polymorphisms were detected in KCNQ1. These findings were likely insignificant based on in silico predictions and the variants’ frequencies in the general population. In KCNE2, a heterozygous c.22A>G, p.(Thr8Ala) mutation with unknown significance was found in three patients. It was present in the database controls with a frequency of 0.0038.ConclusionsKCNQ1 or KCNE2 mutations do not appear to account for somatotropinoma formation, although larger patient series are needed to validate the findings.

Expression of CD163 in hereditary gingival fibromatosis: A possible association with TGF-β1.

Although several studies have discussed some of the molecular and cellular changes associated with hereditary gingival fibromatosis (HGF), its pathogenesis is still largely unclear. This study was directed to detect and outline the degree of relationship between the immunophenotyped macrophages (M2) expressing CD163 and TGF-β1 in patients with gingival overgrowth due to HGF. Biopsies from 20 patients suffering from HGF and 20 normal control subjects were harvested, histologically and immunohistochemically stained then, analyzed and statistically compared and correlated for CD163 immunoexpression and TGF-β1. All HGF specimens expressed TGF-β1 by most of the connective tissue fibroblasts, with statistically high significant mean of area % (2.61±0.41) compared to normal controls (0.11±0.06; P=.001). All control specimens revealed negligible CD163 immunostaining of the few inflammatory cells found with a mean area of % (0.69±0.12), while the specimens of HGF cases showed statistically significant higher CD163 expression (3.39±0.75) at (P=.007). A statistically significant higher mean % of M2 cells expressing CD163 in relation to the total number of the inflammatory cells was revealed in HGF (34.46±2.04) compared to the control group (16.36±2.39; P-value≤.05). Moderate correlation between CD163 and TGF-β1 was detected in HGF (r=.451; P-value<.05). CD163 and TGF-β1 were clearly expressed in HGF cases compared to healthy control patients, with significant correlation. In HGF, the increase in CD 163-positive cells was specific and not dependent on the chronic gingival inflammation.