• Title/Summary/Keyword: Gingival pathology

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GINGIVAL FIBROMATOSIS IN MIXED DENTITION (혼합 치열기 어린이의 치은 섬유종증)

  • Han, Hyo-Jeong;Kim, Jin;Kim, Seong-Oh;Son, Heung-Kyu;Choi, Byung-Jai
    • Journal of the korean academy of Pediatric Dentistry
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    • v.31 no.4
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    • pp.696-700
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    • 2004
  • Gingival fibromatosis is a non-inflammatory oral disease, characterized by slowly progress enlargement of the free and attached gingiva. Gingival fibromatosis may have familial tendency. Gingival enlargement usually begins with the eruption of the permanent dentition but can also develop with the eruption of the primary dentition. In this case, a 6-year-old female had gingival enlargement at birth. There was no familial, medical and pharmacologic history of gingival overgrowth. Treatment is gingivectomy with a rigorous program of oral hygiene. Recurrence of gingival fibromatosis may well be inevitable. Therefore there is no general aggrement as to the timing of surgical intervention. Generally the best time is when all the permanent teeth have erupted. However early intervention can improve oral function and esthetic and psychologic effect.

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Comparative Study of Gingival Changes in Cyclosporine-Induced Nephrotoxicity with Normal and Low Salt Diet (저염식으로 유도한 Cyclosporine 신독성 백서에서의 치은 변화)

  • Lim, Jae-Gye;Kim, Yong-Jin;Park, Yong-Hoon
    • Journal of Periodontal and Implant Science
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    • v.30 no.2
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    • pp.359-374
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    • 2000
  • Cyclosporine A(CsA) is a widely used immunosuppressant for transplant patients and is also used for the treatment of a wide variety of systemic diseases with immunologic disorders. However, its use is frequently limited because of complications such as nephrotoxicity or gingival hyperplasia. Although several hypotheses have been postulated for CsA-induced gingival hyperplasia, i.e. various cytokine effects of inflammatory cells, existence of plaque or CsA itself, but its pathogenesis is still unclear. For experimental chronic CsA toxicity, salt depletion has been shown to increased susceptibility of rodents to the effects of CsA, and this maneuver facilitates production of arteriolopathy and interstitial fibrosis in kidney that mimic the changes found in human. The purpose of this study was to evaluate pathogenesis of CsA-induced gingival hyperplasia by comparing changes between CsA administration groups of normal standard diet and those of low salt diet group. Specific pathogen-free, 20 to 25 days old(120 to 150 g), male Fisher-344 rats(KIST, Korea), 120 to 150g of body weight, were assigned to four groups of six animals each after one week of adaptation period for powder food. Group 1 received olive oil($300{\mu}l/g\;of\;diet$) with normal standard diet(0.4% of sodium)(NSD). Group 2 received CsA(Cypol-N, Jonggundang, Korea; $300{\mu}g/g\;of\;diet$) with normal standard diet(NSD+CsA). Group 3 received same amount of olive oil with low salt diet(0.05 % of sodium, Teklad Premier, U.S.A.)(LSD). Group 4 received same dose of CsA with low salt diet(LSD+CsA). Rats were pair fed and were sacrificed after six weeks. Renal histologic lesions associated with CsA, consisted of cortical interstitial fibrosis, tubular atrophy and hyalinization of arterioles and the impairment of renal function including increase of serum creatinine and decrease of glomerular filtration rate was more severe in low salt diet group. These were proved as the results of activated of renin-angiotensin system in the kidney by low salt condition. Meanwhile the degree of gingival hyperplasia at incisor and molar tooth was less severe in low salt diet group compared with normal sodium diet group. Hyperplastic gingiva showed mild epithelial hyperplasia and expanded underlyng stroma which consisted of matrix increasement, capillary proliferation and dilatation. While the number and the activation of fibroblasts were increased, inflammatory cells were rare in the stroma. The immunohistochemistry for TGF-${\beta}_1$ in the kidney and gingiva revealed stronger positive in LSD+CsA in kidney but in gingiva of NSD+CsA. These results suggested followings; Gingival hyperplasia can be developed without inflammatory cells infiltration and seemed not induced by CsA by itself. The major role for gingival hyperplasia by CsA would be the secondary effect of TGF-${\beta}$, which maybe upregulated by CsA administration. Low salt diet can attenuate this hyperplasia perhaps by decreasing the activation of $TGF-{\beta}$.

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SQUAMOUS CELL CARCINOMA ARISING FROM CHRONIC OSTEOMYELITIS OF THE MANDIBLE (만성 하악골 골수염에서 발생한 편평상피세포암종)

  • Park, Young-Wook;Park, Jung-Min;Jang, Jae-Hyun;Kim, Ji-Hyuck;Kwon, Kwang-Jun;Lee, Suk-Keun
    • Maxillofacial Plastic and Reconstructive Surgery
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    • v.30 no.5
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    • pp.465-472
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    • 2008
  • We experienced a rare case of oral squamous cell carcinoma arisen from gingival tissues overlying prolonged chronic osteomyelitis of the mandible. A 66 years old man complained of unhealed extraction sockets of left mandibular second premolar and first molar, and showed extensive leukoplakia in the gingival tissues of the same area. The inflammation of the socket granuloma became severe and extended into adjacent mandibular proper, resulted in diffuse suppurative chronic osteomyelitis of mandibular body, exhibiting irregular osteolytic changes of mandibular trabecular patterns in mottled radiolucent appearance. The leukoplakia was initially diagnosed under microscope, and the involved gingival tissues were radically removed. Thereafter, the gingival soft tissue inflammation involving the mandibular osteomyelitis was hardly healed for two years. During the period of repeated surgical treatments for the inflamed lesion, nine biopsies were taken sequentially. Until the eighth biopsy, there consistently showed the suppurative osteomyelitis with ingrowing gingival tissues into the bony inflammatory lesion. The gingival epithelium showed the features of leukoplakia but no evidence of malignant changes. However, the ninth biopsy, taken about 2 years after initial diagnosis, showed the early carcinomatous changes of the gingival epithelium. The neoplastic epithelial cells were relatively well differentiated with many keratin pearls, and infiltrated only into underlying connective tissues. So, we presumed that the present case of squamous cell carcinoma was caused by the persistent inflammatory condition of the mandibular osteomyelitis, and also suggest that the leukoplakia should be carefully removed in the beginning to prevent the neoplatic promotion of the chronic inflammation.

Expression of Adhesion Molecule in Inflammatory Gingival Tissue (염증성 치은조직에서 Cell Adhesion Molecule의 발현에 관한 연구)

  • Park, Kyung-Geun;Kim, Eun-Chul;You, Hyung-Keun;Shin, Hyung-Shik
    • Journal of Periodontal and Implant Science
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    • v.26 no.3
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    • pp.655-668
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    • 1996
  • The change in vascular adhesion molecule expression and number of infiltrating leukocytes were investigated irnmunohistochemically in clinically healthy and inflammed gingiva. Monoclonal antibodies to ICAM-1, VCAM-1 and E-cadherin were used to identify positive vessels and leukocyte within gingival biopsies. 10 healthy gingiva and 30 inflammed gingiva was resected by clinical crown lengthening and modified Widman flap operation, respectively. Leukocyte entry into tissues at sites of inflammation is controlled by the interaction between adhesion molecule and endothelium. Because of rapid and severe destructive periodontal disease that is remarkable leukocyte adhesion deficiency, it is very important to unerdstand the mechanism of host defence against periodontal disease. The purpose of this investigation was the characterization of the presence and distribution of the adhesion molecule(ICAM-1, VCAM-1 and Evcadherin) in inflammatory gingival tissues compared to clinically healthy gingiva. The results were as followed; 1. ICAM-1 was distributed on basal layer, endothelium and mononuclear cells 10 healthy gingiva but inflammed gingiva was observed stronger stain than healthy gingiva. 2. Rare expression was observed in both group but few positive VCAM-1 cells were investigated in inflammatory gingival tissues 3. E-cadherin was expressed in only epithelium and reduced expression was observed in inflammatory gingival tissues. ICAM-1, VCAM-1 showed more expression in inflammatory tissues compared to healthy gingiva. Conversely, E-cadherin revealed a opposite result. These finding demonstrate a characteristic distribution and degree of adhesion molecule in healthy and inflammatory gingival tissues. But it is suggested that more detail study be progressive associated with leukocyte adhesion molecule to determine characterization of periodontal disease.

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Immunohistochemical Observation of Plasma Cell Granuloma in Intraoral Chronic Inflammatory Lesions (구강내 만성염증병소에서 보이는 형질세포육아종의 면역조직화학적 관찰)

  • Kim, Yeon-Sook;Lee, Suk-Keun
    • Maxillofacial Plastic and Reconstructive Surgery
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    • v.33 no.1
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    • pp.26-31
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    • 2011
  • Purpose: Chronic inflammatory gingival lesions occur as pyogenic granulomas or non-specific chronic suppurative lesions. Methods: Of the 59 chronic inflammatory gingival lesions examined, plasma cell granuloma (n=14), which showed an intense antibody-mediated immune reaction with the increased infiltration of plasma cells, was observed as a pseudotumor-like gingival overgrowth and myofibroblastic or fibrohistiocytitc proliferation of stromal cells with a heavy collection of plasma cells. The levels of CD3, CD20, CD31, CD68, RANKL, cathepsin G, cathepsin K, lysozyme, TNF${\alpha}$, MMP-2, and MMP-9 in the 14 cases of gingival plasma cell granuloma with immunohistochemical detection were measured to determine the pathogenetic progresses of the plasma cell granuloma compared to the common pyogenic granuloma (n=45) in the gingiva. Results: The gingival lesions of the plasma cell granuloma could be divided into three histological types, plasma cell predominant type (PPT, n=8), mixed inflammatory cell type (MICT, n=2), and sclerosed fibrosis type (SFT, n=4). The PPT showed a condensed infiltration of plasma cells into the perivascular spaces of the granulomatous lesion with frequent formation of Russel's body in their cytoplasm. The MICT showed the concomitant infiltration of many macrophages together with plasma cells, resulting in the diffuse destruction of stromal fibrous tissue. The SFT showed granulomatous lesions replaced gradually by thick collagenous fibrous tissue, resembling an inflammatory pseudotumor. The SFT expressed strongly the lymphocytic markers, CD3 and CD20, and the macrophage/monocyte markers, CD31 and CD68, but showed reduced expression of common inflammatory markers, TNF${\alpha}$, cathepsin G, lysozyme, MMP-2, and MMP-9, as well as the reduced expression of osteoclastogenic markers, RANKL and cathepsin K. Conclusion: These results suggest that a gingival plasma cell granuloma shows variable gene expression for cell-mediated immunity and stromal tissue degeneration, undergoing sclerotic fibrosis with a persistent inflammatory reaction.

DISPLACEMENT OF MAXILLARY LATERAL INCISOR CAUSED BY IDIOPATHIC GINGIVAL FIBROMATOSIS (특발성 치은 섬유종증에 의한 상악 측절치의 변위)

  • Jung, Ji-Sook;Park, Ho-Won;Lee, Ju-Hyun;Seo, Hyun-Woo;Lee, Suk-Keun
    • Journal of the korean academy of Pediatric Dentistry
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    • v.38 no.3
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    • pp.296-302
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    • 2011
  • Idiopathic gingival fibromatosisrarely occurs, but frequently recurred after surgical removal. It usually occurs in generalized symmetrical pattern but sometimes in localized unilateral pattern. The localized pattern usually affects the maxillary molar and tuberosity area. This disease usually causes tooth migration, malocclusion, and problems in eating, speech, and esthetics. A boy showed dense gingival fibromatosis localized at primary maxillary right lateral incisor area at the age of 5 years, and his maxillary right lateral incisor become severely displaced at the age of 9 years. He had no medical and hereditary factors relevant to the gingival fibromatosis. However, the dense fibrous tissue was dominant in his labial gingiva of maxillary right incisors. In order to realign the displaced incisors by orthodontic treatment, the dense fibrous tissue covered the defect space between the central incisor and the displaced lateral incisor was surgically removed. The removed specimen was examined by simple immunohistochemical(IHC) array method. IHC array showed increased expression of CTGF, HSP-70, MMP-1, PCNA, CMG2, and TNF-${\alpha}$ in keratinocytes, fibroblasts, endothelial cells, and macrophages of gingival fibromatosis tissue. Therefore, it was suggested that the gingival fibromatosis be caused by the concomitant overexpression of CTGF, HSP-70, MMP-1, PCNA, CMG2, and TNF-${\alpha}$, and resulted in the fibroepithelial proliferation and the inflammatory reaction of gingival tissue.

Comprehensive Mutation Analysis of PIK3CA, p14ARF, p16INK4a and p21Waf1/Cip1 Genes is Suggestive of a Non- Neoplastic Nature of Phenytoin Induced Gingival Overgrowth

  • Swamikannu, Bhuminathan;Kumar, Kishore S.;Jayesh, Raghavendra S.;Rajendran, Senthilnathan;Muthupalani, Rajendran Shanmugam;Ramanathan, Arvind
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.5
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    • pp.2743-2746
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    • 2013
  • Background: Dilantin sodium (phenytoin) is an antiepileptic drug, which is routinely used to control generalized tonic clonic seizure and partial seizure episodes. A few case reports of oral squamous cell carcinomas arising from regions of phenytoin induced gingival overgrowth (GO), and overexpression of mitogenic factors and p53 have presented this condition as a pathology with potential to transform into malignancy. We recently investigated the genetic status of p53 and H-ras, which are known to be frequently mutated in Indian oral carcinomas in GO tissues and found them to only contain wild type sequences, which suggested a non-neoplastic nature of phenytoin induced GO. However, besides p53 and H-ras, other oncogenes and tumor suppressors such as PIK3CA, p14ARF, p16INK4a and $p21^{Waf1/Cip1}$, are frequently altered in oral squamous cell carcinoma, and hence are required to be analyzed in phenytoin induced GO tissues to be affirmative of its non-neoplastic nature. Methods: 100ng of chromosomal DNA isolated from twenty gingival overgrowth tissues were amplified with primers for exons 9 and 20 of PIK3CA, exons $1{\alpha}$, $1{\beta}$ and 2 of p16INK4a and p14ARF, and exon 2 of $p21^{Waf1/Cip1}$, in independent reactions. PCR amplicons were subsequently gel purified and eluted products were sequenced. Results: Sequencing analysis of the twenty samples of phenytoin induced gingival growth showed no mutations in the analyzed exons of PIK3CA, p14ARF, p16INK4a and $p21^{Waf1/Cip1}$. Conclusion: The present data indicate that the mutational alterations of genes, PIK3CA, p14ARF, p16INK4a and $p21^{Waf1/Cip1}$ that are frequently mutated in oral squamous cell carcinomas are rare in phenytoin induced gingival growth. Thus the findings provide further evidence that phenytoin induced gingival overgrowth as a non-neoplastic lesion, which may be considered as clinically significant given the fact that the epileptic patients are routinely administered with phenytoin for the rest of their lives to control seizure episodes.

THE GROWTH FACTORS EXPRESSION OF CYCLOSPORINE INDUCED GINGIVAL OVERGROWTH (Cyclosporine에 의한 치은증식에서 성장인자들의 발현연구)

  • Kim, Young-Jae;Shim, Kwang-Sup;Hwang, Kyung-Gyun;Oh, Young;Paik, Seung-Sam
    • Maxillofacial Plastic and Reconstructive Surgery
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    • v.27 no.5
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    • pp.438-445
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    • 2005
  • Cyclosporine A(CsA) is a powerful immunossuppresive agent used to prevent graft rejection of organ and treat autoimmune disease. One of the major side effects associated with CsA treatment is the development of gingival overgrowth. The purpose of this study was to evaluate the expression and association of the several growth factors in gingival overgrowth induced CsA using by immunohistochemical technique. Normal tissues as control were obtained from healthy normal gingivae and overgrowth gingival tissues as experiments were obtained from the patients taken the CsA. The expressions of the MMP-1, TIMP-1, TGF$\beta$-1, p21, p53, PCNA were evaluated by immunohistochemical technique. The more overgrowth was detected at the epithelial and connective tissue area in experimental group. The MMP-1, TGF$\beta$-1, p21, p53, PCNA expressions were significantly increased in experimental group. The TIMP-1 expressions was not significantly increased in experimental group. We could conclude that the gingival overgrowth induced CsA was related with the collagen matabolism in connective tissue and also the production of the growth factor from epithelial tissue.

Gingival color change after scaling & subgingival root planing (치석제거술과 치은연하 치근면활택술 후 치은의 색조 변화)

  • Kim, Young-Seok;Lim, Sung-Bin;Chung, Chin-Hyung
    • Journal of Periodontal and Implant Science
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    • v.31 no.3
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    • pp.501-511
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    • 2001
  • Several indices have been developed that use bleeding and color changes as indicators of early gingival pathology. In the presence of gingivitis, vascular proliferation and reduction of keratinization owing to increase redness in gingiva. Descriptions of healthy gingiva are numerous, ranging from pale pink and coral pink to deep red and violet. This terms are not objective. Because of perception of color depends on a lot of factors such as light source, object, observer and so on. It is difficult to make an objective expression. Therefore the using of mechanical equipment is recommended to exclude these variables and observer's vias. The purpose of this study was to evaluate gingival color change after scaling & subgingival root planing. The other purpose of this study was to research the correlation of pocket depth, P.B.I. score and gingival color change. After photo-taking and storaging the image of gingival color into a computer, color change was examine with an image analysis program. Results were as follow; 1. Color of healed gingiva after scaling & subgingival root planing was significantly differ from color of inflamed gingiva(p<0.01). 2. Color of healed gingiva after scaling was similar to color of healed gingiva after subgingival root planing(p<0.05). 3. There was statistically significant correlation between color change of red component and pocket depth after scaling & subgingival root planing(p<0.01). 4. There was no correlation between color change of green, blue component and pocket depth after scaling & subgingival root planing(p<0.01). 5. There was statistically significant correlation between between color change of red component and P.B.I. score after scaling & subgingival root planing(p<0.01). 6. There was no correlation between color changes of green, blue component and P.B.I. score after scaling & subgingival root planing(p<0.01). 7. Increase of pocket depth and P.B.I. score were significantly correlated to the amount of color change(p<0.01). 8. P.B.I. score had a higher correlation with color change than pocket depth(p<0.01).

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Morphological features of Cyclosprin A-induced Gingial Hyperplasia (Cyclosporin A에 의한 치은 과증식의 형태학적 특성)

  • Moon, Hyun-Ju;Kim, Chang-Sung;Suh, Jong-Jin;Park, Ji-Sook;Yoon, Jung-Hoon;Cho, Kyoo-Sung;Choi, Seong-Ho
    • Journal of Periodontal and Implant Science
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    • v.30 no.3
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    • pp.609-619
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    • 2000
  • Cyclosporin A(CsA) is now widely used to treat organ transplant recipients. But CsA has various short-and long-term side effects. Especially, gingival hyperplasia is not easy to resolve since its nature is still unknown. This study discusses the pathogenesis of CsA-induced gingival hyperplasia on the basis of data obtained from light and electron microscopic studies of biopsis from patients on CsA treatment after kidney transplantation. Light microscopically, the multilayered squamous epithelium showed an irregular surface of parakeratosis and deep invaginations in the subepithelial tissue. At lamina propria, we observed bundles of irregularly arranged collagen fiber, some fibroblasts, numerous capillary vessels and a large diffuse infiltration of plasma cells. Ultrastructurally, many fibroblasts, collagen fibers, collagen fibrils were present in lamina propria. On the basis of the data collected, we propose that the morphological features of the dimensional increase in gingival tissue associated with CsA treatment in kidney transplant patients may be considered proliferative fibroblasts, collagen fibers, collagen fibrils in lamina propria.

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