Inflammatory Reactive Hyperplasia Research Articles

Peripheral Ossifying Fibroma in A Pregnant Female – A Case Report

The gingiva is often the site of localized growths that are considered to be reactive rather than neoplastic in nature. Many of these lesions are difficult to be identified clinically and can be identified as specific entity only on the basis of typical and consistent histomorphology. Peripheral ossifying fibroma (POF) is one of the inflammatory reactive hyperplasia of gingiva. It is a non-neoplastic entity, which occurs on the gingiva in response to trauma or irritation. A clinical report of a 26-year-old pregnant female with a large peripheral ossifying fibroma in the anterior maxilla showing significant growth is presented. Keywords: Ossifying fibroma, pyogenic granuloma, trimester, osteogenesis, exostoses.

Clinic analysis of cervical lymph node lesions in children

Objective:Explore the clinical features of cervical lymph node lesions in children with different pathological types, and provide help for the early diagnosis of the disease. Method:The data of 73 children with cervical lymph node disease diagnosed by lymph node biopsy were collected, and the gender composition, age distribution, lymph node characteristics and clinical manifestations of children with different pathological types were analyzed. Result:Among the 73 children with cervical lymph node disease, the incidence of male patients in the benign disease group was less than that of female ones, and the incidence of male patients in the malignant disease group was greater than that of female ones, the difference in gender composition between the two groups was statistically significant（P<0.05）. The benign disease group had the largest proportion in the school-age period（27.4%）, and the malignant disease group had a larger proportion in the preschool period（21.9%） and school-age period（20.5%）, both groups had a relatively smaller proportion in the infant and adolescent period, the difference in age distribution within the group was statistically significant（P<0.01）. Among the various pathological types, the proportion of 73 children with lymph node inflammatory reactive hyperplasia was the largest, 35.6%（26/73）, and was mainly at school age; the second was Hodgkin's lymphoma, accounting for 20.5%（15/73）, mainly in the preschool and school age. The average maximum transverse diameter of lymph nodes in the malignant disease group was greater than that in the benign disease group（P<0.05）. The lymph nodes in the benign disease group were mainly distributed in areas Ⅰ, Ⅱ, and Ⅲ, and the lymph nodes in the malignant disease group were mainly distributed in areas Ⅱ, Ⅲ, Ⅳ, and Ⅴ, there was a statistically significant difference in the distribution of enlarged lymph nodes between the two groups（P<0.01）. Conclusion:Different pathological types of cervical lymph node lesions in children are different in gender composition, age distribution, lymph node size and distribution, and cervical lymph node lesions in children have their own characteristics.

PERIPHERAL OSSIFYING FIBROMA OF MANDIBLE IN A FEMALE PATIENT REPORT OF A CASE

Fibrous growths in the gingiva with the histopathological presence of calcifications are a common occurrence in the oral cavity. These lesions can be neoplastic in nature with either odontogenic or non odontogenic origin or they can be reactive lesions. Peripheral ossifying fibroma (POF) is one of the inflammatory reactive hyperplasia of gingiva. It represents a separate clinical entity rather than a transitional form of pyogenic granuloma and shares unique clinical characteristics and diverse histopathological features.&#x0D; Here, we present a case report of peripheral ossifying fibroma (POF) in an adult female in her fourth decade of life. This case report comprises the growth that occurred in the mandibular posterior region. POF in the age of 45 years, arising in the mandibular posterior region, is an occasional entity. Careful clinical examination and histopathology findings should be correlated to conclude the final diagnosis.

Peripheral ossifying fibroma- A case report with brief review

Peripheral ossifying fibroma (POF) is an inflammatory reactive hyperplasia of gingiva. It occurs frequently in anterior maxilla with a higher predilection for females. It presents as sessile mucosal nodule and more common in second decade of life. It has been suggested as a separate clinical entity rather than a transitional form of pyogenic granuloma. Diagnosis is often challenging as the clinical presentation of POF mimicks other reactive lesions of gingiva. Due to its high recurrence rate of 8.9% to 20%, prompt diagnosis is important. Here, we report a case of 15 year old girl with pedunculated lesion in gingival and clinically diagnosed as traumatic fibroma.

Clinical and histopathological study of four diverse cases of peripheral ossifying fibroma: A case series

Peripheral ossifying fibroma (POF) is an inflammatory reactive hyperplasia of gingiva. It presents as a diverse lesion with respect to the size, site, gender, age of incidence, clinical appearance, histological, and radiographic presentations. Here, we present a case series of four cases of POF. All the four cases show the clinical, histological, and radiographic diversity of POF posing a diagnostic dilemma. Local excisional biopsy was performed in all the four cases, and the specimens were subjected to histopathological examination which revealed Case 1 to be peripheral cemento-ossifying fibroma, whereas, Case 2, 3, and 4 came out to be POF. Clinically, it becomes difficult to differentiate between the various reactive lesions of the gingiva. This emphasizes upon the role of biopsy for all such lesions. All the local etiological factors should be completely removed, and patients must be put on regular follow-up for evaluation of any recurrences.

MP20-01 CYTOTOXIC NECROTIZING FACTOR-1 (CNF-1) TOXIN IN UROPATHOGENIC E. COLI: IS THERE A ROLE FOR VIRULENCE IN URINARY TRACT INFECTION?

prostate development, reactive hyperplasia, and prostate cancer, but the mechanisms and cell types expanded within the epithelium are unclear. The purpose of this study is to determine if survivin, a known survival and proliferative factor in the prostate, is involved in a specialized protected progenitor cell population that expands as part of repair and recovery in response to prostatic inflammation. METHODS: We initiated inflammatory reactive hyperplasia in mice using our bacterially induced acute inflammation model, harvesting daily for 5 days after inflammation initiation; these were compared to non-inflamed vehicle-instilled prostates. We counted previously characterized prostate epithelial progenitor cells (PEPCs) by their characteristic CD133þ/Sca-1þ/CD44þ/CD117þ/Linprogenitor cell pattern by flow cytometry. We quantified survivin expression in inflamed prostates with both immunofluorescence and immunoblotting. We then determined the co-localization of survivin with PEPCs by immunofluorescence post-sorting. Finally, the dependence of inflammation-driven PEPC expansion was determined by inflaming survivin inhibitortreated mice (LQ7-7F) and determining PEPC expansion and survivin expression as described above. RESULTS: Inflammation induced PEPC expansion 6-fold in the prostate, increasing the percent of PEPCs within the epithelium from 0.2% to 1.2%. Simultaneously, survivin was up-regulated 5-fold as measured by western, and IF showed that survivin expression was increased throughout the inflammatory period, as it was expressed in less than 1% of cells (exclusively basal) in control prostates but increased to 15% of the epithelium by day 2, and 50% of the epithelium by day 5, suggesting that it is preferentially the survivin-positive fraction of cells that expand during inflammatory reactive hyperplasia. Finally, pretreatment of inflamed mice with the survivin inhibitor attenuated both PEPC expansion and the survivinpercent fraction by 50%,while having minimal effect on inflammation itself. CONCLUSIONS: Our data indicate that inflammation induces the expansion of a specialized survivin-expressing progenitor cell population in the prostate, in a surviving-dependent fashion.

Hyperactive lesions of gingiva associated with severe alveolar bone loss: A rare finding.

Pyogenic granuloma (PG) is an inflammatory reactive hyperplasia of connective tissue. It usually arises in response to various stimuli such as low-grade local irritation, traumatic injury, hormonal factors or certain kinds of drugs. It predominantly occurs in the second decade of life in young females and rarely may cause significantly alveolar bone loss. It managed by conservative surgical excision and removal of causative irritants. This paper presents the case of a PG in a 55-year-old male with severe alveolar bone loss in the affected site, managed by surgical intervention.

Pyogenic Granuloma in Eight-Year-Old Child Associated with Bone Loss and Displacement of Tooth Bud: A Unique Case

ABSTRACT Pyogenic granuloma (PG) is one of the inflammatory reactive hyperplasia affecting the oral tissues. It is a relatively common mucocutaneous lesion seen in the oral cavity. It is predominantly seen in young females. Soft tissue enlargements of the oral cavity often represent a diagnostic challenge, because a diverse group of pathologic processes can produce such lesions. An enlargement may represent a variation of normal anatomic structures, inflammation, developmental anomalies, cyst and neoplasm. Here, we report an exceptional case of PG of unknown etiology in 8-year-old male child patient in alveolar crest associated with bone resorption and displacement of tooth bud. How to cite this article Jain M, Singhal S, Goyal M, Sharma B. Pyogenic Granuloma in Eight-Year-Old Child Associated with Bone Loss and Displacement of Tooth Bud: A Unique Case. Int J Experiment Dent Sci 2015;4(2):134-136.

Peripheral ossifying fibroma

Peripheral ossifying fibroma (POF) is one of the inflammatory reactive hyperplasia of gingiva. It represents a separate clinical entity rather than a transitional form of pyogenic granuloma and shares unique clinical characteristics and diverse histopathological features. We present a case of POF in a 65-year-old male patient in the posterior maxillary gingiva, the clinical presentation of which differs from the usual presentation. Differential diagnosis and some interesting facts of POF are discussed.

1577 INFLAMMATION EXPANDS PUTATIVE PROGENITOR CELLS IN HYPERPLASTIC PROSTATES

You have accessJournal of UrologyBenign Prostatic Hyperplasia: Basic Research1 Apr 20121577 INFLAMMATION EXPANDS PUTATIVE PROGENITOR CELLS IN HYPERPLASTIC PROSTATES Marloes Zoetemelk, Jason Myers, Edward Srour, Hal Broxmeyer, Liang Wang, and Travis Jerde Marloes ZoetemelkMarloes Zoetemelk Indianapolis, IN More articles by this author , Jason MyersJason Myers Indianapolis, IN More articles by this author , Edward SrourEdward Srour Indianapolis, IN More articles by this author , Hal BroxmeyerHal Broxmeyer Indianapolis, IN More articles by this author , Liang WangLiang Wang Indianapolis, IN More articles by this author , and Travis JerdeTravis Jerde Indianapolis, IN More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2012.02.1349AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Inflammation is a very consistent histological feature of BPH, but mechanisms by which inflammation promotes epithelial proliferation during BPH are poorly understood. One consistent feature of the reactive prostatic microenvironment is the reactivation of developmental features. Since expansion of progenitor cells is also a hallmark developmental feature, we determined if inflammation expands the putative progenitor cell population in the mouse prostate. METHODS We initiated inflammatory reactive hyperplasia in mice using our bacterially−induced acute inflammation model. Prostates were harvested 1-5 days after inflammation initiation since this is the time point of maximal proliferative response in the mouse prostate; these were compared to uninflamed control prostates. Two methods of determining progenitor cell expansion were performed: 1) Sphere−forming epithelial cells were cultured in anchorage−independent conditions; and 2) Flow cytometry was performed to identify Prostate Epithelial Progenitor Cells (PEPCs) based on the presence of hematopoietic lineage−negative, 4 marker−positive cells (Sca1, CD133, CD44, and CD117) previously shown to be capable of full prostate generation in vivo. Finally, we determined the spatial location of PEPC expansion in inflamed prostates by immunohistochemistry for the most selective of these markers, CD117. RESULTS Although the total number of sphere−forming cells was not significantly increased by inflammation, the growth capacity of these cells in culture increased substantially, as the number of medium−sized spheres (5−20 cells diameter) and large spheres (>20 cells diameter) increased 3 and 10−fold, respectively from inflamed prostates. The total cells per sphere were doubled from inflamed prostates, and BrdU incorporation was also statistically increased. Flow cytometry indicated that inflammation increased 4−marker cell population from 0.2% of epithelial cells in controls to 1.2% in inflamed tissues. IHC showed that rare CD117+ cells were located in the basal layer of the epithelium in the control tissues but were expanded to both the basal and luminal layers of inflamed tissues. CONCLUSIONS Our data indicate that inflammation induces the proliferation of putative PEPCs. Determining the mechanism of how PEPCs expand will lead to better understanding of how the prostate microenvironment utilizes the developmental system during repair and recovery, and how this might be co−opted during prostate diseases. © 2012 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 187Issue 4SApril 2012Page: e639 Peer Review Report Advertisement Copyright & Permissions© 2012 by American Urological Association Education and Research, Inc.MetricsAuthor Information Marloes Zoetemelk Indianapolis, IN More articles by this author Jason Myers Indianapolis, IN More articles by this author Edward Srour Indianapolis, IN More articles by this author Hal Broxmeyer Indianapolis, IN More articles by this author Liang Wang Indianapolis, IN More articles by this author Travis Jerde Indianapolis, IN More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

A clinical and fine needle aspiration cytology study of gingiva in acute leukemia

Background:Oral manifestations are frequently the initial signs of acute leukemia, prompting the patient to consult the dentist first. The gingival tissue is one site commonly involved either by leukemic infiltration or by inflammatory reactive hyperplasia, causing gingival enlargement. The gingival infiltration may also be present without gingival enlargement. Early recognition of clinical findings in the oral cavity leads to its timely diagnosis and management. Since biopsy is highly contraindicated, gingival fine needle aspiration cytology was performed to assess its diagnostic value in detecting gingival infiltration in acute leukemia patients.Materials and Methods:Fifty patients of acute leukemia received clinical and gingival cytological examination. The cases were diagnosed based on bone marrow aspiration findings and classified according to the French–American–British criteria. The absence or presence of intraoral findings was recorded. Site for gingival fine needle aspiration cytology was selected.Results:Leukemic gingival infiltration was found to be more common in acute lymphoblastic leukemia, while the characteristic oral findings were seen more commonly in acute myeloblastic leukemia. All the eight cases of acute lymphoblastic leukemia that were positive for leukemic gingival infiltration showed no clinical evidence of gingival enlargement. In terms of leukemic gingival infiltration, L2 subtype was the only subtype involved, while M5 was more commonly involved than M4 subtype. Two cases of L2 subtype showed gingival enlargement due to local factors like plaque/calculus rather than due to leukemic infiltration.Conclusion:The technique was found to be safe and of definitive diagnostic value in detecting gingival infiltration in acute leukemia patients.

1432 INSULIN-LIKE GROWTH FACTORS MEDIATE INFLAMMATION-DRIVEN PROLIFERATION OF THE MOUSE PROSTATE

You have accessJournal of UrologyProstate Cancer: Basic Research VIII1 Apr 20101432 INSULIN-LIKE GROWTH FACTORS MEDIATE INFLAMMATION-DRIVEN PROLIFERATION OF THE MOUSE PROSTATE Travis Jerde, Eliza McFarland, Sanghee Lee, and Wade Bushman Travis JerdeTravis Jerde Madison, WI More articles by this author , Eliza McFarlandEliza McFarland Medford, MA More articles by this author , Sanghee LeeSanghee Lee Madison, WI More articles by this author , and Wade BushmanWade Bushman Madison, WI More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2010.02.1125AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Inflammation in the prostate is of considerable importance to urological research because of its association with prostate cancer. Yet, mechanisms by which inflammation promotes cancerous or benign prostatic growth remain obscure. Insulin-like growth factor (IGF) signaling plays a role in prostate development and is postulated to drive prostate tumor and benign prostatic growth in men. Since inflammation is associated with growing prostate cancer, we sought to determine if IGF signaling is involved in inflammation-induced epithelial proliferation. METHODS We initiated inflammatory reactive hyperplasia in mice using our bacterially-induced acute inflammation model. Prostates were harvested 1, 2, 3, 5, 7, and 14 days post-instillation. IGF-1 and IGF-2 expression was determined by RT-PCR, and peptide concentration and release were determined by ELISA. IGF receptor activation was quantified by immunoblotting and spatially detected by immunohistochemistry using phospho-specific antibodies to activated IGF receptor. Normal and cancerous human prostate specimens were also stained for IGF receptor activation. Additional inflamed and control animals were treated with an IGF receptor antagonist (picropodophyllin [PPP]) or vehicle i.p. twice daily for 3 days. Inflammatory index, proliferation, IGF receptor activation, and IGF target pathway activity (phosphorylated Akt) were determined. RESULTS Inflammation caused a significant increase in IGF-1 expression and regulated release within two days of inducing inflammation. This correlated with substantially increased proliferative index and IGF receptor activation. The human prostatic epithelium showed substantial induction of IGF signaling in areas juxtaposed to inflammation. IGF inhibition substantially reduced proliferation rates and hyperplastic response of the mouse prostate. PPP treatment predictably reduced IGF receptor activation and Akt pathway activation, but had minimal effect on inflammation itself indicating that IGF inhibition targets proliferation of the epithelium and stroma but not inflammatory infiltrate. CONCLUSIONS Our data indicate that IGF plays a critical role in the hyperplastic response of the prostate to inflammation. While using IGF inhibition therapeutically has been previously proposed based on an associative increase in gene expression, our work provides clear evidence for a causative role for IGF in inflammation-induced growth and establishes IGF signaling as a logical therapeutic target in reducing epithelial expansion in the prostate. © 2010 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 183Issue 4SApril 2010Page: e552 Advertisement Copyright & Permissions© 2010 by American Urological Association Education and Research, Inc.MetricsAuthor Information Travis Jerde Madison, WI More articles by this author Eliza McFarland Medford, MA More articles by this author Sanghee Lee Madison, WI More articles by this author Wade Bushman Madison, WI More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...