Metaplasia: A condition in which there is a change of one adult cell type to another similar adult cell type.Barrett Esophagus: A condition with damage to the lining of the lower ESOPHAGUS resulting from chronic acid reflux (ESOPHAGITIS, REFLUX). Through the process of metaplasia, the squamous cells are replaced by a columnar epithelium with cells resembling those of the INTESTINE or the salmon-pink mucosa of the STOMACH. Barrett's columnar epithelium is a marker for severe reflux and precursor to ADENOCARCINOMA of the esophagus.Precancerous Conditions: Pathological processes that tend eventually to become malignant. (From Dorland, 27th ed)Gastric Mucosa: Lining of the STOMACH, consisting of an inner EPITHELIUM, a middle LAMINA PROPRIA, and an outer MUSCULARIS MUCOSAE. The surface cells produce MUCUS that protects the stomach from attack by digestive acid and enzymes. When the epithelium invaginates into the LAMINA PROPRIA at various region of the stomach (CARDIA; GASTRIC FUNDUS; and PYLORUS), different tubular gastric glands are formed. These glands consist of cells that secrete mucus, enzymes, HYDROCHLORIC ACID, or hormones.Gastritis: Inflammation of the GASTRIC MUCOSA, a lesion observed in a number of unrelated disorders.Gastritis, Atrophic: GASTRITIS with atrophy of the GASTRIC MUCOSA, the GASTRIC PARIETAL CELLS, and the mucosal glands leading to ACHLORHYDRIA. Atrophic gastritis usually progresses from chronic gastritis.Goblet Cells: A glandular epithelial cell or a unicellular gland. Goblet cells secrete MUCUS. They are scattered in the epithelial linings of many organs, especially the SMALL INTESTINE and the RESPIRATORY TRACT.Stomach Neoplasms: Tumors or cancer of the STOMACH.Esophagus: The muscular membranous segment between the PHARYNX and the STOMACH in the UPPER GASTROINTESTINAL TRACT.Primary Myelofibrosis: A de novo myeloproliferation arising from an abnormal stem cell. It is characterized by the replacement of bone marrow by fibrous tissue, a process that is mediated by CYTOKINES arising from the abnormal clone.Helicobacter Infections: Infections with organisms of the genus HELICOBACTER, particularly, in humans, HELICOBACTER PYLORI. The clinical manifestations are focused in the stomach, usually the gastric mucosa and antrum, and the upper duodenum. This infection plays a major role in the pathogenesis of type B gastritis and peptic ulcer disease.Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the ESOPHAGUS and the beginning of the DUODENUM.Helicobacter pylori: A spiral bacterium active as a human gastric pathogen. It is a gram-negative, urease-positive, curved or slightly spiral organism initially isolated in 1982 from patients with lesions of gastritis or peptic ulcers in Western Australia. Helicobacter pylori was originally classified in the genus CAMPYLOBACTER, but RNA sequencing, cellular fatty acid profiles, growth patterns, and other taxonomic characteristics indicate that the micro-organism should be included in the genus HELICOBACTER. It has been officially transferred to Helicobacter gen. nov. (see Int J Syst Bacteriol 1989 Oct;39(4):297-405).Cardia: That part of the STOMACH close to the opening from ESOPHAGUS into the stomach (cardiac orifice), the ESOPHAGOGASTRIC JUNCTION. The cardia is so named because of its closeness to the HEART. Cardia is characterized by the lack of acid-forming cells (GASTRIC PARIETAL CELLS).Mucins: High molecular weight mucoproteins that protect the surface of EPITHELIAL CELLS by providing a barrier to particulate matter and microorganisms. Membrane-anchored mucins may have additional roles concerned with protein interactions at the cell surface.Duodenitis: Inflammation of the DUODENUM section of the small intestine (INTESTINE, SMALL). Erosive duodenitis may cause bleeding in the UPPER GI TRACT and PEPTIC ULCER.Mucin 5AC: A gel-forming mucin that is primarily found on the surface of gastric epithelium and in the RESPIRATORY TRACT. Mucin 5AC was originally identified as two distinct proteins, however a single gene encodes the protein which gives rise to the mucin 5A and mucin 5C variants.Intestines: The section of the alimentary canal from the STOMACH to the ANAL CANAL. It includes the LARGE INTESTINE and SMALL INTESTINE.Esophagoscopy: Endoscopic examination, therapy or surgery of the esophagus.Ossification, Heterotopic: The development of bony substance in normally soft structures.Mucous Membrane: An EPITHELIUM with MUCUS-secreting cells, such as GOBLET CELLS. It forms the lining of many body cavities, such as the DIGESTIVE TRACT, the RESPIRATORY TRACT, and the reproductive tract. Mucosa, rich in blood and lymph vessels, comprises an inner epithelium, a middle layer (lamina propria) of loose CONNECTIVE TISSUE, and an outer layer (muscularis mucosae) of SMOOTH MUSCLE CELLS that separates the mucosa from submucosa.Gastroscopy: Endoscopic examination, therapy or surgery of the interior of the stomach.Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.Mucin-2: A gel-forming mucin found predominantly in SMALL INTESTINE and variety of mucous membrane-containing organs. It provides a protective, lubricating barrier against particles and infectious agents.Adenocarcinoma: A malignant epithelial tumor with a glandular organization.Mucin-6: A gel-forming mucin that is predominantly associated with the gastric epithelium.Pyloric Antrum: The region between the sharp indentation at the lower third of the STOMACH (incisura angularis) and the junction of the PYLORUS with the DUODENUM. Pyloric antral glands contain mucus-secreting cells and gastrin-secreting endocrine cells (G CELLS).Chief Cells, Gastric: Epithelial cells that line the basal half of the GASTRIC GLANDS. Chief cells synthesize and export an inactive enzyme PEPSINOGEN which is converted into the highly proteolytic enzyme PEPSIN in the acid environment of the STOMACH.Esophageal Neoplasms: Tumors or cancer of the ESOPHAGUS.Esophagogastric Junction: The area covering the terminal portion of ESOPHAGUS and the beginning of STOMACH at the cardiac orifice.Epithelium: One or more layers of EPITHELIAL CELLS, supported by the basal lamina, which covers the inner or outer surfaces of the body.Mucus: The viscous secretion of mucous membranes. It contains mucin, white blood cells, water, inorganic salts, and exfoliated cells.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Gastroesophageal Reflux: Retrograde flow of gastric juice (GASTRIC ACID) and/or duodenal contents (BILE ACIDS; PANCREATIC JUICE) into the distal ESOPHAGUS, commonly due to incompetence of the LOWER ESOPHAGEAL SPHINCTER.Gastric Mucins: Mucins that are found on the surface of the gastric epithelium. They play a role in protecting the epithelial layer from mechanical and chemical damage.Duodenum: The shortest and widest portion of the SMALL INTESTINE adjacent to the PYLORUS of the STOMACH. It is named for having the length equal to about the width of 12 fingers.Stomach Diseases: Pathological processes involving the STOMACH.Stomach Ulcer: Ulceration of the GASTRIC MUCOSA due to contact with GASTRIC JUICE. It is often associated with HELICOBACTER PYLORI infection or consumption of nonsteroidal anti-inflammatory drugs (NSAIDS).Keratin-7: A type II keratin found associated with KERATIN-19 in ductal epithelia and gastrointestinal epithelia.Hyperplasia: An increase in the number of cells in a tissue or organ without tumor formation. It differs from HYPERTROPHY, which is an increase in bulk without an increase in the number of cells.Respiratory Mucosa: The mucous membrane lining the RESPIRATORY TRACT, including the NASAL CAVITY; the LARYNX; the TRACHEA; and the BRONCHI tree. The respiratory mucosa consists of various types of epithelial cells ranging from ciliated columnar to simple squamous, mucous GOBLET CELLS, and glands containing both mucous and serous cells.Keratin-20: A type I keratin expressed predominately in gastrointestinal epithelia, MERKEL CELLS, and the TASTE BUDS of the oral mucosa.Apocrine Glands: Large, branched, specialized sweat glands that empty into the upper portion of a HAIR FOLLICLE instead of directly onto the SKIN.Helicobacter felis: A species of HELICOBACTER that colonizes in the STOMACH of laboratory MICE; CATS; and DOGS. It is associated with lymphoid follicular hyperplasia and mild GASTRITIS in CATS.Duodenal Ulcer: A PEPTIC ULCER located in the DUODENUM.Endoscopy, Gastrointestinal: Endoscopic examination, therapy or surgery of the gastrointestinal tract.Bile Reflux: Retrograde bile flow. Reflux of bile can be from the duodenum to the stomach (DUODENOGASTRIC REFLUX); to the esophagus (GASTROESOPHAGEAL REFLUX); or to the PANCREAS.Keratins: A class of fibrous proteins or scleroproteins that represents the principal constituent of EPIDERMIS; HAIR; NAILS; horny tissues, and the organic matrix of tooth ENAMEL. Two major conformational groups have been characterized, alpha-keratin, whose peptide backbone forms a coiled-coil alpha helical structure consisting of TYPE I KERATIN and a TYPE II KERATIN, and beta-keratin, whose backbone forms a zigzag or pleated sheet structure. alpha-Keratins have been classified into at least 20 subtypes. In addition multiple isoforms of subtypes have been found which may be due to GENE DUPLICATION.Bronchi: The larger air passages of the lungs arising from the terminal bifurcation of the TRACHEA. They include the largest two primary bronchi which branch out into secondary bronchi, and tertiary bronchi which extend into BRONCHIOLES and PULMONARY ALVEOLI.Thalidomide: A piperidinyl isoindole originally introduced as a non-barbiturate hypnotic, but withdrawn from the market due to teratogenic effects. It has been reintroduced and used for a number of immunological and inflammatory disorders. Thalidomide displays immunosuppressive and anti-angiogenic activity. It inhibits release of TUMOR NECROSIS FACTOR-ALPHA from monocytes, and modulates other cytokine action.Research Support, U.S. Gov't, Non-P.H.S.Research Support, U.S. Gov't, P.H.S.Research Support, Non-U.S. Gov'tResearch Support, U.S. Government

Hybrid capture II, a new sensitive test for human papillomavirus detection. Comparison with hybrid capture I and PCR results in cervical lesions. (1/1094)

AIM: To test a new assay for the detection of human papillomavirus (HPV) DNA, hybrid capture II (HC II), compared with the previous commercialized hybrid capture I (HC I) and polymerase chain reaction (PCR) results on cervical scrapes from fresh cone excision biopsy samples. METHODS: The three methods were used on cervical scrapes from 42 fresh cone excision biopsy samples. There were nine metaplastic and inflammatory lesions, five low grade lesions, and 28 high grade lesions. PCR was performed using the general primers GP5+/GP6+. The viral load of high risk HPV DNA was estimated by the ratio of relative light units to positive control values in the samples. RESULTS: The sensitivity of HC I for the detection of high grade lesions was 71.4%, while it was 92.8% for HC II and 96.4% for the PCR. Considering only the absence of detectable cervical in situ neoplasia, the specificity was 88.9% for HC I, 66.7% for HC II, and 66.7% for PCR. With HC II, for a ratio of cervical sample to normal control of > 200, the sensitivity for the detection of high grade lesion was only 34.6% with a specificity of 66.7%. CONCLUSIONS: HPV detection with the HC II assay is more sensitive than the previous HC I and represents a more convenient and easier test than PCR for routine use. Nevertheless the viral load estimated with this test cannot be a reliable predictive indicator of high grade lesions.  (+info)

Precancerous lesions in two counties of China with contrasting gastric cancer risk. (2/1094)

BACKGROUND: Gastric cancer (GC) is one of the most common cancers worldwide and shows remarkable geographical variation even within countries such as China. Linqu County in Shandong Province of northeast China has a GC rate that is 15 times higher than that of Cangshan County in Shandong, even though these counties are within 200 miles of each other. METHOD: In order to evaluate the frequency of precancerous gastric lesions in Linqu and Cangshan Counties we examined 3400 adults in Linqu County and 224 adults in Cangshan County. An endoscopic examination with four biopsies was performed in each individual of the two populations. RESULTS: The prevalence of intestinal metaplasia (IM) and dysplasia (DYS) was 30% and 15.1%, respectively, in Linqu compared to 7.9% and 5.6% in Cangshan (P < 0.01). Within these histological categories, advanced grades were found more often in Linqu than in Cangshan. The prevalences of IM and DYS were more common at each biopsy site in Linqu, where the lesions also tended to affect multiple sites. CONCLUSIONS: The findings of this study support the concept that IM and DYS are closely correlated with risks of GC and represent late stages in the multistep process of gastric carcinogenesis.  (+info)

KRAS mutations predict progression of preneoplastic gastric lesions. (3/1094)

Eight hundred sixty-three subjects with atrophic gastritis were recruited to participate in an ongoing chemoprevention trial in Narino, Colombia. The participants were randomly assigned to intervention therapies, which included treatment to eradicate Helicobacter pylori infection followed by daily dietary supplementation with antioxidant micronutrients in a 2 x 2 x 2 factorial design. A series of biopsies of gastric mucosa were obtained according to a specified protocol from designated locations in the stomach for each participant at baseline (before intervention therapy) and at year three. A systematic sample of 160 participants was selected from each of the eight treatment combinations. DNA was isolated from each of these biopsies (n = 320), and the first exon of KRAS was amplified using PCR. Mutations in the KRAS gene were detected using denaturing gradient gel electrophoresis and confirmed by sequence analysis. Of all baseline biopsies, 14.4% (23 of 160) contained KRAS mutations. Among those participants with atrophic gastritis without metaplasia, 19.4% (6 of 25) contained KRAS mutations, indicating that mutation of this important gene is likely an early event in the etiology of gastric carcinoma. An important association was found between the presence of KRAS mutations in baseline biopsies and the progression of preneoplastic lesions. Only 14.6% (20 of 137) of participants without baseline KRAS mutations progressed from atrophic gastritis to intestinal metaplasia or from small intestinal metaplasia to colonic metaplasia; however, 39.1% (9 of 23) with baseline KRAS mutations progressed to a more advanced lesion after 3 years [univariate odds ratio (OR), 3.76 (P = 0.05); multivariate OR adjusted for treatment, 3.74 (P = 0.04)]. In addition, the specificity of the KRAS mutation predicted progression. For those participants with G-->T transversions at position 1 of codon 12 (GGT-->TGT), 19.4% (5 of 17) progressed (univariate OR, 2.4); however, 60.0% (3 of 5) of participants with G-->A transitions at position 1 of codon 12 (GGT-->AGT) progressed (univariate OR, 8.7; P = 0.004 using chi2 test).  (+info)

Apoptotic activity is increased in parallel with the metaplasia-dysplasia-carcinoma sequence of the bronchial epithelium. (4/1094)

A high level of apoptotic activity and an independence of apoptosis from the expression of p53 and bcl-2 have been observed in non-small-cell lung carcinoma. We examined 44 samples of normal, metaplastic and premalignant (i.e. mild, moderate and severe dysplasias and carcinoma in situ) bronchial epithelia to evaluate whether differences in the apoptotic activity could already be seen in the stages preceding squamous cell carcinoma of the lung (SQCLC). Apoptotic cells and bodies were visualized by 3' end labelling. The expression of p53 and members of the bcl-2 gene family, such as bcl-2, bax and mcl-1, were determined immunohistochemically with specific antibodies. The relative number of apoptotic cells and bodies [apoptotic index (AI%)] was already increased threefold as the normal bronchial epithelium changed to squamous metaplasia, and the AIs of the dysplastic lesions were about four times higher than those of the normal epithelium. Apoptosis was significantly associated with cell proliferation, as determined by proliferating cell nuclear antigen (PCNA) immunohistochemistry. However, the extent of apoptosis did not correlate with the expression of p53, bcl-2, bax and mcl-1. We conclude that, in the metaplasia-dysplasia-carcinoma sequence in the lung, the elevation of the AI% is an early event associated with cell proliferation activity, but is independent of the expression of p53, bcl-2, mcl-1 and bax.  (+info)

Intestinal metaplasia of human stomach displays distinct patterns of mucin (MUC1, MUC2, MUC5AC, and MUC6) expression. (5/1094)

Intestinal metaplasia is a well-established premalignant condition of the stomach that is characterized by mucin carbohydrate modifications defined by histochemical methods. The purpose of the present study was to see whether the expression of mucin core proteins was modified in the different types of intestinal metaplasia and to evaluate the putative usefulness of mucins as "molecular markers" in this setting. We used a panel of monoclonal antibodies with well-defined specificities to MUC1, MUC2, MUC5AC, and MUC6 to characterize the expression pattern of mucins. In contrast to normal gastric mucosa, the complete form or type I intestinal metaplasia (n = 20) displayed little or no expression of MUC1, MUC5AC, or MUC6 in the metaplastic cells and strong expression of the intestinal mucin MUC2 in the goblet cells of all cases. The incomplete forms of intestinal metaplasia, type II (n = 25) and type III (n = 16), expressed MUC1 and MUC5AC in every case, both in goblet and in columnar cells. MUC6 was also expressed in 16 cases of type II intestinal metaplasia and in 11 cases of type III intestinal metaplasia. The intestinal mucin MUC2 was expressed in every case of incomplete intestinal metaplasia, mostly in goblet cells. The mucin expression profile in the different types of intestinal metaplasia allows the identification of two patterns: one defined by decreased levels of expression of "gastric" mucins (MUC1, MUC5AC, and MUC6) and expression of MUC2 intestinal mucin, which corresponds to type I intestinal metaplasia, and the other defined by coexpression of "gastric mucins" (MUC1, MUC5AC, and MUC6) together with the MUC2 mucin, encompassing types II and III intestinal metaplasia. Our results challenge the classical sequential pathway of intestinal metaplasia (from type I to type III via a type II intermediate step).  (+info)

Helicobacter pylori-induced chronic active gastritis, intestinal metaplasia, and gastric ulcer in Mongolian gerbils. (6/1094)

The establishment of persisting Helicobacter pylori infection in laboratory animals has been difficult, but in 1996 Hirayama reported the development of a successful Mongolian gerbil model. The present study was undertaken with two aims: to better characterize the normal histological structure and histochemical properties of the gastric mucosa of the Mongolian gerbil; and to evaluate the progression of the histopathological features of H. pylori-induced gastritis in this animal model for one year after the experimental infection. Seventy-five Mongolian gerbils were used. Mongolian gerbils were sacrificed at 2, 4, 8, 12, 26, 38, and 52 weeks after H. pylori inoculation. Sections prepared from stomachs immediately fixed in Carnoy's solution were stained with hematoxylin and eosin and Alcian blue at pH 2.5/periodic acid-Schiff, a dual staining consisting of the galactose oxidase-cold thionin Schiff reaction and paradoxical Concanavalin A staining, and with immunostaining for H. pylori and BrdU. H. pylori infection induced in the Mongolian gerbil a chronic active gastritis, in which a marked mucosal infiltration of neutrophils on a background of chronic inflammation became detectable 4 weeks after inoculation and continued up to 52 weeks. Intestinal metaplasia and gastric ulcers appeared after 26 weeks in some of the animals, whereas others developed multiple hyperplastic polyps. The Mongolian gerbil represents a novel and useful model for the study of H. pylori-induced chronic active gastritis and may lend itself to the investigation of the epithelial alterations that lead to intestinal metaplasia and gastric neoplasia.  (+info)

Pathologic changes induced in respiratory tract mucosa by polycyclic hydrocarbons of differing carcinogenic activity. (7/1094)

Seven aromatic polycyclic hydrocarbons (PCHs) were investigated for their toxic effects on respiratory mucosa: benzo(e)pyrene (BeP), pyrene, anthracene, benz(a)anthracene(BaA), dibenz(a,c)anthracene(DBacA), benzo (a)pyrene (BaP), and dimethylbenz(a)anthracene (DMBA). The compounds were chosen because they comprise a spectrum of PCHs ranging from noncarcinogens, to initiators, to weak and strong carcinogens. All of them except DMBA are environmentally relevant chemicals. The chemicals were tested over an 8-week period. Heterotopic tracheal transplants were continously exposed and the histopathologic effects induced by the various PCHs were periodically assessed semiquantitatively. All PCHs exhibited varying degrees of toxicity for respiratory epithelium and submucosa. BeP clearly showed the least toxicity followed by pyrene and anthracene. BaA and DBacA caused marked epithelial and submucosal changes. In addition to epithelial hyperplasia, undifferentiated epithelium and squamous metaplasia developed. Marked mononuclear infiltration occurred in the subepithelial connective tissue. With BaP the epithelial and submucosal changes were similar but were much stronger. DMBA was the most toxic substance, causing epithelial necrosis followed by generalized keratinizing squamous metaplasia; the subepithelial changes consisted of an early acellular exudate and, later (at 8 weeks), marked condensation and hyalinization of the lamina propria. The toxic response pattern of the tracheal mucosa to carcinogenic agents was characterized by the chronicity of epithelial and connective tissue damage, as opposed to the short-lived hyperplastic and inflammatory response elicited by the noncarcinogens and weak initiators.  (+info)

Helicobacter pylori infection enhances glandular stomach carcinogenesis in Mongolian gerbils treated with chemical carcinogens. (8/1094)

Helicobacter pylori (Hp) is thought to be a stomach carcinogen from epidemiological findings. To determine the effects of infection with the bacteria on experimental carcinogenesis, a study of the glandular stomach of Mongolian gerbils (MGs) was performed. Male MGs were treated with N-methyl-N'-nitro-N-nitrosoguanidine followed by inoculation with Hp or infected with Hp followed by N-methyl-N'-nitro-N-nitrosoguanidine administration. Animals were killed at week 50, and their excised stomachs underwent microbiological and histopathological examinations. In addition, a serological investigation was performed. The incidences of adenocarcinomas were significantly higher in animals treated with 60 or 300 p.p.m. N-methyl-N'-nitro-N-nitrosoguanidine for 10 weeks followed by Hp inoculation or Hp followed by 20 p.p.m. N-methyl-N'-nitro-N-nitrosoguanidine for 30 weeks than in the respective controls. Moreover, tumour-bearing animals had higher titres of anti-Hp antibodies than tumour-free animals. Of interest was the finding that a dose of 100 p.p.m. N-methyl-N'-nitro-N-nitrosoguanidine given to infected gerbils eradicated the Hp in about half the animals, with a concomitant reduction in the promoting effect. No tumours were found in animals infected with Hp without N-methyl-N'-nitro-N-nitrosoguanidine or non-treated gerbils. Hp infection enhances glandular stomach carcinogenesis in MGs treated with N-methyl-N'-nitro-N-nitrosoguanidine. Animals with high titres of anti-Hp antibodies are at greatest risk of developing neoplasms.  (+info)

  • The aim of this study was to investigate the prevalence and histopathologic characteristics of entrapped adipose with or without osseous metaplasia in RCC nephrectomy specimens and to determine if this finding impacted the preoperative imaging interpretation. (
  • While intratumoral adipose and/or osseous metaplasia can be observed within RCC, it is extremely rare for the radiologic diagnostic impression to have been confounded by histologically identified entrapped adipose. (
  • There is minimal information in the literature regarding the frequency of intratumoral adipose and osseous metaplasia in RCC [ 1 ]. (
  • The aim of this investigation is to determine the prevalence, impact on preoperative imaging, and histopathologic characteristics of intratumoral adipose and osseous metaplasia in RCC. (
  • RCC nephrectomy cases with intratumoral adipose and/or osseous metaplasia at The Ohio State University Wexner Medical Center from 2010 to 2015, inclusive, were prospectively diagnosed with metaplasia documented by a single genitourinary pathologist (D.L.Z.) at the time of initial diagnosis. (
  • Adipose and osseous metaplasia documentation was performed as part of routine evaluation of RCC nephrectomy cases. (
  • Osseous metaplasia was defined as intratumoral calcification with the presence of lacunae and/or bone marrow elements. (
  • To minimize carryover artifact from biopsy and histologic processing, which can mimic intratumoral adipose without osseous metaplasia, only deposits adherent to the surrounding tissue were included. (
  • All slides were analyzed to determine the size of the largest intratumoral focus of adipose and/or osseous metaplasia (in which adipocytes are often present as a part of the recapitulation of bone marrow) and the distance of the deposit from the nearest tumor edge/capsule. (
  • In the presence of inflammation, SPEM can advance into a more proliferative metaplasia with increased expression of intestine-specific transcripts. (
  • Pathology and immunohistochemical analyses were used to determine depletion efficiency, metaplasia, and proliferation. (
  • The aim of this study is to determine whether Paneth cell hyperplasia or metaplasia characteristically occurs in the colons of children with newly diagnosed idiopathic inflammatory bowel disease (IBD). (
  • Paneth cell metaplasia (PCM) has been most often described in idiopathic inflammatory bowel disease (IBD), both ulcerative colitis (UC) and Crohn's disease (CD). (
  • Squamous metaplasia should not be confused with regeneration, since regenerating epithelial cells can assume a flattened morphology (stretching out to cover a denuded basement membrane). (
  • All showed Paneth Cell Metaplasia. (
  • Paneth cell metaplasia (PCM) is well described in adults but little is known about the distribution of colonic Paneth cells and the occurrence of PCM in a paediatric population. (
  • A key issue in otitis media is mucous cell metaplasia which is responsible for mucous hypersecretion and persistence of the disease. (
  • However, little is known about the molecular mechanisms of mucous cell metaplasia in otitis media. (
  • On the other hand, SAM-pointed domain-containing Ets transcription factor (SPDEF), a member of the "Ets" transcription factor family, has been reported to trigger the mucous cell metaplasia of pulmonary infectious diseases or athsma. (
  • Atoh1 and SPDEF could be the therapeutic targets for otitis media associated with mucous cell metaplasia which is frequently considered "intractable" in the clinical settings. (
  • Glandular metaplasia is a type of metaplasia where irritated tissue converts to a glandular form. (
  • This type of metaplasia is less clearly seen as an adaptive response. (
  • Osseous metaplasia is characterized by mature-appearing bone in the renal parenchyma. (
  • Osseous metaplasia needs to be distinguished from mineralization. (
  • Osseous metaplasia should be recorded but need not be graded. (
  • Mucinous metaplasia was confirmed by PAS and Mucin stains, and plasmacytosis was confirmed by immunohistochemistry for CD138 and MUM1 markers. (
  • The etiology of zoon's balanitis as well as the significance of mucinous metaplasia in these setting are unclear and need to be further investigated. (
  • This is a case of a Nile monitor that suffered fibrous osteodystrophy and chondroid metaplasia after being fed mostly muscle tissue for over two years. (
  • 7) Some authors make a distinction between a primary form, which represents an active cartilaginous metaplasia , and a secondary form that is characterized by less cellular atypia, which is a passive process that involves intra-articular loss of fragments secondary to trauma, arthropathies, or arthritis. (
  • The principal clinical differential diagnosis are extraskeletal mesenchimal chondrosarcoma, giant cell tumor of the tendon sheath with foci of cartilaginous metaplasia , calcifying aponeurotic fibroma, synovial chondromatosis, and nodular chondrometaplasia. (