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Two cases of sclerotic fibromas directly related to the tendon sheath are presented. Fibroma in these 2 cases consisted of hypocellular, homogeneous collagen bundles that were closely related to the subjacent tendon sheath, and were described by the term 'sclerotic fibroma of tendon sheath'. It is possible that the sclerotic fibroma may arise from fibroma of tendon sheath and that common pathomechanisms exist between these two types of fibroma.
Peripheral odontogenic fibroma (WHO type) is an uncommon lesion of the gingiva; 18 well-documented cases have been published. It is considered to be the extraosseous counterpart of the central odontogenic fibroma. Because of the paucity of reported cases, the full histomorphologic spectrum of this lesion has not yet been established. This article presents nine cases of peripheral odontogenic fibroma that illustrate the variety of its histopathologic findings. The connective tissue ranged from loose (almost myxomatous) to markedly cellular to relatively acellular and well-collagenized. Islands and/or strands of odontogenic epithelium were present in all lesions. Matrix of mineralized material was present in three cases, and juxtaepithelial hyalinization was seen in one case. To avoid the introduction of additional diagnostic terms, we suggest that all these lesions be considered a spectrum of the peripheral odontogenic fibroma (WHO type). We also suggest that the term WHO type be used to distinguish peripheral odontogenic fibromas from the peripheral ossifying fibroma with which they have often been confused.
The peripheral odontogenic fibroma (WHO type) is a relatively rare, benign, unencapsulated, exophytic gingival mass of fibrous connective tissue. Odontogenic epithelium is found within the gingival mass, but usually appears to play a minor role when compared to the fibrous component. According to the present concept, cases reported in the literature under the terms "odontogenic gingival epithelial harmartoma" "hamartoma of the dental lamina" and "peripheral ameloblastic fibrodentinoma" are actually examples of peripheral odontogenic fibroma. Review of the literature revealed only 30 acceptable cases that fit the present concept of peripheral odontogenic fibroma. Because of the paucity of reported cases, the histomorphological spectrum and the clinical features of this lesion have not yet been fully established. This article presents five new cases of peripheral odontogenic fibroma. The connective tissue ranged from markedly cellular to relatively acellular well collagenized. Islands and strands of epithelium were present in all five cases: in four they were scanty and in one abundant. A matrix of mineralized material was present in four cases. The peripheral odontogenic fibroma must be differentiated histologically from peripheral ossifying fibroma, which is a reactive lesion, and from the peripheral ameloblastoma and the calcifying epithelial odontogenic tumour.
Chondromyxoid fibroma is a benign bone tumor that arises most commonly in the metaphysis of long bones in young adults. The cytogenetic features of this tumor are not well known. In this study, four chondromyxoid fibromas were karyotyped after short-term cell culture. All of the tumors contained clonal rearrangements of chromosome 6, and each of these rearrangements involved band 6q13. Two tumors contained a pericentromeric inversion, inv (6)(p25q13), which was described recently in chondromyxoid fibroma. 6q13 rearrangements are not associated with other types of bone and soft tissue tumors, and the inv (6)(p25q13) is reported only in chondromyxoid fibroma. Hence, this cytogenetic marker might be helpful in distinguishing chondromyxoid fibroma from chondrosarcoma and other histologic mimics. The consistent occurrence of 6q13 rearrangements suggests a specific oncogenic mechanism in chondromyxoid fibroma, most likely involving oncogene activation.
The odontogenic fibroma is a rare tumor that has generated controversy, perhaps disproportionately to its importance in the family of odontogenic tumors. The clinical and radiographic features are well documented but the histologic aspects have generated controversy. The behavior is benign, and published accounts indicate a low recurrence rate following treatment by curettage. The tumor recognized by the World Health Organization (WHO) is the legitimate odontogenic fibroma. Histologic variants include the granular cell type and the hybrid odontogenic fibroma giant cell-like tumor. Although the extraosseous "peripheral" odontogenic fibroma presents as a gingival enlargement clinically indistinguishable from other gingival lesions, its histomorphology is similar to the central tumor. A normal dental follicle around the crown of an unerupted tooth may histologically mimic the odontogenic fibroma and other odontogenic tumors.
Recurrent digital fibroma of infancy generally is considered a sporadic tumor of childhood. We describe the case of a mother with recurrent digital fibroma at a young age who gave birth to a daughter with focal dermal hypoplasia, coloboma of the iris and eyelids, anal atresia, and extensive limb malformations. When the infant was 3 months old, fibromas started to appear at the fingertips. The cases of three additional patients are described, with a similar combination of multiple digital fibromas, pigmented marks on the temporal region, and limb malformations. One of these patients has consanguineous parents. The clinical findings overlap partially with Gorlin-Goltz syndrome, which has been renamed by some authors "microphthalmia with linear skin defects" (MLS). Since the skin signs are clearly different, however-more like those of Setleis syndrome ("forceps mark" temporal dysplasia)-the patients described here seem to have a new combination of congenital malformations. Deletion of distal Xp, known to occur in some MLS patients, was not detected using cosmids in fluorescence in situ hybridization. This pattern of digital fibroma with congenital malformations seems to represent a new syndrome.
Nevoid basal cell carcinoma (NBCC) syndrome is an autosomal dominant disorder characterized by distinctive congenital malformations and a variety of benign and malignant neoplasms, including ovarian fibromas. We describe pathologic and cytogenetic findings in a large unilateral ovarian fibroma from a 12-year-old female with NBCC syndrome. The pathologic findings were characteristic for ovarian fibroma, but were unusual for the ovarian fibromas associated with NBCC syndrome because of the absence of calcification, the lack of bilaterality, and the presence of focal hypercellularity. The karyotype of tumor tissue showed complex numerical and structural abnormalities. Although there is frequent loss of heterozygosity of 9q22.3 and mutations in the PTCHgene in Gorlin syndrome, the ovarian fibroma in this case did not have cytogenetically detectable abnormalities of chromosome 9.
The case of bilateral ovarian fibromas occurring in an 8-year-old black girl is reported. These lesions occur rarely in premenarchal females and may be a manifestation of Nevoid Basal Cell Syndrome. Calcifications are reported to occur rarely in ovarian fibromas but seem to occur frequently in fibromas in children. Management is guided by the benignity of the lesion and consists of surgical excision of the fibroma. Preservation of normal ovarian tissue is recommended with the acknowledged risk of recurrence of the fibroma.
Three different but probably related central lesions of the jaws have been referred to previously as odontogenic fibromas. They are (1) hyperplastic dental follicles, (2) a fibrous neoplasm having a histologic appearance similar to that of a dental follicle, and (3) a more complicated lesion, illustrated in a WHO publication, consisting of fibrous connective tissue with varying amounts of odontogenic epithelium, dentin, and/or material resembling cementum. The terms simple odontogenic fibroma and odontogenic fibroma (WHO type) are proposed, respectively, for lesions 2 and 3 above. Some examples of lesion 3 may be confused histologically with the calcifying epithelial odontogenic tumor. More information is required on the biologic behavior of both 1 and 2. A central fibroma of the jaws should be considered a desmoplastic fibroma if it does not appear to have arisen from the odontogenic apparatus and is not a neurofibroma.
We report 32 cases of fibroma of tendon sheath. Most cases presented as a painless mass in the distal portion of an extremity. Ganglion cyst was the most frequent clinical diagnosis. The median patient age was 30.5 years, and 60% of the patients were male. Only one lesion is known to have recurred. The lesions, which averaged 1.5 cm, were light tan, firm, and nodular. Histologic features common to all lesions were (a) a predominantly fibrous matrix containing (b) fibroblast-like spindle cells. Elongated, slitlike spaces were observed in many lesions, and nine cases had areas closely resembling nodular fasciitis. Myofibroblasts and fibroblasts were observed in the three cases studied by electron microscopy. The histologic findings were similar to those previously described for fibroma of tendon sheath. Although slitlike spaces are present in most instances, this finding is not specific for fibroma of tendon sheath, nor is it invariably present. Fasciitis-like changes have been noted in previous series. Our findings, as well as those from prior studies, indicate that fibromas of tendon sheath are heterogeneous. The diagnosis is made only after other fibrous, nodular lesions of the extremities are excluded. Fasciitis-like lesions heretofore classified as fibroma of tendon sheath are more appropriately classified as tenosynovial counterparts of nodular fasciitis.
We retrospectively analyzed the proliferative activity and the centromeric copy number of chromosomes 8, 12, and 17 in three cases of fibrosarcoma and eight cases of cellular fibroma of the ovary using MIB-1 immunostaining, DNA flow cytometry, and fluorescence in situ hybridization (FISH) on paraffin-embedded tissue specimens. In our study, both the MIB-1 labeling index (LI) and the proliferative index (% of cells in S + G2 + M phase) in fibrosarcomas were higher than those in cellular fibromas. The FISH analysis demonstrated the sole abnormality of a gain of trisomy 12 cells in all eight cases of cellular fibroma. Both a gain of trisomy 12 cells and a gain of tetrasomy 12 cells were observed in one case of fibrosarcoma. A gain of trisomy 8 cells was observed in all two fibrosarcomas in which signals were detected. By contrast, neither a gain of trisomy 8 cells nor a gain of tetrasomy 12 cells was observed in any of the eight cases of cellular fibroma. Chromosome 17 showed disomy in all eleven cases. On the basis of these findings, a gain of trisomy 8 cells is therefore considered to be an adequately effective marker to distinguish between cellular fibroma and fibrosarcoma of the ovary, and it may also be related to the proliferative activity of fibrosarcoma of the ovary.
Nuchal-type fibroma is a distinct subcutaneous and dermal fibrous tissue proliferation that has been previously definitely identified in one patient with Gardner's syndrome and has been possibly present in two others. Gardner's syndrome is an autosomal-dominant condition with variable expressivity that comprises epidermoid cysts, fibrous tumors, osteomas, intestinal polyposis, as well as other findings. We report two cases of nuchal-type fibroma presenting in a 13-year-old boy in the right upper back and in his 60-year-old grandfather in the upper chest at the posterior axillary line. Both individuals carried a diagnosis of Gardner's syndrome and neither of them had diabetes. Although the boy has as of now only presented with cutaneous manifestations of Gardner's syndrome, his grandfather has exhibited both cutaneous and intestinal evidence of this syndrome. In addition, the boy's mother and her sister have documented Gardner's syndrome. Light microscopic findings of nuchal-type fibroma from both patients include paucicellular, haphazardly arranged collagen bundles with entrapped adipose tissue. A marked diminution of elastic fibers was noted with Van-Gieson stains. The lesions were diffusely positive for CD34 and contained a few factor XIIIa-positive cells. Electron microscopic analysis revealed no differences between the collagen comprising the nuchal-type fibroma as compared with control dermal collagen obtained from skin away from the tumor. These cases strengthen the view that there is an association between nuchal-type fibroma and Gardner's syndrome.
The present investigation concerns 113 patients with peripheral giant cell granulomas, 52 patients with central giant cell granulomas and 18 patients with non-ossifying fibromas of the long bones. The purpose was to analyze the possible equivalence of central giant cell granulomas with non-ossifying fibromas. Non-ossifying fibromas occur at a lower mean age than central giant cell granulomas and moreover, although central giant cell granulomas may exhibit areas that are histologically similar to non-ossifying fibromas, the presence of other features, especially bone formation, warrants a recognition of central giant cell granulomas and non-ossifying fibromas as separate entities.
PURPOSE: To describe the morphologic and signal intensity characteristics on magnetic resonance (MR) images of fibromas and fibrothecomas. MATERIALS AND METHODS: MR images of 11 female patients with histologically proved fibromas or fibrothecomas were reviewed, and morphologic and signal intensity characteristics of the lesions were analyzed. MR imaging findings were correlated with histologic findings. RESULTS: All fibromas and fibrothecomas showed homogeneous low signal intensity on T1-weighted images. On T2-weighted images, the two smallest lesions showed homogeneous low signal intensity, and eight of the other nine lesions showed predominantly low signal intensity. Edema was noted only in larger lesions, and cystic degeneration was noted only in three of the largest lesions. On T2-weighted images, the percentage of low signal intensity in the lesion was not found to be related to lesion size, and the percentage of low signal intensity in fibromas was not significantly different from that in fibrothecomas (P = .55). Many lesions showed heterogeneous signal intensity; the solid component was distributed peripherally, and the cystic component was located centrally or eccentrically. Free intraperitoneal fluid was noted in 10 of 11 lesions and was not significantly correlated with lesion size (r = .52 and P = .10). CONCLUSION: Because of their predominantly low signal intensity on T2-weighted images, fibromas and fibrothecomas display a relatively specific appearance on MR images.
OBJECTIVE AND IMPORTANCE: Desmoplastic fibroma is a benign bone tumor that can be locally aggressive. It usually occurs in the long bones and mandible. We report on a patient with a desmoplastic fibroma arising in the temporal bone and review previously published cases of desmoplastic fibroma originating within the cranium. CLINICAL PRESENTATION: A 43-year-old woman presented with a 12-year history of progressively worsening head asymmetry. Magnetic resonance imaging and computed tomography demonstrated a mass originating from the bone and involving the adjacent soft tissues. INTERVENTION: A temporal parietal craniectomy was performed with excision of a large tumor involving the bone. An acrylic cranioplasty was used to replace the bone. Pathological examination of the lesion identified desmoplastic fibroma of the cranium. After surgery, the patient's cranial asymmetry was corrected. CONCLUSION: Desmoplastic fibroma of the cranium is rare. Surgical resection is the treatment of choice.
We studied matrix composition and gene expression pattern in chondromyxoid fibromas on the protein and the messenger RNA levels. We could clearly identify focal chondrocytic differentiation within chondromyxoid fibroma by the expression and deposition of type II collagen, which is a marker of chondrocytic cell differentiation. We also were able to show expression of collagen types I, III, and VI in the neoplasm. The major tumor portion was, however, characterized by the presence of hydrated proteoglycans and only minor amounts of collagens, a matrix composition responsible for the myxoid matrix appearance of most parts of these neoplasms. By analyzing cytoprotein expression, we found S-100 protein restricted to cells of the chondroid areas, suggesting S-100 protein staining to be of little help as a positive diagnostic marker for chondromyxoid fibroma. Our data show a specific matrix composition of chondromyxoid fibroma, not previously found in other mesenchymal neoplasms, including chondroblastoma, osteochondroma, enchondroma, and chondrosarcoma. This justifies chondromyxoid fibroma as a specific neoplastic entity, both clinically and biologically.
OBJECTIVES: The fibroma of mesocolon transverse is a rare lesion occurring primarily in age about 45-55 of years. The rarity of these lesions and the absence of characteristic clinical findings makes diagnosis difficult. STUDY DESIGN: The authors describe a case of fibroma mesocolon transverse in woman aged 75 years which became directed to Department of Gynecology & Obstetric in Hospital of Słupsk on account suspicions of ovarian tumor. RESULTS: Fibroma mesocolon transverse usually present as abdominal distention of long duration, pain, vomiting, less frequently as a palpable abdominal mass. Rarely they cause an acute abdominal surgical crisis clinically resembling appendicitis with peritonitis. Ultrasonography was the diagnostic method of choice. Other diagnostic modalities included intravenous pyelogram, barium enema examination, upper gastrointestinal tract series, CT scan and MRI in selected patients exclude gastrointestinal and genitourinary cysts and tumors. Histologically, several specific types could be distinguished of intra-abdominal lesions: lymphangioma, nonpancreatic pseudocyst, enteric duplication tumor, mesothelial tumor, enteric tumor, torsion of an omental segmental infarction cyst, hydatic omental cyst, omental fibromatosis tumor, ectopic ovarian cyst of the omentum, benign teratoma of the omentum or mesocolon. Treatment of choice of fibroma mesocolon transverse is always surgical (enucleation or resection of fibroma). Morbidity and mortality should be very low because of modern surgical techniques and follow-up procedures.
A survey of 4342 oral pathology reports accumulated over a five-year period was performed. Diagnoses were 1090 irritation fibromas and 116 giant cell fibromas. A statistical comparison was then made between the giant cell fibromas and the irritation fibromas to determine if there were any differences between these two lesions with respect to sex or race predilection, age distribution, or location in the oral cavity. Finally, various staining techniques were performed on the giant cell fibromas in an attempt to ascertain the origin of the giant cells present in these lesions. The results will be discussed in this paper.