Fibroma

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Maneesha Nandimandalam, M.B.B.S.[2],Simrat Sarai, M.D. [3]

Fibromas are benign tumors that are composed of fibrous or connective tissue. They can grow in all organs, arising from mesenchymal tissue. The term “fibroblastic” or “fibromatous” is used to describe tumors of the fibrous connective tissue. There is no classification system established for fibroma. Based on the pathophysiology and location of the tumor, fibroma may be classified into hard fibroma, soft fibroma, angiofibroma, cystic fibroma, chondromyxoid fibroma, desmoplastic fibroma, nonossifying fibroma, ossifying fibroma, nuchal fibroma, collagenous fibroma, fibroma of tendon sheath, perifollicular fibroma, pleomorphic fibroma, uterine fibroma, neurofibroma, and ovarian fibroma. On gross pathology, polypoid lesion which is usually small, is characteristic findings of oral fibroma. On microscopic histopathological analysis, fibrous stroma, collagen bundles, prominent vessels, and overlying squamous mucosa with hyperkeratosis and focal ulceration are characteristic findings of oral fibroma. On gross pathology, well circumscribed, metaphyseal lesion, and fragments of white-grey rubbery tissue are characteristic findings of chondromyxoid fibroma. On microscopic histopathological analysis, spindle cells or stellate cells in a myxoid or chondroid stroma, lobules with hypocellular centers and hypercellular peripheries, giant cells in a hypercellular periphery, and scattered calcifications are characteristic findings of chondromyxoid fibroma. On gross pathology, fleshy, fibrous, yellow or tan-brown lesion with variable areas of haemorrhage are characteristic findings of non-ossifying fibroma. On microscopic histopathological analysis, spindle cells without cytologic atypia are arranged in a storiform pattern, scattered chronic inflammatory cells and benign giant cells, foam cells and hemosiderin deposition, and mitoses are characteristic findings of non-ossifying fibroma. On gross pathology, discrete mass that is well delineated from surrounding bone, tan-white, rubbery cut surface, firm to gritty and no encapsulation are characteristic findings of ossifying fibroma. On microscopic histopathological analysis, haphazardly distributed lamellated bony spicules on a background of fibrous stroma, a zonal architecture with a center of immature bone surrounded by more mature lamellar bone, and central spicules of woven bony trabeculae are lined by a layer of osteoblasts are characteristic findings of ossifying fibroma. Common causes of oral fibroma include trauma or chronic irritation. There are no established causes for chondromyxoid fibroma, non-ossifying fibroma, cemento-ossifying fibroma, and ossifying fibroma. Patients of all age groups may develop fibromas. However, the majority of fibromas are observed in adults. Fibromas usually affects men and women equally, however certain fibromas may show gender predilection. Fibromas are most often observed in adults, but they may occur in individuals of any age and either sex. The majority of patients with fibroma are asymptomatic. The most common symptoms of fibroma include pain and swelling of the affected area. Biopsy is the diagnostic study of choice for fibroma.

Ossifying fibroma was first described in 1872 by Menzel. In the year 1927 Montgomery coined the term “ossifying fibroma”. Chondromyxoid fibroma was first described in year 1948 by H L Jaffe and L Lichtenstein. The non-ossifying fibroma (NOF) was first recognized in 1941 by Sontag and Pyle. Desmoplastic fibroma was first described in year 1958 by H L Jaffe.

There is no classification system established for fibroma. Based on the pathophysiology and location of the tumor, fibroma may be classified into hard fibroma, soft fibroma, angiofibroma, cystic fibroma, chondromyxoid fibroma, desmoplastic fibroma, nonossifying fibroma, ossifying fibroma, nuchal fibroma, collagenous fibroma, fibroma of tendon sheath, perifollicular fibroma, pleomorphic fibroma, uterine fibroma, neurofibroma, and ovarian fibroma.

On gross pathology, polypoid lesion which is usually small, is characteristic findings of oral fibroma. On microscopic histopathological analysis, fibrous stroma, collagen bundles, prominent vessels, and overlying squamous mucosa with hyperkeratosis and focal ulceration are characteristic findings of oral fibroma. On gross pathology, well circumscribed, metaphyseal lesion, and fragments of white-grey rubbery tissue are characteristic findings of chondromyxoid fibroma. On microscopic histopathological analysis, spindle cells or stellate cells in a myxoid or chondroid stroma, lobules with hypocellular centers and hypercellular peripheries, giant cells in a hypercellular periphery, and scattered calcifications are characteristic findings of chondromyxoid fibroma. On gross pathology, fleshy, fibrous, yellow or tan-brown lesion with variable areas of haemorrhage are characteristic findings of non-ossifying fibroma. On microscopic histopathological analysis, spindle cells without cytologic atypia are arranged in a storiform pattern, scattered chronic inflammatory cells and benign giant cells, foam cells and hemosiderin deposition, and mitoses are characteristic findings of non-ossifying fibroma. On gross pathology, discrete mass that is well delineated from surrounding bone, tan-white, rubbery cut surface, firm to gritty and no encapsulation are characteristic findings of ossifying fibroma. On microscopic histopathological analysis, haphazardly distributed lamellated bony spicules on a background of fibrous stroma, a zonal architecture with a center of immature bone surrounded by more mature lamellar bone, and central spicules of woven bony trabeculae are lined by a layer of osteoblasts are characteristic findings of ossifying fibroma.

Common causes of oral fibroma include trauma or chronic irritation. There are no established causes for chondromyxoid fibroma, non-ossifying fibroma, cemento-ossifying fibroma, and ossifying fibroma.

Patients of all age groups may develop fibromas. However, the majority of fibromas are observed in adults. Fibromas usually affects men and women equally, however certain fibromas may show gender predilection. Fibromas are most often observed in adults, but they may occur in individuals of any age and either sex.

There are no established risk factors for fibroma.

According to the United States Preventive Services Task Force, screening for fibroma is not recommended among the general population.

Oral fibroma must be differentiated from squamous papilloma, giant cell fibroma, neurofibroma, peripheral giant cell granuloma, mucocele, and benign and malignant salivary gland tumors. Non-ossifying fibroma must be differentiated from fibrous cortical defect, aneurysmal bone cyst, chondromyxoid fibroma, fibrous dysplasia, desmoplastic fibroma, giant cell tumor of bone, and spindle cell lesions of bone. Ossifying fibroma must be differentiated from ossifying fibroma, fibrous dysplasia, adamantinoma, and osteoid osteoma. Chondromyxoid fibroma must be differentiated from aneurysmal bone cyst (ABC), giant cell tumor of bone (GCT), non ossifying fibroma, chondroblastoma, chondrosarcoma, and phosphaturic mesenchymal tumor. Desmoplastic fibroma must be differentiated from giant cell tumour of bone (GCT), non ossifying fibroma (NOF), fibrous dysplasia, low grade fibrosarcoma, unicameral bone cyst, chondromyxoid fibroma, periosteal desmoids, eosinophilic granuloma, low-grade intraosseous osteosarcoma, adamantinoma, and distant metastasis.

Common complications of ossifying and non-ossifying fibroma include pathological fractures. Depending on the type of the fibroma, the prognosis may vary. However, the prognosis is generally regarded as excellent for nonossifying fibroma. Ossifying fibromas tend to regress over time. Ossifying fibroma is noninvasive tumor. It will recur if it is excised before skeletal maturity. Excision after skeletal maturity is usually successful. Oral fibromas are benign tumors. Recurrence of oral fibromas is possible, however, if the offending irritant persists. Desmoplastic fibromas are benign and locally aggressive tumors. Desmoplastic fibroma is a rare benign intraosseous tumor neoplasm. Desmoplastic fibroma has a recurrence rate of approximately 37% to 72%. The average rate of recurrence after curettage has been reported to be approximately 55%.

The majority of patients with fibroma are asymptomatic. The most common symptoms of fibroma include pain and swelling of the affected area.

Common physical examination findings of oral fibroma include sessile, dome-shaped mass, 1-2 cm in diameter, pale pink in color, and firm, non-tender on palpation. Common physical examination findings of non-ossifying fibromas include localized tenderness or swelling over a lesion. Common physical examination findings of cemento-ossifying fibromas include a sessile or pedunculated mass, mass may be ulcerated and generally has a diameter of less than 2 cm, and diffuse expansion of jaw on right maxillary posterior area, extending anteroposteriorly from distal of upper right second premolar to tuberosity region. Common physical examination findings of desmoplastic fibroma include tenderness over the affected area and palpable mass may be present.

X-ray may be helpful in the diagnosis of fibroma. Findings on x-ray suggestive of a particular fibroma depends on the type of the fibroma. Findings on x-ray suggestive of non-ossifying fibromas include sharply demarcated, asymmetrical, and cortically based lucencies with a thin sclerotic rim. Findings on x-ray suggestive of ossifying fibromas include well-circumscribed lesion, intracortical osteolysis with a characteristic sclerotic band, cortical expansion, and a lytic thinning of the diaphyseal cortical bone with interspersed sclerosis. Findings on x-ray suggestive of chondromyxoid fibroma include a lobulated, eccentric radiolucent lesion. Findings on x-ray suggestive of desmoplastic fibroma include a lytic bone lesions with a geographic pattern of bone destruction and a narrow zone of transition and non-sclerotic margins.

CT scan may be helpful in the diagnosis of fibroma. Findings on x-ray suggestive of a particular fibroma depends on the type of the fibroma. Findings on CT scan of ossifying fibroma include a well-circumscribed lesion, intracortical osteolysis with a characteristic sclerotic band, and moderate cortical expansion. Findings on CT scan of non- ossifying fibroma include sharply demarcated, asymmetrical, cortically based lucencies with a thin sclerotic rim. Findings on CT scan of chondromyxoid fibroma include a mild cortical expansion and characteristic lack of mineralization within chondromyxoid fibromas. Findings on CT scan of cemento-ossifying fibroma include a well circumscribed masses which expand the underlying bone.

MRI may be helpful in the diagnosis of fibroma. On MRI, fibromas appear isointense or hypointense on T1 sequences and hyperintense on T2 sequences.

Ultrasound may be helpful in the diagnosis of fibroma. Findings on ultrasound suggestive of fibroma include solid, hypoechoic masses with ultrasound beam attenuation.

Other imaging studies for ossifying fibroma include bone scan, which demonstrates mild hyperemia and moderate bone uptake during healing. However, in general they are negative.

Biopsy is the diagnostic study of choice for fibroma.

There are no much options available in medical therapy for most of the fibromas, but for some one’s like uterine fibroma does have medical therapy. Gonadotropin-releasing hormone analogues like Leuprolide, Buserelin, Nafarelin, Deslorelin, Histrelin, Goserelin are commonly used. GnRH analogues with add-back therapy like progestins alone, estrogen alone, combined estrogen and progesterone, tibolone, and raloxifene.

Benign fibromas can be removed or left alone. A physician should examine the fibroma and determine whether it may be malignant. For most fibromas the definitive treatment is complete excision. The standard treatment for uterine fibroids include uterus resection (hysterectomy. Segmentary myomectomy is a conservative surgical procedure that consists of resecting the tumor, with the preservation of uterus and, therefore the reproductive function. Bilateral uterine artery embolisation is used as an alternative approach to surgery.

There are no primary preventive measures for fibroma.

There is no secondary prevention for fibromas.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Maneesha Nandimandalam, M.B.B.S.[2],Simrat Sarai, M.D. [3]

Ossifying fibroma was first described in 1872 by Menzel. In the year 1927 Montgomery coined the term “ossifying fibroma”. Chondromyxoid fibroma was first described in the year 1948 by H L Jaffe and L Lichtenstein. The non-ossifying fibroma (NOF) was first recognized in 1941 by Sontag and Pyle. Desmoplastic fibroma was first described in the year 1958 by H L Jaffe.

• Chondromyxoid fibroma was first described in the year 1948 by H L Jaffe and L Lichtenstein.^[1]
• Desmoplastic fibroma was first described in the year 1958 by H L Jaffe.^[2]
• Giant cell fibroma was first described in the year 1974 by Weathers and Callihan.^[3]
• Solitary fibrous tumor (SFT) was first described in the pleura in 1931. The first discussion of its clinical and pathological properties was by Klemperer and Rabin.
• Pleural fibroma was first mentioned in the scientific literature by Wagner. The first discussion of its clinical and pathological properties was by Klemperer and Rabin.
• Elastofibroma was first described in the year 1959 by O H Jarvi and A E Saxon.
• Ossifying fibroma was first described in 1872 by Menzel. In the year 1927 Montgomery coined the term “ossifying fibroma”.
• The non-ossifying fibroma (NOF) was first recognized in 1941 by Sontag and Pyle.^[4]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Maneesha Nandimandalam, M.B.B.S.[2],Simrat Sarai, M.D. [3]

There is no classification system established for fibroma. Based on the pathophysiology and location of the tumor, fibroma may be classified into hard fibroma, soft fibroma, angiofibroma, cystic fibroma, chondromyxoid fibroma, desmoplastic fibroma, nonossifying fibroma, ossifying fibroma, nuchal fibroma, collagenous fibroma, fibroma of tendon sheath, perifollicular fibroma, pleomorphic fibroma, uterine fibroma, neurofibroma, and ovarian fibroma.^[1]

Based on the pathophysiology and location of the tumor fibroma may be classified into the following types, which is shown below in a tabular form:^{[2][3][4] [5][6][7][8] [9][10][11] [12][13] [14]}

Type of Fibroma	Features
Hard Fibroma	The hard fibroma (fibroma durum) consists of many fibers and a few cells, e.g. in the skin it is called dermatofibroma (fibroma simplex or nodulus cutaneous). A special form is the keloid, which derives from hyperplastic growth of scars.
Soft Fibroma	The soft fibroma (fibroma molle) or fibroma with a shaft (acrochordon, skin tag, fibroma pendulans) consist of many loosely connected cells and less fibrous tissue. They mostly appear on the neck, armpits or groin.
Other types of fibroma	The fibroma cavernosum or angiofibroma It consists of many dilated vessels, it is a vasoactive tumor occurring almost exclusively in adolescent males. The cystic fibroma (fibroma cysticum) It has central softening or dilated lymphatic vessels. Myxofibroma The myxofibroma (fibroma myxomatodes) is produced by liquefaction of the underlying soft tissue. Cemento-ossifying fibroma The cemento-ossifying fibroma is hard and fibrous, most frequently seen on the jaw or in the mouth, sometimes in connection with a fracture or another type of injury. Other fibromas: Chondromyxoid fibroma Desmoplastic fibroma Nonossifying fibroma Ossifying fibroma Nuchal fibroma Collagenous fibroma Fibroma of tendon sheath Perifollicular fibroma Pleomorphic fibroma Uterine fibroma Neurofibroma
Ovarian Fibroma	It appears in the sex cord-stromal tumor group of ovarian neoplasms. Upon gross pathological inspection, ovary fibromas are firm and white or tan. Variants with edema are especially likely to be associated with Meigs’ syndrome. On microscopic examination, there are intersecting bundles of spindle cells producing collagen. There may be thecomatous areas (fibrothecoma). The presence of an ovarian fibroma can cause ovarian torsion in some cases.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Maneesha Nandimandalam, M.B.B.S.[2], Simrat Sarai, M.D. [3]

On gross pathology, polypoid lesion which is usually small, are characteristic findings of oral fibroma. On microscopic histopathological analysis, fibrous stroma, collagen bundles, prominent vessels, and overlying squamous mucosa with hyperkeratosis and focal ulceration are characteristic findings of oral fibroma. On gross pathology, well circumscribed, metaphyseal lesion, and fragments of white-grey rubbery tissue are characteristic findings of chondromyxoid fibroma. On microscopic histopathological analysis, spindle cells or stellate cells in a myxoid or chondroid stroma, lobules with hypocellular centers and hypercellular peripheries, giant cells in a hypercellular periphery, and scattered calcifications are characteristic findings of chondromyxoid fibroma. On gross pathology, fleshy, fibrous, yellow or tan-brown lesion with variable areas of haemorrhage are characteristic findings of non-ossifying fibroma. On microscopic histopathological analysis, spindle cells without cytologic atypia are arranged in a storiform pattern, scattered chronic inflammatory cells and benign giant cells, foam cells and hemosiderin deposition, and mitoses are characteristic findings of non-ossifying fibroma. On gross pathology, discrete mass that is well delineated from surrounding bone, tan-white, rubbery cut surface, firm to gritty and no encapsulation are characteristic findings of ossifying fibroma. On microscopic histopathological analysis, haphazardly distributed lamellated bony spicules on a background of fibrous stroma, a zonal architecture with a center of immature bone surrounded by more mature lamellar bone, and central spicules of woven bony trabeculae are lined by a layer of osteoblasts are characteristic findings of ossifying fibroma.^[1][2]

Type of fibroma	Location	Gross pathology	Microscpoic pathology	Genetics and Immunohistochemistry	Associated conditions
Ovarian Fibroma [3][4][5][6][7][8][9][10]	Ovary	The tumor shows homogeneous and solid in appearance with a yellowish-white pigment tinge Necrosis and hemorrhage may or may not be present	Dense cellular proliferations of spindle fibroblast-like cells, which are arranged in a fascicular pattern with ovoid to spindle-shaped nuclei and a scant cytoplasm Tumor cells multiply in a trabecular pattern with a collagen band that is distributed around the stroma Absence of significant cytological atypia	None	Ovarian fibromas are associated with ascites in approximately 40% of cases and with pleural effusions in a small percentage of cases Meigs syndrome: consists of an ovarian fibroma with ascites and a pleural effusion Fibromas are seen in approximately 75% of patients with nevoid basal cell carcinoma syndrome (Gorlin syndrome)
Oral Fibroma [11][12][13]	Buccal mucosa	A round-to-ovoid polypoid lesion, smooth-surfaced, and firm sessile or pedunculated mass 1 mm to 2 cm in diameter in size,hyperkeratotic or ulcerated surface Known for repeated trauma	Histologically similar to fibrous papule Fibrous stroma is a key feature Collagen bundles may be present	None	Multiple oral fibromas may be seen in Cowden disease
Chondromyxoid fibroma [14][15][16][17][18][19][20][21][22]	Proximal tibia metaphysis Distal femoral metaphysis	Well circumscribed, metaphyseal lesion, and fragments of white-grey rubbery tissue are noted	Spindle cells or stellate cells in a myxoid or chondroid stroma Lobules with hypocellular centers and hypercellular peripheries Giant cells in the hypercellular periphery Scattered calcifications. No true hyaline cartilage formation is seen No mitotic activity is seen	GRM1 gene fusion or promoter swapping noted It can be associated with a translocation at t(1;5)(p13;p13)	None
Uterine fibroma [23][24][25][26][27][28][29][30][31][32][33]	Intra-uterine: Intramural leiomyoma Subserosal leiomyoma Submucosal leiomyoma Extra-uterine: Broad ligament leiomyoma Cervical leiomyoma Parasitic leiomyoma Diffuse uterine leiomyomatosis	Round, well circumscribed (but not encapsulated), solid nodules that are white or tan, and show whorled appearance	Spindle cells arranged in fascicles. Fascicular appearance: Adjacent groups of cells have their long axis perpendicular to one another. Whorled arrangement of cells. These cells are uniform in size and shape, with scarce mitoses. There are three benign variants: bizarre (atypical); cellular; and mitotically active. The appearance of prominent nucleoli with perinucleolar halos should alert the pathologist to investigate the possibility of the extremely rare hereditary leiomyomatosis and renal cell cancer (Reed) syndrome.	When multiple fibroids are present they frequently have unrelated genetic defects. Specific mutations of the MED12 protein have been noted in 70% of fibroids. If a mother had fibroids, risk in the daughter is about three times higher than average. Researchers have found that only a few specific genes or cytogenetic deviations are associated with uterine leiomyomas. An association with fatty acid synthase has been reported. CD10 positive SMA positive Desmin positive H-caldesmon positive p16 negative Ki-67 negative	A syndrome (Reed’s syndrome) that causes uterine leiomyomata along with cutaneous leiomyomata and renal cell cancer has been reported. This is associated with a mutation in the gene that produces the enzyme fumarate hydratase, located on the long arm of chromosome 1 (1q42.3-43). Inheritance is autosomal dominant.
Ossifying Fibroma [34][35][36][37][38][39][40]	Tibia: predilection for the cortex of the tibial diaphysis. Femur	Discrete mass that is well delineated from surrounding bone, tan-white, rubbery cut surface, firm to gritty and no encapsulation	They comprise of haphazardly distributed lamellated bony spicules on a background of fibrous stroma The lesion has a zonal architecture with a center of immature bone surrounded by more mature lamellar bone. The central spicules of woven bony trabeculae are lined by a layer of osteoblasts. The background is a loose and storiform fibrous tissue.	Ossifying fibromas are keratin positive – isolated cells accepted by some. It is osteonectin, neurofibromin, and S-100 protein positive.	Clonal chromosomal abnormalities such as trisomies of chromosomes 7, 8, 12 ,21, and/or 22 Adamantinoma
Non-ossifying Fibroma [41][42][43]	Metaphysis of distal femur or proximal tibia (80%) Cortical	Fleshy, fibrous, yellow or tan-brown lesion with variable areas of haemorrhage are noted	Spindle cells without cytologic atypia are arranged in a storiform pattern. Scattered chronic inflammatory cells and benign giant cells. Foam cells and hemosiderin deposition are present. Mitoses are seen but cytologic atypia is absent.	Clonal rearrangements in chromosomes 1, 3, 4, 11, and 14 are noted in NOFs (non-ossifying fibroma) of bone	Neurofibromatosis-type 1 (NF1) Fibrous dysplasia Jaffe-Campanacci syndrome
Desmoplastic Fibroma [44][45][46][47][48][49][50]	Mandible (22%) and the metaphysis of long bones (56%). Pelvis		Lamellar bone Fibrotic marrow space has following features: Collagen Low cellularity Spindle cells without significant atypia On histopathology, desmoplastic fibromas are identical to soft tissue desmoid tumors, with abundant collagenous stroma and little cellularity or pleomorphism. The main cell types that are seen include the following: Fibroblasts Myofibroblasts Undifferentiated mesenchymal cells	Strong positive for the adhesion protein β-Catenin Weak positive labelling for S-100 No positive stain for the proliferation marker Ki67	No associated conditions
Pleural Fibroma [51][52][53][54][55][56][57][58][59][60][61][62]	80% of pleural fibromas originate in the visceral pleura, while 20% arise from parietal pleura.		Composed of irregularly arranged fascicles comprising of spindle cells with collagen separation. They originate from submesothelial mesenchymal cells. Myxoid or cystic degeneration can occur.	Recurrent somatic fusions of the two genes, STAT6, located at chromosomal region 12q13, have been identified in pleural fibromas.	Some pleural fibromas are associated with the paraneoplastic Doege–Potter syndrome, which is caused by tumor production of IGF-2. Hypoglycaemia: 2-4% 6, thought to be due to production of IGF-2 Hypertrophic pulmonary osteoarthropathy (HPOA): ~20% 6: thought to be due to abnormal production of hyaluronic acid
Cardiac Fibroma [63][64][65][66][67][68][69][70][71][72]	Ventricular septum and left ventricular free wall.	Well defined, solitary, intramyocardial lesions with smooth margins and usually large, with a mean diameter of ~5 cm	Usually have no foci of cystic change, hemorrhage, or necrosis. Calcification is common	None	There is an increased prevalence of cardiac fibromas in Gorlin syndrome.
Renal Medullary Fibroma [73][74][75]	Renal medulla	Small, and white well circumscribed nodule in medulla typically less than 3mm are characteristic findings of renal medullary fibroma	Small polygonal/stellate cells Abundant loose/myxoid stroma Entrapped renal tubules may be present	None	No associated conditions
Cemento-ossifying Fibroma [76][77][78][79][80][81][82][83][84][85]	Maxillary gingiva is involved more often than the mandibular gingiva	Solid, sessile or pedunculated mass, which is often ulcerated, and generally has a diameter of less than 2 cm are characteristic findings of cemento-ossifying fibroma.	Cemento -ossifying tumors are composed of fibrous tissue, calcified tissue resembling bone and/or cementum. The bone-like component is predominant reminiscent of woven bone and is found in more ‘mature’ lesions. In some instances, this entity has been divided into cementifying fibroma and ossifying fibroma depending on the relative amounts of the tumor’s constituent tissues. Surface ulceration is common	None	No associated conditions
Desmoplastic Fibroblastoma [86][87][88][89][90][91]	Shoulder region		Spindle cells or stellate cells without nuclear atypia Acellular stroma with abundant collagen Myxoid areas may be present Mitoses is rare	FOSL1 gene is involved in the pathogenesis of desmoplastic fibroblastoma, llq 12 breakpoint described as being characteristic. Beta-catenin -ve Positive in desmoid-type fibromatosis Desmin negative S-100 negative CD34 negative MSA positive Alpha-SMA positive	No associated conditions
Elastofibroma [92][93][94][95][96][97][98]	Subscapular region.	I’ll defined, nonencapsulated, rubbery, firm, white lesion with interspersed fat and with moderate demarcation to surrounding tissue are characteristic findings of elastofibroma. The tumors can be quite large (up to 20 cm), although most are around 5 cm.	Thick bundles of collagen and elastin fibers are characteristic findings of elastofibroma. Admixture of heavy dense bands of collagenous tissue dissected by fat and abnormal elastic fibers. The elastic fibers are coarse, thick, and darkly eosinophilic, often fragmented into globules, creating a “string of pearls” or “pipe cleaner” appearance. Because of degeneration, the elastic fibers will appear as globules with a serrated or “prickled” edge.	There are alterations of short arm of chromosome 1 Multifocality may suggest systemic enzymatic defect, resulting in abnormal elastogenesis The elastic fibers will be visible on a Weigert or von Gieson elastic stains.	No associated conditions
Sclerotic Fibroma [99][100][101][102][103][104][105][106][107]	Skin, may be solitary or multifocal		Well-delineated but unencapsulated mass of densely collagenized, hypocellular fibrous tissue with a storiform pattern, and prominent clefts between collagen bundles are characteristic findings of elastofibroma.	CD34 Vimentin positive	Cowden syndrome
Giant cell fibroma [108][109][110][111][112][113][114][115]	Mandibular gingiva, followed by the maxillary gingiva, the tongue, and the palate.	Sessile or pedunculated nodule that is smaller than 1cm in diameter are characteristic findings of giant cell fibroma. Often, it has a bosselated or somewhat papillary surface.	An unencapsulated mass of fibrous connective tissue that contains numerous characteristic large, plump, stellate and spindle-shaped fibroblasts, some of which are multinucleated. The surface epithelium is often atrophic and corrugated.	None	No associated conditions
Peripheral Odontogenic Fibroma [116][117][118][119][120]	Mandible	Firm, slowly growing, sessile, and nodular growth of the gingiva are characteristic findings of peripheral odontogenic fibroma.	An unencapsulated mass of interwoven cellular fibrous connective tissue that contains scattered nests or strands of odontogenic epithelium It consists of cellular fibrous connective tissue parenchyma with non neoplastic islands, strands of columnar or cuboidal odontogenic epithelium. Myxoid foci, osteoid, cementoid, or dystrophic calcifications are sometimes seen. Generally, the surface is not ulcerated.	None	No associated conditions

Type of fibroma	Gross image	Microscopic image
Ovarian fibroma
Oral fibroma
Chondromyxoid fibroma
Uterine fibroma
Ossifying Fibroma
Cardiac fibroma
Giant cell fibroma
Peripheral odontogenic fibroma
Elastofibroma
Desmoplastic fibroblastoma
Renal medullary fibroma
Pleural fibroma

The normal physiology of [name of process] can be understood as follows:

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Genes involved in the pathogenesis of [disease name] include:

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• [Gene3]

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The development of [disease name] is the result of multiple genetic mutations such as:

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Type of fibroma	Location	Gross pathology	Microscpoic pathology	Genetics and Immunohistochemistry	Associated conditions
Ovarian Fibroma [3][4][5][6][7][8][9][10]	Ovary	The tumor shows homogeneous and solid in appearance with a yellowish-white pigment tinge Necrosis and hemorrhage may or may not be present	Dense cellular proliferations of spindle fibroblast-like cells, which are arranged in a fascicular pattern with ovoid to spindle-shaped nuclei and a scant cytoplasm Tumor cells multiply in a trabecular pattern with a collagen band that is distributed around the stroma Absence of significant cytological atypia	None	Ovarian fibromas are associated with ascites in approximately 40% of cases and with pleural effusions in a small percentage of cases Meigs syndrome: consists of an ovarian fibroma with ascites and a pleural effusion Fibromas are seen in approximately 75% of patients with nevoid basal cell carcinoma syndrome (Gorlin syndrome)
Oral Fibroma [11][12][13]	Buccal mucosa	A round-to-ovoid polypoid lesion, smooth-surfaced, and firm sessile or pedunculated mass 1 mm to 2 cm in diameter in size,hyperkeratotic or ulcerated surface Known for repeated trauma	Histologically similar to fibrous papule Fibrous stroma is a key feature Collagen bundles may be present	None	Multiple oral fibromas may be seen in Cowden disease
Chondromyxoid fibroma [14][15][16][17][18][19][20][21][22]	Proximal tibia metaphysis Distal femoral metaphysis	Well circumscribed, metaphyseal lesion, and fragments of white-grey rubbery tissue are noted	Spindle cells or stellate cells in a myxoid or chondroid stroma Lobules with hypocellular centers and hypercellular peripheries Giant cells in the hypercellular periphery Scattered calcifications. No true hyaline cartilage formation is seen No mitotic activity is seen	GRM1 gene fusion or promoter swapping noted It can be associated with a translocation at t(1;5)(p13;p13)	None
Uterine fibroma [23][24][25][26][27][28][29][30][31][32][33]	Intra-uterine: Intramural leiomyoma Subserosal leiomyoma Submucosal leiomyoma Extra-uterine: Broad ligament leiomyoma Cervical leiomyoma Parasitic leiomyoma Diffuse uterine leiomyomatosis	Round, well circumscribed (but not encapsulated), solid nodules that are white or tan, and show whorled appearance	Spindle cells arranged in fascicles. Fascicular appearance: Adjacent groups of cells have their long axis perpendicular to one another. Whorled arrangement of cells. These cells are uniform in size and shape, with scarce mitoses. There are three benign variants: bizarre (atypical); cellular; and mitotically active. The appearance of prominent nucleoli with perinucleolar halos should alert the pathologist to investigate the possibility of the extremely rare hereditary leiomyomatosis and renal cell cancer (Reed) syndrome.	When multiple fibroids are present they frequently have unrelated genetic defects. Specific mutations of the MED12 protein have been noted in 70% of fibroids. If a mother had fibroids, risk in the daughter is about three times higher than average. Researchers have found that only a few specific genes or cytogenetic deviations are associated with uterine leiomyomas. An association with fatty acid synthase has been reported. CD10 positive SMA positive Desmin positive H-caldesmon positive p16 negative Ki-67 negative	A syndrome (Reed’s syndrome) that causes uterine leiomyomata along with cutaneous leiomyomata and renal cell cancer has been reported. This is associated with a mutation in the gene that produces the enzyme fumarate hydratase, located on the long arm of chromosome 1 (1q42.3-43). Inheritance is autosomal dominant.
Ossifying Fibroma [34][35][36][37][38][39][40]	Tibia: predilection for the cortex of the tibial diaphysis. Femur	Discrete mass that is well delineated from surrounding bone, tan-white, rubbery cut surface, firm to gritty and no encapsulation	They comprise of haphazardly distributed lamellated bony spicules on a background of fibrous stroma The lesion has a zonal architecture with a center of immature bone surrounded by more mature lamellar bone. The central spicules of woven bony trabeculae are lined by a layer of osteoblasts. The background is a loose and storiform fibrous tissue.	Ossifying fibromas are keratin positive – isolated cells accepted by some. It is osteonectin, neurofibromin, and S-100 protein positive.	Clonal chromosomal abnormalities such as trisomies of chromosomes 7, 8, 12 ,21, and/or 22 Adamantinoma
Non-ossifying Fibroma [41][42][43]	Metaphysis of distal femur or proximal tibia (80%) Cortical	Fleshy, fibrous, yellow or tan-brown lesion with variable areas of haemorrhage are noted	Spindle cells without cytologic atypia are arranged in a storiform pattern. Scattered chronic inflammatory cells and benign giant cells. Foam cells and hemosiderin deposition are present. Mitoses are seen but cytologic atypia is absent.	Clonal rearrangements in chromosomes 1, 3, 4, 11, and 14 are noted in NOFs (non-ossifying fibroma) of bone	Neurofibromatosis-type 1 (NF1) Fibrous dysplasia Jaffe-Campanacci syndrome
Desmoplastic Fibroma [44][45][46][47][48][49][50]	Mandible (22%) and the metaphysis of long bones (56%). Pelvis		Lamellar bone Fibrotic marrow space has following features: Collagen Low cellularity Spindle cells without significant atypia On histopathology, desmoplastic fibromas are identical to soft tissue desmoid tumors, with abundant collagenous stroma and little cellularity or pleomorphism. The main cell types that are seen include the following: Fibroblasts Myofibroblasts Undifferentiated mesenchymal cells	Strong positive for the adhesion protein β-Catenin Weak positive labelling for S-100 No positive stain for the proliferation marker Ki67	No associated conditions
Pleural Fibroma [51][52][53][54][55][56][57][58][59][60][61][62]	80% of pleural fibromas originate in the visceral pleura, while 20% arise from parietal pleura.		Composed of irregularly arranged fascicles comprising of spindle cells with collagen separation. They originate from submesothelial mesenchymal cells. Myxoid or cystic degeneration can occur.	Recurrent somatic fusions of the two genes, STAT6, located at chromosomal region 12q13, have been identified in pleural fibromas.	Some pleural fibromas are associated with the paraneoplastic Doege–Potter syndrome, which is caused by tumor production of IGF-2. Hypoglycaemia: 2-4% 6, thought to be due to production of IGF-2 Hypertrophic pulmonary osteoarthropathy (HPOA): ~20% 6: thought to be due to abnormal production of hyaluronic acid
Cardiac Fibroma [63][64][65][66][67][68][69][70][71][72]	Ventricular septum and left ventricular free wall.	Well defined, solitary, intramyocardial lesions with smooth margins and usually large, with a mean diameter of ~5 cm	Usually have no foci of cystic change, hemorrhage, or necrosis. Calcification is common	None	There is an increased prevalence of cardiac fibromas in Gorlin syndrome.
Renal Medullary Fibroma [73][74][75]	Renal medulla	Small, and white well circumscribed nodule in medulla typically less than 3mm are characteristic findings of renal medullary fibroma	Small polygonal/stellate cells Abundant loose/myxoid stroma Entrapped renal tubules may be present	None	No associated conditions
Cemento-ossifying Fibroma [76][77][78][79][80][81][82][83][84][85]	Maxillary gingiva is involved more often than the mandibular gingiva	Solid, sessile or pedunculated mass, which is often ulcerated, and generally has a diameter of less than 2 cm are characteristic findings of cemento-ossifying fibroma.	Cemento -ossifying tumors are composed of fibrous tissue, calcified tissue resembling bone and/or cementum. The bone-like component is predominant reminiscent of woven bone and is found in more ‘mature’ lesions. In some instances, this entity has been divided into cementifying fibroma and ossifying fibroma depending on the relative amounts of the tumor’s constituent tissues. Surface ulceration is common	None	No associated conditions
Desmoplastic Fibroblastoma [86][87][88][89][90][91]	Shoulder region		Spindle cells or stellate cells without nuclear atypia Acellular stroma with abundant collagen Myxoid areas may be present Mitoses is rare	FOSL1 gene is involved in the pathogenesis of desmoplastic fibroblastoma, llq 12 breakpoint described as being characteristic. Beta-catenin -ve Positive in desmoid-type fibromatosis Desmin negative S-100 negative CD34 negative MSA positive Alpha-SMA positive	No associated conditions
Elastofibroma [92][93][94][95][96][97][98]	Subscapular region.	I’ll defined, nonencapsulated, rubbery, firm, white lesion with interspersed fat and with moderate demarcation to surrounding tissue are characteristic findings of elastofibroma. The tumors can be quite large (up to 20 cm), although most are around 5 cm.	Thick bundles of collagen and elastin fibers are characteristic findings of elastofibroma. Admixture of heavy dense bands of collagenous tissue dissected by fat and abnormal elastic fibers. The elastic fibers are coarse, thick, and darkly eosinophilic, often fragmented into globules, creating a “string of pearls” or “pipe cleaner” appearance. Because of degeneration, the elastic fibers will appear as globules with a serrated or “prickled” edge.	There are alterations of short arm of chromosome 1 Multifocality may suggest systemic enzymatic defect, resulting in abnormal elastogenesis The elastic fibers will be visible on a Weigert or von Gieson elastic stains.	No associated conditions
Sclerotic Fibroma [99][100][101][102][103][104][105][106][107]	Skin, may be solitary or multifocal		Well-delineated but unencapsulated mass of densely collagenized, hypocellular fibrous tissue with a storiform pattern, and prominent clefts between collagen bundles are characteristic findings of elastofibroma.	CD34 Vimentin positive	Cowden syndrome
Giant cell fibroma [108][109][110][111][112][113][114][115]	Mandibular gingiva, followed by the maxillary gingiva, the tongue, and the palate.	Sessile or pedunculated nodule that is smaller than 1cm in diameter are characteristic findings of giant cell fibroma. Often, it has a bosselated or somewhat papillary surface.	An unencapsulated mass of fibrous connective tissue that contains numerous characteristic large, plump, stellate and spindle-shaped fibroblasts, some of which are multinucleated. The surface epithelium is often atrophic and corrugated.	None	No associated conditions
Peripheral Odontogenic Fibroma [116][117][118][119][120]	Mandible	Firm, slowly growing, sessile, and nodular growth of the gingiva are characteristic findings of peripheral odontogenic fibroma.	An unencapsulated mass of interwoven cellular fibrous connective tissue that contains scattered nests or strands of odontogenic epithelium It consists of cellular fibrous connective tissue parenchyma with non neoplastic islands, strands of columnar or cuboidal odontogenic epithelium. Myxoid foci, osteoid, cementoid, or dystrophic calcifications are sometimes seen. Generally, the surface is not ulcerated.	None	No associated conditions

Type of fibroma	Gross image	Microscopic image
Ovarian fibroma
Oral fibroma
Chondromyxoid fibroma
Uterine fibroma
Ossifying Fibroma
Cardiac fibroma
Giant cell fibroma
Peripheral odontogenic fibroma
Elastofibroma
Desmoplastic fibroblastoma
Renal medullary fibroma
Pleural fibroma

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Maneesha Nandimandalam, M.B.B.S.[2], Simrat Sarai, M.D. [3]

Common causes of oral fibroma include trauma or chronic irritation. There are no established causes for chondromyxoid fibroma, non-ossifying fibroma, cemento-ossifying fibroma, and ossifying fibroma. Although there are some associated factors for the development of some fibromas like ovarian fibroma, uterine fibroma.

Type of fibroma	Causes/ associated factors
Ovarian Fibroma[1][2]	Obesity Tamoxifen therapy Early menarche Infertility Nulliparity African race Estrogen
Non-ossifying Fibroma [3][4]	Clonal rearrangements in chromosomes 1, 3, 4, 11, and 14
Uterine Fibroma [5]	Genetic changes Estrogen and progesterone Insulin-like growth factor
Oral Fibroma	Trauma or chronic irritation
Chondromyxoid Fibroma [6][7]	Clonal rearrangement of chromosome 6

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Maneesha Nandimandalam, M.B.B.S.[2], Simrat Sarai, M.D. [3]

Patients of all age groups may develop fibromas. However, the majority of fibromas are observed in adults. Fibromas usually affects men and women equally, however certain fibromas may show gender predilection. Fibromas are most often observed in adults, but they may occur in individuals of any age and either sex.

The prevalence of non-ossifying fibroma is estimated to be 30-40 % of all normal children.

Non-ossifying fibromas are the most common fibrous bony lesions in children and adolescents, with a peak incidence at 10-15 years old. Non-ossifying fibromas are not seen beyond the age of 30 years, as they spontaneously heal. The age of presentation of the isolated mandibular non-ossifying fibroma appears to differ from that of the long bones in that the mandibular NOF appears at an older average age at diagnosis. The overall incidence of non-ossifying fibromas in the long bones is 30–40 % of children over the age of 2 with the highest incidence between ages 4 and 8 years.

Males are more commonly affected with non-ossifying fibromas of the long bones than females. The male to female ratio is approximately 2 to 1. Females are more commonly affected with mandibular NOF than males.

The incidence of desmoplastic fibroma is approximately 0.11% of all primary bone tumors.^[1][2]

The median age at presentation is 21 years.

Desmoplastic fibromas affects men and women equally.

Ovarian fibromas represent 4% of all ovarian neoplasms. They tend to occur mostly during perimenopause and postmenopause.^[3][4][5]

Patients of all age groups may develop ovarian fibroma. However, they are most frequently seen in middle-aged women. The median age at diagnosis is 52 years. Ovarian fibromas commonly affects individuals during perimenopause and postmenopause. They are rare in children.

Ossifying fibromas most frequently occur in young children (less than 10 years of age). The median age at diagnosis for females and for males is 13 years and 10 years respectively.^[6][7]

Ossifying fibromas affects men and women equally.

A chondromyxoid fibroma (CMF) is an extremely rare benign cartilaginous neoplasm which accounts for < 1% bone tumours.^[8][9][10]

Chondromyxoid fibromas affects men and women equally.

Patients of all age groups may develop chondromyxoid fibroma. However, they are most frequently seen in second and third decades. Approximately 75% of cases occur before the age of 30 years. The location of chondromyxoid fibroma(CMF) varies with age. It is found predominantly in long bones between 1 and 10 years, while the distribution of localization becomes equal between the long bones, flat bones and ribs in the fourth decade. According to some authors, the average age for intracranial CMF is 37 – 39 years. It is 32.7years (range 15-50 years) among patients who have frontal CMF.The duration of the symptoms before diagnosis varies between 10 days and 20 years.^[11]

Cardiac fibromas primarily affects children, the majority of cases are detected in infants or in utero. They are the second most common benign primary cardiac tumour in children after cardiac rhabdomyoma and second commonest fetal cardiac tumor.^[12]

Pleural fibromas affects men and women equally.^[13][14]

Pleural fibromas usually presents in the 6th to 7th decades.

Cemento-ossifying fibromas are most frequently diagnosed during the third and fourth decades. Occasionally, they are identified in children, in which case they are a more aggressive variant and are known as juvenile aggressive cemento-ossifying fibromas. Patients of all age groups may develop cemento-ossifying fibroma. Cemento-ossifying fibroma commonly affects individuals 10-20 years of age.^{[15][16][17][18]}

Females are more commonly affected with cemento-ossifying fibromas than males. The female to male ratio is approximately 3 to 2.

Oral fibromas are the most common oral cavity tumors.^[19]

Patients of all age groups may develop oral fibromas. However, they are most commonly seen in older adults, usually 30-50 years old. It affects 1-2% of adults. It is the most common oral cavity tumour.

Females are more commonly affected with oral fibromas than males. The female to male ratio is approximately 2 to 1.

Patients of all age groups may develop giant cell fibroma. The majority of cases of giant cell fibroma are diagnosed in persons aged 10-30 years.^{[20][21][22][23]}

Giant cell fibromas affects men and women equally.

Elastofibroma commonly affects individuals older than 50 years of age. Elastofibroma is a rare disease that tends to affect elderly population (< 0.001% of soft tissue tumors).^[24][25]

Females are more commonly affected with elastofibroma than males. The female to male ratio is approximately 5 to 1.

Uterine fibromas occur in approximately 25% of women of reproductive age. Approximately 40% of women by age 40 years develop uterine fibromas. Uterine fibromas commonly affects females after puberty, they commonly accelerate in growth during pregnancy and involute with menopause. Uterine fibromas commonly affects individuals older than 30 years of age. Approximately 20% to 80% of women develop fibroids by the age of 50.^{[26][27][28][29][30]}

In 2013, it was estimated that 171 million women were affected by uterine fibromas worldwide.^{[31][32][33][34]}

Uterine fibromas usually affects individuals of the African race. Caucasian females are less likely to develop uterine fibromas. African American women are two to three times more likely to get fibroids than Caucasian women. In African-American women fibroids seem to occur at a younger age, grow more quickly, and are more likely to cause symptoms.According to the National Institute of Environmental Health Sciences, eighty percent of African American women will develop benign uterine fibroid tumors by their late 40s.^[35][36][37]

It is a rare lesion

Patients of all age groups may develop peripheral odontogenic fibroma. Peripheral odontogenic fibroma commonly affects individuals ranged from 5 to 65 years of age.^[38][39][40]

Peripheral odontogenic fibromas affects men and women equally.

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There are no established risk factors for fibroma. Moreover the risk factors varies with the individual types of fibromas.

• Frequent milk and soybean consumption^[1][2][3][4]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Maneesha Nandimandalam, M.B.B.S.[2], Simrat Sarai, M.D. [3]

According to the United States Preventive Services Task Force, screening for fibroma is not recommended among the general population.

According to the United States Preventive Services Task Force, screening for fibroma is not recommended among the general population.^[1]

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Oral fibroma must be differentiated from squamous papilloma, giant cell fibroma, neurofibroma, peripheral giant cell granuloma, mucocele, and benign and malignant salivary gland tumors. Non-ossifying fibroma must be differentiated from fibrous cortical defect, aneurysmal bone cyst, chondromyxoid fibroma, fibrous dysplasia, desmoplastic fibroma, giant cell tumor of bone, and spindle cell lesions of bone. Ossifying fibroma must be differentiated from ossifying fibroma, fibrous dysplasia, adamantinoma, and osteoid osteoma. Chondromyxoid fibroma must be differentiated from aneurysmal bone cyst (ABC), giant cell tumor of bone (GCT), non-ossifying fibroma, chondroblastoma, chondrosarcoma, and phosphaturic mesenchymal tumor. Desmoplastic fibroma must be differentiated from giant cell tumor of bone (GCT), non- ossifying fibroma (NOF), fibrous dysplasia, low grade fibrosarcoma, unicameral bone cyst, chondromyxoid fibroma, periosteal desmoids, eosinophilic granuloma, low-grade intraosseous osteosarcoma, adamantinoma, and distant metastasis.

Type of Fibroma	Differential Diagnosis
Ovarian fibroma	Large pedunculated subserosal uterine leiomyoma Thecoma Leiomyoma Fibrosarcoma Metastatic metaplastic carcinoma Endometriosis with extensive fibrosis.
Non-ossifying fibroma	Fibrous cortical defect Aneurysmal bone cyst Chondromyxoid fibroma Fibrous dysplasia Desmoplastic fibroma Giant cell tumor of bone Spindle cell lesions of bone
Ossifying Fibroma	Fibrous dysplasia Adamantinoma Osteoid osteoma
Chondromyxoid Fibroma	Aneurysmal bone cyst (ABC) Giant cell tumor of bone (GCT) Non ossifying fibroma Chondroblastoma Chondrosarcoma Phosphaturic mesenchymal tumor
Desmoplastic Fibroma	Giant cell tumor of bone (GCT) Non ossifying fibroma (NOF) Fibrous dysplasia Low grade fibrosarcoma Unicameral bone cyst Chondromyxoid fibroma Periosteal desmoids Eosinophilic granuloma Low-grade intraosseous osteosarcoma Adamantinoma Distant metastasis
Pleural Fibroma	Considerations for extremely well defined lesions include: Pleural lipoma Pleural fibrosarcoma Intercostal nerve neurilemoma (schwannoma) If not extremely well defined, broader considerations include: Organised inflammation Peripheral bronchogenic carcinoma Solitary pleural metastasis Also consider the differential for a single pleural mass which includes the following: Pleural tumors Solitary fibrous tumour of the pleura (pleural fibroma) Mesothelioma Localised mediastinal malignant mesothelioma Metastatic pleural disease, particularly from adenocarcinomas Pleural lymphoma Invasive thymoma Lipoma Pleural effusion Empyema Haemothorax Ewing sarcoma of chest wall, Askin tumor Intercostal nerve neurilemmoma Splenosis Tuberculosis
Renal Medullary Fibroma	Renal myxoma
Cemento-ossifying Fibroma	Fibrous dysplasia Ameloblastic fibro odontoma Odontoma Calcifying epithelial odontogenic tumour (Pindborg tumour) Odontogenic cyst Calcifying odontogenic cyst (Gorlin cyst) Osteochondroma Osteosarcoma Chondrosarcoma
Desmoplastic fibroblastoma (Collagenous fibroma)	Fibromatosis Elastofibroma Low-grade fibromyxoid sarcoma.
Ameloblastic Fibroma	Ameloblastoma
Giant cell fibroma	Squamous Papilloma Irritation fibroma Pyogenic granuloma Peripheral giant cell granuloma.
Oral Fibroma	Squamous Papilloma Giant cell fibroma Neurofibroma Peripheral giant cell granuloma Mucocele Benign and malignant salivary gland tumors
Uterine Fibroma	Uterine leiomyosarcoma Uterine smooth muscle tumors of uncertain malignant potential Uterine lipoleiomyoma Ovarian masses Focal myometrial contraction (Braxton Hicks contraction): especially if seen during pregnancy Focal adenomyosis
Peripheral odontogenic fibroma	Inflammatory gingival hyperplasia Peripheral cemento-ossifying fibroma Peripheral giant cell granuloma
Elastofibroma	Spindle cell lipoma Nuchal-type fibroma Fibromatosis colli

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Common complications of chondromyxoid, ossifying and non-ossifying fibroma include pathological fractures. Depending on the type of the fibroma, the prognosis may vary. However, the prognosis is generally regarded as excellent for nonossifying fibroma. Ossifying fibromas tend to regress over time. Ossifying fibroma is noninvasive tumor. It will recur if it is excised before skeletal maturity. Excision after skeletal maturity is usually successful. Oral fibromas are benign tumors. Recurrence of oral fibromas is possible, however, if the offending irritant persists. Desmoplastic fibromas are benign and locally aggressive tumors. Desmoplastic fibroma is a rare benign intraosseous tumor neoplasm. Desmoplastic fibroma has a recurrence rate of approximately 37% to 72%. The average rate of recurrence after curettage has been reported to be approximately 55%.

• Clinically, cemento-ossifying fibroma manifest as a slow-growing intrabony mass that is normally well delimited and asymptomatic, although over time the lesion may become large enough to cause facial deformation. Cemento-ossifying fibroma is a benign fibro-osseous maxillary tumor. It is a slow-growing lesion. Approximately one-half of all cases are asymptomatic, the growth of the tumor over time may lead to facial asymmetry, with the appearance of a mass causing facial discomfort or mandibular expansion, and the possible displacement of dental roots. Juvenile aggressive cemento-ossifying fibroma presents in children and is clinically more aggressive and pathologically more vascular.^[1]

• Central cemeto-ossifying fibromas are a distinct form of benign fibro-osseous lesions of the maxilla and mandible. Central cemento-ossifying fibromas are asymptomatic if they are not expanded. Therefore, they are generally not diagnosed until the tumor has had time to produce calcifications. Central cemento-ossifying fibromas are typically well-circumscribed, they maintain a round shape, expand the surrounding cortical bone without cortical expansion, and may cause tooth divergence. The expanded tumors may involve the nasal septum, orbital floor, and infraorbital foramen. At the time of diagnosis, maxillary central cemento-ossifying fibromas are large; indicating the ability of the tumor to expand freely within the maxillary sinus.^{[2][3][4][5][6]}

• Chondromyxoid fibroma (CMF) is a rare, slow-growing, benign bone tumor of chondroblastic derivation. Approximately 70% of patients with chondromyxoid fibroma have symptoms at the time of diagnosis; the remaining lesions are found incidentally. Chondromyxoid fibroma (CMF) represents less than 1% of all benign bone neoplasms. It is a slow-growing, locally destructive tumor.^[7] Pain is the most common symptom and may be present for years. While typically mild, the pain may become severe with time, and night symptoms may be present. Patients may also report stiffness and swelling. As a consequence of slow growth of the tumor, pathologic fractures have been rarely reported. Chondromyxoid fibroma is an unusual benign tumor of cartilaginous tissues.^{[8][9][10][11][12]}

• A history of chronic irritation to the area or trauma followed by the development of a sessile, firm mass is characteristic of oral fibroma. The majority of fibromas represent reactive focal fibrous hyperplasia due to local irritation or trauma. The fibroma may occur in any area, although the areas most frequently affected include the areas most easily traumatized, such as the tongue, buccal mucosa, and labial mucosa. They are benign lesions and they do not have malignant potential and recurrence is mostly as a result of failure to eliminate the irritation. Oral fibroma generally presents as a painless, sessile, ovoid or round, broad based growth. Oral fibromas develop over weeks or months to reach a maximum size which is approximately 1 cm in diameter, but can sometimes be larger.^{[13][14][15][16]}

• Desmoplastic fibroma (DF) is an extremely rare benign intraosseous tumor with locally aggressive and infiltrative characteristics. The clinical presentation of desmoplastic fibroma is nonspecific and usually presents as pain over the affected area and occasionally as a palpable mass, although pathologic fracture has been described previously as a common reason for seeking treatment. Desmoplastic fibroma has also been presented as an incidental finding. The most common sites of involvement are the mandible and the metaphysis of long bones. Biologically and histologically, desmoplastic fibroma mimics extra-abdominal desmoid tumor of soft tissue. Morphologically a distinction between desmoplastic fibroma and aggressive fibromatosis (desmoid tumor) is not possible.^[17][18][19]

• Nonossifying fibroma (NOF) is a common type of benign fibrous lesion that occurs in the metaphysis of the long bones of the lower extremities. While the NOF occurs with relative frequency in the long bones, NOF of the mandible and other areas of the skeleton are rare. The majority of NOFs are asymptomatic; however, those that are particularly large may cause chronic pain and/or pathologic fracture in the long bones. Diagnosis of NOF in the long bones is usually based upon the characteristic clinical and radiographic appearance. Typically the NOF appears as an asymptomatic multiloculated lesion often identified incidentally during radiographic evaluation indicated for another reason. Mandibular lesions of the NOF may be asymptomatic or may present with expansion. Non-ossifying fibromas are typically self-limiting and spontaneous resolution at skeletal maturity is usually seen. This spontaneous regression, usually starting at the end of adolescence, has been observed to occur over periods of 29–52 months. Recurrence is rare. The clinical behavior of mandibular NOF appears to be that of a benign lesion with no reports of recurrence, as seen in the long bones.^{[20][21][22][23]}

• Adnexal / ovarian torsion^[24][25][26]

• Pathological fracture(s)
• Limb bowing

• Pathological fractures

• Pathological fractures

• Rarely invasion of adjacent venous channels leading to intravenous leiomyomatosis ^{[27][28][29][30][31]}
• Rarely (0.1-0.5%), they undergo malignant degeneration into leiomyosarcomas
• In extremely rare instances, lesions capable of metastasizing without malignant transformation: benign metastasizing leiomyoma
• Fibroids may undergo torsion, leading to acute pelvic pain
• Hemoperitoneum
• Hypovolemic shock from massive haemorrhage

• Generally, the prognosis for nonossifying fibroma is excellent. They usually fill in during adolescence. The risk of recurrence is usually lower than for other benign tumors.^[32]

• Oral fibromas are benign tumors. Recurrence of oral fibromas is possible, however, if the offending irritant persists.

• Ovarian fibromas are almost always benign.

• Ossifying fibromas tend to regress over time. For locally aggressive lesions, surgical resection is often curative although recurrence has been reported. Ossifying fibroma is noninvasive tumor. It will recur if it is excised before skeletal maturity. Excision after skeletal maturity is usually successful.^[33][34]

• The majority of pleural fibromas tend to be benign and slow growing. Approximately 78% to 88% of SFT’s(solitary fibrous tumors) are benign and 12% to 22% are malignant. In approximately 10 to 25 percent of cases recurrence of the tumor can occur. Late relapse, even for benign tumors, is common.
• Approximately 63% of patients with malignant pleural fibromas will have a recurrence of their tumor, of which more than half will succumb to disease progression within 2 years.
• Among tumors classified as malignant, approximately 10 to 40 percent of those destined to metastasize will do so after five years, and they may recur up to 20 years after initial presentation . Prolonged survival after pleural fibroma recurrence is possible, particularly for those who are amenable to re-resection. Patients with multiple synchronous metastases that are not amenable to surgical intervention, usually have a poor prognosis.
• Recurrence in pleural fibromas may be due to following causes:
• Incomplete resection
• Tumor seeding within the pleura, peritoneum or meninges, or distant hematogenous spread.
• The most common sites of distant metastasis in SFT at all sites are lung, liver, bone, and brain

• Chondromyxoid-fibroma are benign lesions and malignant degeneration is rare. Chondromyxoid-fibromas have a high recurrence rate of approximately 25%.

• Recurrence following complete excision of cemento-ossifying fibroma is generally considered to be uncommon. However, in some series, it has been reported to be approximately 16%.

• Desmoplastic fibromas are benign and locally aggressive tumors. Desmoplastic fibroma is a rare benign intraosseous tumor neoplasm. It is usually a localized lesion with propensity for cortical bone perforation and recurrence. They are considered to be a bony counterpart of soft tissue desmoid tumors and are histologically identical. ^[35] Desmoplastic fibroma has a recurrence rate of approximately 37% to 72%. The average rate of recurrence after curettage has been reported to be approximately 55%.^[17]

• Sclerotic fibroma is an uncommon benign fibrous neoplasm and may be solitary or multifocal.

• About 1 out of 1000 lesions are or become malignant, typically as a leiomyosarcoma on histology. A sign that a lesion may be malignant is growth after menopause. There are a number of rare conditions in which fibroids metastasize. They still grow in a benign fashion, but can be dangerous depending on their location.

• Recurrence is rare

• Giant cell fibroma is a benign non-neoplastic lesion. Recurrence is rare.

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