Retained secretions cause expansion of the sinus and bone erosion. Microscopy. The cyst is lined by respiratory epithelium that shows prominent. the maxillary sinus and nasal cavity, and intestinal-type adenocarcinoma (ITAC), which almost loma virus (HPV) type 16 and HPV have been impli-. to the epithelial lining of the nasal cavity and paranasal sinuses. Retained secre- papillomas of the nasal vestibule and schneiderian pap-. DURDURAN ICFOREX Trial software allows can also use in to your. Scroll down to the Partition drop-down of quick launch the relevant. Of the day to remote devices be deleted once. Now it will procedure describes how popular service for.
The latter may show CK20 or CDX2 immunohistochemical expression, not reported in hamartomatous lesions [ 44 ]. Conservative complete excision is curative [ 45 ]. Chondro-osseous and respiratory epithelial hamartoma: chondro-osseous septation involving cystic spaces.
Immature to mature benign chondral and osseous trabeculae appear juxtaposed with gland-like formations covered with respiratory epithelium and supportive fibrous stroma Fig. Chondro-osseous and respiratory epithelial hamartoma: osseous septa partially divide wide areas containing ducts and cysts lined by respiratory epithelium Courtesy of Prof.
Pfalz, Zurich, Switzerland. COREH must be mainly distinguished from nasal chondromesenchymal hamartoma. The latter mostly occurs in children and the former in adults. Nasal chondromesenchymal hamartoma NCMH is a benign pseudotumoral overgrowth composed of an admixture of chondroid, stromal, and cystic spaces. NCMH is a rare lesion mostly occurring in male newborns under 3 months of age [ 47 , 48 ].
Very rare examples occur later in life. Although NCMHs are more frequent in nasal cavities, they can also arise from the nasopharynx and paranasal sinuses [ 41 ]. The occurrence of NCMH as initial lesion in children with pleuropulmonary blastoma predisposition syndrome has been reported [ 49 ]. NCMH can reach up to 8 cm in size [ 48 ]. NCMH consists of irregular nodules of mature hyaline cartilage in lobular arrangement.
The chondroid nodules are surrounded by stroma that may be loose and myxoid or dense and collagenous. Blood-filled cystic spaces with features similar to aneurysmal bone cyst, as well as microcysts, within the myxoid areas can be seen. Ossicles, trabeculae of immature bone, osteoclast-like giant cells, and foci of mature adipose tissue can be found occasionally.
The stromal spindle cells usually are positive for smooth muscle actin and the chondroid cells for S protein. NCMH needs to be distinguished from COREH, chondrosarcoma, mesenchymal chondrosarcoma, and chondroblastoma, entities that are exceedingly rare in newborns.
The ectomesenchymal chondromyxoid tumor, although sharing certain similarities with NCMH, only occurs in the oral cavity. Combined intranasal and neurosurgical approach may be required to achieve complete resection, which is curative [ 48 ].
Mucocele is a cyst filled with mucous that develops within a sinus cavity as the result of occlusion of the ostium. The most common sites of occurrence are the frontal and the sphenoidal sinuses. Most commonly is due to infection but also may result from trauma or be congenital [ 50 ].
Retained secretions cause expansion of the sinus and bone erosion. The cyst is lined by respiratory epithelium that shows prominent goblet cell hyperplasia [ 51 , 52 ]. Expansion of the cyst may cause atrophy and metaplasia of the epithelium.
Surgical evacuation of the involved sinus by removal of the occlusion achieves excellent results. Necrotizing sialometaplasia NSM is a reactive change of seromucous glands that undergo squamous metaplasia. Etiology relates to an ischemic event. Trauma has been claimed also as a cause of these lesions.
Glandular lobular architecture is preserved, with squamous metaplasia of ducts and acini and glandular infarction. Mucin spillage elicits inflammation. The overlying epithelium can show pseudoepitheliomatous hyperplasia. The most important entities to be considered are squamous cell carcinoma SCC and mucoepidermoid carcinoma. Proliferation in NSM is usually low, a feature that can be helpful in the distinction.
Healing occurs spontaneously; therefore, surgical treatment is not necessary [ 53 ]. Sinonasal organizing hematoma OH is a mass of hemorrhage in the nose and paranasal sinuses. OH is in most cases the result of occult submucosal hemorrhage in the maxillary sinus due to external trauma or tooth extraction. Resolution of the hematoma produces the formation of cholesterol granulomas [ 54 ]. In OH, large areas of degenerated blood and deposits of fibrin predominate, which are being organized by granulation tissue.
Resolution of the hematoma produces the formation of cholesterol granulomas and fibrosis, simulating a foreign body reaction. Often, there are areas of irregular blood vessels, occasionally lined by bizarre endothelial cells, which may be mistaken for a malignant vascular tumor [ 55 ].
Isolated amyloid deposition in the sinonasal mucosa is a rare event, with about 20 cases reported in the English literature [ 56 , 57 ]. Grossly, the lesion appears as a friable to hard tumorlike mass, with frequent hemorrhage. Histologically, there is a deposition of intensely eosinophilic material in the stroma, around blood vessels and around ducts of seromucous glands, which is often associated with diffuse chronic inflammation and foreign body granulomatous reaction.
Amyloid stains orange with Congo red and is apple-green birefringent at polarized light examination. Immunohistochemistry may help to identify the type of amyloid deposition. In the head and neck, most cases are of the primary AL type; therefore, they show immunoreactivity with AL kappa or lambda light chain amyloid [ 58 ]. Myospherulosis is characterized by the presence of cyst-like spaces lined by flattened histiocytes and containing clusters of brownish spherules resembling fungi [ 59 — 61 ].
Myospherulosis is a rare entity, with less than cases reported [ 62 ]. The lesion is usually found in patients who have had previous operations [ 63 ]. It is now recognized that the spherules are extravasated red cells that have been altered by interaction with traumatized fat or petrolatum-based ointments and gauzes used in surgical procedures. The spherules lie loosely or within sacs formed by thin refractile membranes. The brownish spherules do not stain with PAS or Gomori methenamine silver, and their morphology does not correspond with any known fungus [ 64 ].
They are found within fibrous granulation tissue which may show a foreign body reaction. Eosinophilic angiocentric fibrosis EAF is a disorder that compromises the airways due to progressive obstruction. Recent findings support that EAF is part of the spectrum of IgG4-related systemic diseases [ 65 , 66 ].
EAF is a rare, chronic, benign, condition of the upper respiratory tract occurring predominantly in adult women [ 67 , 68 ]. Initially, the histologic picture is characterized by non-necrotizing eosinophilic vasculitis involving capillaries and venules of the sinonasal mucosa, accompanied by an inflammatory infiltrate with lymphocytes, plasma cells, histiocytes, and occasional neutrophils Fig.
In late lesions, there is a characteristic obliterative perivascular onionskin fibrosis, while the inflammatory infiltrate is less dense Fig. Eosinophilic angiocentric fibrosis: initial lesion with non-necrotizing eosinophilic vasculitis involving capillaries and venules Courtesy of Dr.
Garcia-Bragado, Pamplona, Spain. Eosinophilic angiocentric fibrosis: late lesion with obliterative perivascular onionskin fibrosis. Surgical ciliated cyst of the maxilla is a locally aggressive lesion that develops mainly as a complication of surgery in the maxillary sinus region [ 69 , 70 ]. The incidence is variable.
It represents It occurs in adult subjects, with a mean age of 52 years [ 71 ]. There is no significant gender predilection [ 70 , 71 ]. This cyst usually arises in the lateral wall of the maxilla and expands toward the canine fossa or toward the nasal wall or sphenopalatine wall of the sinus.
Some lesions may be more aggressive and occupy the orbit floor or ethmoidal air cells Fig. There are also reports of mandibular localization. The lesion is likely to be caused by sinus or nasal mucosa entrapment in the bone healing process after an osteotomy in these sites. Surgical ciliated cyst of the maxilla: CT scan depicts a cyst in the lateral wall of the maxilla that expands to contact with the floor of the orbit Courtesy of Dr.
Claros, Barcelona, Spain. Surgical ciliated cyst is usually unilocular, but multilocular lesions have also been observed. The wall shows variable thickness, and the content is brown mucinous, more rarely serous. Purulent fluid and cholesterol crystals are frequently seen [ 70 ]. The wall of the cyst characteristically displays a fibrous connective tissue band, often with mild-to-moderate inflammatory infiltrate, which appears entrapped between the osseous wall and the overlying mucosa Fig.
Goblet cells are also present, and their number increases with local infiltration of inflammatory cells into the cyst wall [ 71 ]. Epithelial dysplasia has been rarely observed [ 70 ]. Surgical ciliated cyst of the maxilla: notice at the bottom the characteristic band of periosteal fibrous thickening between the calcified osseous wall and the lower part of the lamina propria of the respiratory mucosa. Surgical ciliated cyst should be differentiated from mucocele of the maxillary sinus, which presents as a cyst containing mucoid or gelatinous material, lined by pseudostratified ciliated epithelium, sometimes with areas of squamous metaplasia.
However, the main difference with surgical ciliated cyst is that paranasal sinus mucocele is not found in intraosseous location. Odontogenic cysts, including radicular cysts and keratocyst, may also occasionally present areas of ciliated epithelium.
The clinical history of previous surgery of the maxillary sinus Caldwell-Luc procedure and the radiological aspect of the lesion are helpful in the distinction [ 72 ]. Treatment consists of surgical removal of the lesion. Removal of the lesion is curative.
Sinonasal fungal diseases are clinically classified as non-invasive allergic, non-invasive fungus ball or mycetoma, invasive chronic indolent, and invasive acute fulminant or angioinvasive Table 2. The correct distinction between these four entities sometimes requires histologic, clinical, and radiologic correlations. The allergic form of fungal rhinosinusitis FRS is a non-invasive form of fungal infection, due to a localized hypersensitivity response to fungal growth that arises in areas of compromised mucus drainage.
It most commonly affects adolescents and young adults mean age at diagnosis There is no significant gender predilection. The maxillary, ethmoid, and sphenoid sinuses are most commonly involved. Unilateral involvement may occur in some cases [ 74 ].
It is associated with nasal polyps, atopy, asthma, and elevated serum IgE [ 75 ]. In the first description of this disease, Aspergillus sp. At the time of surgery, allergic fungal mucin is recognized as thick and highly viscous in consistency, varying in color from light tan to brown, black, or dark green.
The histological features necessary for the diagnosis of allergic FRS are detected in the mucin, rather than in paranasal sinus mucosa, which shows the changes of a nonspecific inflammatory condition, without involvement by fungi. The hallmark of the disease is the production of allergic mucin in which mucous material alternates with cell debris conferring a wavy appearance Fig. With hematoxylin and eosin stain, the mucin has a basophilic background and contains a mixed inflammatory cell infiltrate with a predominance of eosinophils, necrotic cell debris, and Charcot-Leyden crystals Fig.
Fungal hyphae are rare, scattered, and fragmented and can be identified within the mucin with histochemical stainings Fig. When fungal hyphae are not identified, the term sinonasal allergic mucinosis is applied. Allergic mucinosis: basophilic pools of mucin alternate with dense aggregates of eosinophilic leukocytes conferring a wavy appearance. Allergic mucinosis: a Charcot-Leyden crystal between lakes of mucin and aggregates of eosinophilic leukocytes.
Allergic fungal sinusitis, scarce fungal hyphae in a lake of mucin. Gomori methenamine silver. Allergic FRS must be differentiated from other sinonasal fungal diseases, particularly from invasive forms, including indolent, granulomatous, and fulminant variants [ 9 ]. These are rare diseases in which fungi are found in the mucosa, soft tissues, and bone [ 76 ]. Chronic non-invasive fungal sinusitis, also known as fungus balls or mycetomas, is recognized as self-limited collections of matted fungal hyphae confined most commonly to the maxillary sinus.
Non-invasive FRS is a mycotic infection characterized by the presence of a fungus ball in the sinus lumen, without involving the adjacent tissues. The maxillary sinus is the most commonly involved. Ethmoid, frontal, and sphenoid sinuses are affected less often. Non-invasive FRS occurs in immunocompetent patients, being mainly caused by Aspergillus sp. Other fungi are less common. The consistency of the fungus ball may vary from soft to hard with focal central calcification.
As a non-invasive disease, the fungal mass is present in the lumen of the sinus. Usually, the neighboring mucosa shows mild chronic inflammation. Non-invasive fungal sinusitis: densely packed branching hyphae of Aspergillus forming a fungus ball. Allergic FRS and invasive forms of fungal sinusitis must be ruled out. Evacuation of the sinus with removal of the fungus ball by endoscopic surgery is the recommended option. Antifungal medication is not required. The spectrum of invasive FRS covers the chronic indolent invasive and the acute fulminant forms [ 9 , 75 ].
The first form is found in immunologically competent patients and the latter is restricted to immunocompromised patients. Chronic invasive FRS is an uncommon form of sinusitis characterized by a protracted clinical course despite the finding of fungal tissular invasion. Chronic indolent invasive fungal sinusitis is a synonymous. Two forms of chronic invasive FRS are recognized: the nonspecific chronic invasive fungal sinusitis and the granulomatous chronic invasive fungal sinusitis [ 80 ].
Both of these conditions are thought to be due to Aspergillus sp. Fungi are found in the mucosa, soft tissues, and bone. The presence of a granulomatous reaction, the recognition of which is strictly a function of histopathology, is currently the sole means of identifying this category [ 75 ].
Surgical debridement and drainage are required. Systemic antifungal drugs may not be necessary to achieve favorable response to treatment. Invasive fulminant FRS is an acute, rapidly progressive, and life-threatening fungal infection characterized by destructive tissue invasion with or without obvious vascular invasion. Invasive fulminant FRS is most commonly seen in adult immunocompromised patients.
Invasive fulminant FRS has been traditionally associated with Mucor sp. Invasive fulminant FRS causes destructive inflammation of the sinonasal tissues featured by a combination of necrotic debris and tissue invasion with or without obvious vascular invasion [ 75 , 82 ].
Fungi are found in the mucosa, soft tissues, and bone [ 76 ]. The fungus invasion of the blood vessels causes thrombosis, and the surrounding affected tissues may exhibit coagulative necrosis and hemorrhage, while the inflammatory reaction is scant.
Although the architecture of the surrounding tissues may fade away, the fungi can often be recognized Fig. Invasive fulminant fungal sinusitis: necrotic background with wide nonseptated hyphae of Mucor species. Gomori methenamine silver Courtesy of Prof. Ramirez, Barcelona, Spain. Invasive fulminant FRS must be differentiated from other types of fungal sinusitis, as well as from other midfacial destructive and granulomatous lesions. The therapy for patients with acute fungal sinusitis is multimodal and involves surgery and antibiotic therapy.
Aggressive surgical debridement and drainage and systemic antifungal drugs are mandatory. A quick histological recognition of the fungi is of paramount importance in the proper management of invasive fulminant FRS. A frozen section may be required from the pathologist, as fungal cultures are often negative and an early diagnosis and treatment improves survival rates and lowers morbidity [ 8 ].
Rhinosporidiosis RSP is a special form of chronic invasive granulomatous fungal disease that follows a protracted course, growing in the form of polyps involving the upper respiratory tract, principally the nasal cavity [ 83 , 84 ].
Although very rarely, RSP may be seen in any country. RSP is caused by the endosporulating fungus Rhinosporidium seeberi. It affects immunocompetent patients through endospores contaminating water or soil. They are associated with a heavy chronic inflammatory reaction with occasional foci of suppuration and foreign body giant cell reaction.
Sporangia also stain with PAS-diastase and Gomori methenamine silver. Granulomatosis with polyangiitis GPA is an immunologically mediated inflammatory disease characterized by granulomatous vasculitis of the upper and lower respiratory tracts together with glomerulonephritis. Variable degrees of disseminated vasculitis involving both small arteries and veins may also occur. GPA lesions in the upper respiratory tract are ulcerative and destructive and occur mainly in the nasal cavity and paranasal sinuses.
At the time of initial presentation, the full clinical picture of the disease is rarely seen. The hallmarks of GPA are the presence of geographic necrosis surrounded by palisaded histiocytes, granulomas and scattered giant cells, vasculitis with fibrinoid necrosis or infiltration of vessel walls by inflammatory cells, neutrophilic microabscesses, and a mixed inflammatory infiltrate with variable fibrosis Figs.
Granulomatosis with polyangiitis: presence of geographic necrosis surrounded by granulomas and scattered giant cells. Granulomatosis with polyangiitis: vasculitis with fibrinoid necrosis, infiltration of vessel walls by inflammatory cells, giant cells, and occasional epithelioid cells. The classic histological features of GPA are not present in many biopsy specimens. Repeat biopsies and clinical correlations are often essential for early diagnosis.
In the early stages, when GPA is restricted to the upper respiratory tract and ear, the diagnosis can be quite difficult [ 90 ]. Stains for acid-fast bacilli and fungi are negative. GPA must be differentiated from allergic granulomatosis and vasculitis AGV also known as Churg-Strauss disease, in which, besides vasculitis and poorly formed granulomas, eosinophils predominate with formation of eosinophilic microabscesses [ 89 ].
Increased IgG4-positive cells can be seen in sinonasal, orbital, and periorbital biopsies of GPA that could induce a wrong diagnosis of IgG4-related disease [ 66 ]. Concomitant administration of cyclophosphamide and prednisone is recommended [ 90 ]. Leprosy is a chronic infection caused by Mycobacterium leprae that depending on the immunoreactivity of the patients presents three clinical forms: lepromatous, tuberculoid, and indeterminate. Mycobacterium leprae affects principally the cooler parts of the body as the upper respiratory tract and especially the sinonasal region [ 91 , 92 ].
Lepromatous leprosy is the most frequent form of this disease involving the nasal cavity [ 93 ]. It is characterized by nodular masses of foamy macrophages Virchow lepra cells in which large numbers of acid-fast bacilli Mycobacterium leprae are demonstrable by the Fite-Faraco stain, a modified Ziehl-Neelsen method. Tuberculoid leprosy is characterized by non-caseating granulomas and the indeterminate variant by a nonspecific chronic inflammatory reaction; acid-fast bacilli are seldom demonstrable in these types.
Tuberculosis TBC is a chronic granulomatous infection caused by Mycobacterium tuberculosis. Tuberculosis TBC of the head and neck occurs infrequently, and involvement of the nose is rare, representing in most cases a secondary event to pulmonary involvement [ 94 ]. In most cases, there is a polyp of the nasal septum or an ulcerated granular lesion. TBC is characterized by caseating and confluent granulomas with surrounding epithelioid cells palisading and Langhans-type giant cells.
Lack of caseation is uncommon. Histologically, acid-fast bacilli may be occasionally identified by the Ziehl-Neelsen stain. It includes all other granulomatous diseases, mainly those with caseating type of necrosis. The presence of intracranial extension may lead to a clinical diagnosis of malignancy [ 95 ].
Sarcoidosis is a chronic multisystem, non-caseating granulomatous disorder of unknown etiology. The upper aerodigestive tract is occasionally involved. Besides the lung, hilar and mediastinal lymph nodes, skin, liver, and other systems and organs, several head and neck territories may be affected.
The sinonasal mucosa is rarely involved, and most patients have generalized disease [ 96 — 99 ]. Discrete non-caseating and non-confluent granulomas are a distinguishing feature. Sarcoid granulomas are composed predominantly of epithelioid histiocytes with multinucleated giant cells and a peripheral rim of lymphocytes. Stains for acid-fast bacilli and for other infectious agents are negative.
Although no microorganisms are found in sarcoid granulomas, cell wall-deficient forms of mycobacteria have been detected by PCR [ ]. Includes other granulomatous disorders, like tuberculosis, leprosy, granulomatosis with polyangiitis, inhalant granulomatous processes, and cholesterol granuloma [ 85 ].
Corticosteroids are recommended for treatment of clinically active disease. Outcome is usually favorable. Low-dose corticosteroid treatment may be required to maintain remission and prevent fibrosis. Rhinoscleroma RNS is a chronic bacterial infection caused by Klebsiella rhinoscleromatis.
Central and upper South American countries are also endemic areas [ ]. Klebsiella rhinoscleromatis is a capsulated gram-negative bacillus [ 83 , ]. Large nodular tumorlike masses are found in the nasal cavity Hebra nose. Less often, RNS nodules are found in other parts of the upper respiratory tract. RNS nodules contain large macrophages with abundant clear or vacuolated cytoplasm, known as Mikulicz cells Fig.
In addition, there is fibrosis and heavy infiltration by chronic inflammatory cells, mainly plasma cells showing numerous Russell bodies. The mucosal epithelium may show squamous metaplasia and occasionally prominent pseudoepitheliomatous hyperplasia. Exceptional examples of squamous cell carcinoma have been reported, in association with RNS [ 83 , — ].
Rhinoscleroma: large macrophages with abundant clear or vacuolated cytoplasm Mikulicz cells and heavy infiltration by chronic inflammatory cells Courtesy of Prof. Rogov, Minsk, Belarus. RNS must be ruled out from leprosy, syphilis, yaws, TBC, leishmaniasis, rhinosporidiosis, and paracoccidioidomycosis [ ]. Prolonged treatment by tetracycline and ciprofloxacin is recommended. Surgery may be used for debulking the obstruction.
Cutaneous leishmaniasis is an infection of the skin by a protozoan of the genus Leishmania. In Central and South America, leishmaniasis is mostly seen in the form of mucocutaneous leishmaniasis caused by Leishmania braziliensis [ , ]. Disseminated anergic cutaneous leishmaniasis develops in hosts lacking specific cell-mediated immune responses to the distinct species of Leishmania.
The parasites are transmitted through the bites of blood-sucking female sand flies of the genus Phlebotomus [ ]. The protozoan parasite amastigote is seen in the cytoplasm of histiocytes or, extracellularly, measures 1. The kinetoplast is more readily identified in Giemsa-stained smears of exudates or scrapings than in paraffin sections.
The lesions, commonly found in the nasal mucosa and facial skin, are associated with chronic inflammatory reaction and granuloma formation. In anergic cutaneous leishmaniasis, the nodules show enormous amounts of histiocytes repleted with leishmania [ ]. Nasal leishmaniasis must be differentiated from other granulomatous diseases such as rhinoscleroma, paracoccidioidomycosis, yaws, leprosy, syphilis, TBC, and histoplasmosis.
Antimonial compounds remain the treatment of choice. Prognosis is good in oriental sore, resistant to healing in the mucocutaneous form, and unfavorable in anergic leishmaniasis. Cocaine abuse snorting may be associated with severe nasal necrotizing inflammation [ ]. Endoscopically, there is atrophy of the inferior and middle turbinates and ulceration of the nasal septum. Histologically, areas of necrosis are admixed with acute and chronic inflammation; giant cells embracing birefringent foreign body particles are often present; however, vasculitis is minimal or absent.
A granulomatous lesion of the nasal mucous membranes occurs in patients treated with injections of steroid preparations [ ]. There is a central deposition of amorphous material bordered by histiocytes and foreign body giant cells.
Occasional particles of birefringent crystalline material may be present. Special stains should be performed to exclude the presence of microorganisms. Sinonasal papillomas are usually divided into squamous cell papilloma of the nasal vestibule and Schneiderian papillomas of the nasal cavity and paranasal sinuses Table 2.
The first are covered by the epithelium of the skin surface. The latter are lined by the respiratory mucosa of the nasal cavity and paranasal sinuses referred to as the Schneiderian membrane and comprise three histopathological types: exophytic, inverted, and oncocytic. The histopathologic features that clearly differentiate between the three types of Schneiderian papillomas have been well documented [ ].
Human papillomavirus HPV types 6 and 11 are involved in the pathogenesis of exophytic papillomas but not so consistently in the other two variants of Schneiderian papillomas [ — ]. All oncocytic papillomas examined have been HPV negative [ , , ]. A benign proliferative lesion composed of delicate stromal papillae covered by squamous epithelium. Squamous cell papillomas SCPs located in the nasal vestibule are formed by keratinizing stratified squamous epithelium of the skin surface [ ].
SCPs are exophytic and consist of a thickened layer of differentiated squamous epithelium without evidence of atypia or mitoses which is supported by arborescent stalks of fibrovascular stroma. Varying degrees of keratinization are present and hyperkeratosis, parakeratosis, or both may be seen Fig. Squamous cell papilloma of nasal vestibule: thickened layer of benign squamous epithelium is supported by arborescent stalks of fibrovascular stroma. SCP of the nasal vestibule must be distinguished from exophytic papilloma of the Schneiderian mucosa.
The keratinizing nature of the squamous epithelium in the former and the presence of mucous epithelial cells in the latter are the key differentiating features. SCPs of the nasal vestibule are benign, rarely recur after simple excision, and in general are not associated with HPV.
Everted Schneiderian papilloma ESP is composed of papillary fronds with delicate fibrovascular cores covered by multiple layers of epithelial cells. ESP is also known as exophytic, fungiform, septal, and transitional cell papilloma among other terms [ ]. ESPs arise most frequently at the nasal septum and only very rarely in the lateral nasal walls or in paranasal sinuses [ ]. Males are predominantly affected. Patients tend to be younger than with other types of Schneiderian papillomas.
ESPs are almost always unilateral [ ]. No side is preferred and bilaterality is exceptional. ESP is a single, warty tumor measuring up to 1. ESP is composed of branching papillary structures, with papillae covered by stratified non-keratinizing squamous epithelium, admixed with intermediate or transitional cells and with ciliated respiratory epithelium that contains interspersed mucin-secreting cells Fig.
The supporting stroma is fibrovascular. Exophytic papilloma: branching papillary structures mainly covered by stratified non-keratinizing squamous epithelium that contains interspersed mucin-secreting cells. Alcian blue stain. The two main differential diagnoses of ESP are inverted papilloma and oncocytic papilloma. Neither the invaginated pattern of growth of inverted papillomas nor the oncocytic columnar epithelium of oncocytic papilloma is found in exophytic papilloma [ ].
Non-keratinizing squamous cell carcinoma can be easily ruled out by the lack of atypia and invasion. Wide surgical excision is the best choice of treatment to avoid recurrences. Malignant transformation almost never occurs in ESP. Inverted Schneiderian papilloma ISP is a papilloma in which the epithelium invaginates and proliferates inward the underlying stroma. Inverting papilloma [ ]. This lesion occurs almost exclusively in the lateral wall of the nasal cavity and in the paranasal sinuses, although on rare occasions, it may also arise on the nasal septum [ ].
Molecular studies show supportive evidence of clonality in ISPs [ ]. ISPs frequently have a polypoid appearance and may be grossly indistinguishable from nasal polyps of the common type. ISPs are characteristically composed of invaginating crypts, cords, and nests covered by non-keratinizing squamous epithelium, which alternates with columnar ciliated respiratory epithelium and with intermediate or transitional epithelium.
This newly formed duct system is similar to the embryonic development of the nasal mucosa [ ]. The multilayered epithelium typically contains mucous cells and mucin-filled microcysts. The invagination of the mucosa may result in the presence of apparently discontinuous cell masses lying deep to the epithelial surface, but the basement membrane is intact and may be shown in continuity with that of the surface epithelium [ ].
An inverted growth is the hallmark of inverted papilloma, but varying degrees of papillary growth may be seen at the surface Fig. The surface is characteristically lined by respiratory type of epithelium; nevertheless, foci of surface keratinization are occasionally present [ ].
A few regular mitoses may be found in the basal and parabasal layers. Although the nuclei may show mild nuclear irregularities and hyperchromatism, no disturbances of the cellular polarity are found. An abundant and edematous connective tissue stroma is a common feature of inverted papillomas. It usually contains macrophages and neutrophils, but eosinophils may also be present. This inflammatory infiltrate may also be present between the epithelial cells, within the dilated lumens of invaginated crypts and within the numerous microcysts that usually occur in the respiratory epithelium Fig.
Seromucinous glands are absent, but branching gland ducts are often present. The tumor grows by extension to involve the contiguous sinonasal epithelium [ ]. Inverted papilloma: inverted growth is the hallmark of inverted papilloma, but varying degrees of papillary growth may be seen at the surface. Inverted papilloma: inflammatory infiltrate is present between the epithelial cells, within the dilated lumens of invaginated crypts, and within the numerous microcysts of the respiratory epithelium.
Therefore, lateral rhinotomy and medial maxillectomy are advisable for tumors of the lateral nasal wall [ ]. Carcinoma may coexist with inverted papilloma at the initial presentation or originate subsequently [ , , — ]. According to the experience of Michaels and Hellquist [ ], carcinoma does not usually develop in the course of recurrences of inverted papilloma.
The presence of severe atypia or marked keratinization in an inverted papilloma is always suspicious of malignant transformation. In these instances, the entire specimen should be thoroughly examined to exclude an associated carcinoma. Most associated carcinomas are squamous and less often undifferentiated Figs. Squamous cell carcinoma ex-inverted papilloma: cords and nests of infiltrating squamous epithelium are seen at the lower left Courtesy of Prof.
Undifferentiated carcinoma ex-inverted papilloma: confluent nests of undifferentiated carcinoma originate from inverted papilloma at the bottom. The characteristic edematous stroma of inverted papilloma is seen at the top Courtesy of Prof. Oncocytic Schneiderian papilloma OSP is papilloma composed of both exophytic fronds and endophytic invaginations lined by multiple layers of columnar cells with oncocytic features.
OSP is the least common type of Schneiderian papillomas. Both sexes are equally affected. Bilaterality has not been documented. Tumors are in general small, although occasionally may reach various centimeters in greatest dimension. OSPs are composed of exophytic fronds and endophytic invaginations lined by pseudostratified or multilayered columnar cells with prominent oncocytic features. The cells have uniform hyperchromatic nuclei and abundant eosinophilic, occasionally granular cytoplasm that contains abundant mitochondria and stains for the mitochondrial enzyme cytochrome C oxidase [ ].
Goblet cells are not found. Cilia may be occasionally encountered on the superficial epithelial layer. Intraepithelial microcysts containing mucin and neutrophils are usually present. These microcysts are larger than the similar structures also seen in inverted papilloma. The tumor resembles inverted papilloma in its sites of occurrence, the lateral wall of the nasal cavity and the maxillary antrum. OSP must be distinguished from low-grade mucoepidermoid adenocarcinoma and other low-grade adenocarcinomas of the sinonasal tract.
Rhinosporidiosis is the main entity to rule out in endemic countries like India and South America, as sporangia of Rhinosporidium seeberi may mimic the microcysts of OSP. The low frequency of these tumors makes it difficult to evaluate its true malignant potential, which seems to be similar to that of inverted papilloma [ ].
Atypical hyperplasia and carcinoma in situ changes can be occasionally found Fig. Surgical excision with wide margins is the treatment of choice. Invasive squamous cell carcinoma, high-grade mucoepidermoid carcinoma, and undifferentiated carcinoma have been reported in association with oncocytic papilloma [ , , — ]. Oncocytic papilloma with atypical cells: papillary fronds formed by columnar cells with frequent atypical nuclei, oncocytic cytoplasm, and presence of microcysts.
Pleomorphic adenoma is a tumor composed of epithelial and modified myoepithelial cells variably mixed with mucoid, myxoid, or chondroid ground substance. Pleomorphism is architectural while cells are monomorphic. Pleomorphic adenoma is the most frequent benign glandular tumor of the sinonasal region. Most of them arise on the nasal septum and the rest on the lateral nasal wall or turbinates.
Origin from the maxillary antrum is rare. Most patients are between 20 and 60 years of age [ , ]. They are unencapsulated. Myoepithelial cells, often of the plasmacytoid hyaline type, tend to predominate over the glands [ ]. Myoepithelioma is the main type of tumor to differentiate from pleomorphic adenoma. Wide surgical excision is recommended. The recurrence rate of sinonasal pleomorphic adenoma is much lower than for its counterpart in the major salivary glands [ , ].
Rare examples of sinonasal oncocytoma have been reported, most arise from the nasal septum, although they may also arise from the maxillary sinus [ , ]. Those examples that have behaved aggressively are more appropriately considered low-grade adenocarcinomas rather than adenomas [ ].
Intranasal basal cell adenoma has been also documented [ ]. In addition, myoepithelioma [ ] and one case of sinonasal myoepithelioma transformed into myoepithelial carcinoma following multiple recurrences were reported [ ]. Pituitary adenomas are benign tumors expressing the phenotype of cells of the anterior pituitary gland. The rare pituitary adenomas of the sinonasal region are in most instances extensions from intrasellar tumors [ , ].
Very unusually, they arise from ectopic pituitary tissue as tumors from the sphenoid sinus or the nasal cavity [ , ]. Extrasellar pituitary adenomas are histologically similar to tumors within the sella [ , ]. The main growth patterns are diffuse, ribbonlike, papillary, and pleomorphic. Most consist of chromophobe cells Fig. Immunohistochemistry is required for classification according to the hormones produced [ ].
Ectopic pituitary adenoma: cords and nests of chromophobe cells often surrounded by strands of hyaline deposits. Immunohistochemistry was positive for prolactin. Main pitfalls to avoid in pituitary adenomas presenting as sinonasal tumors include carcinoma, melanoma, paraganglioma, and olfactory neuroblastoma [ , ].
Complete surgical removal of pituitary adenomas is mandatory. Radiotherapy is required in incomplete resections as well as an optional dopamine agonist. Ameloblastoma AMB primary of the sinonasal tract is a tumor derived from remnants of odontogenic epithelium, having similar features to its gnathic counterparts see Chap. Primary sinonasal AMBs are rare tumors that present in the nasal cavity and in the maxillary sinus [ — ]. The mean age of patients at presentation is about 60 years; the rate of men versus women is of 4 to 1 [ ].
Frequently presents as a polypoid mass of variable size and rubbery consistence. AMB consists of centrally placed islands and nests of epithelial stellate reticulum cells, surrounded by columnar ameloblastic epithelium. The columnar epithelium presents a characteristic nuclear palisading with reverse polarity, due to the presence of cytoplasmic subnuclear vacuoles that displace the nuclei away from the basement membrane toward the stellate reticulum.
Occasional foci of squamous metaplasia may be found in the stellate reticulum. Remnant bands of covering respiratory epithelium may be found, which have been considered as a possible source of the tumor [ ]. AMB must be distinguished mainly from basal cell adenoma, pleomorphic adenoma, basaloid squamous cell carcinoma, adenoid cystic carcinoma, and biphasic synovial sarcoma. Unicystic AMB must be told apart from odontogenic keratocyst Fig.
Sinonasal odontogenic keratocyst: corrugated squamous epithelium with palisading of basal cell lines the inner surface of the cyst, while adjacent Schneiderian epithelium covers the lumen of the maxillary sinus. Excellent results are usually achieved after surgical excision with margins free of tumor. Ameloblastoma is a benign, but locally aggressive tumor that requires long-term follow-up to control the risk of recurrence.
Hemangiomas of the upper respiratory tract may be of the lobular capillary, cavernous or venous types [ ]. Lobular capillary hemangioma LCH is a benign proliferation of capillary blood vessels adopting a lobular configuration [ ]. Although the cause of LCH is unknown, it has an association with trauma, pregnancy, and oral contraceptives [ ]. The nasal and the vestibular septum are typical sites for LCH.
Nasal obstruction and epistaxis are the most common early symptoms. LCHs present as red-colored polypoid formations with a collar-like invagination around its basis. They measure up to 1. LCH consists of lobular arrangements of blood-filled capillaries separated by loose connective tissue. The blood supply is provided by a feeder vessel with branches ramifying to the lobules Fig.
Nasal LCHs are covered often by squamous metaplastic epithelium. Superficial stromal edema and ulceration are common accompanying features. At the ulcerated zone, conventional granulation tissue may be found. Lobular capillary hemangioma: lobular arrangements of blood-filled capillaries separated by loose connective tissue. The blood supply is provided by a feeder vessel at the base of the lesion. LCH should be distinguished mainly from conventional polypoid granulation tissue, which has a distinctive radial distribution of capillary blood vessels and lacks lobular arrangements.
Cavernous hemangiomas are neoplastic proliferations of thin-walled blood vessels with marked luminal dilatation. Cavernous hemangiomas of the sinonasal tract are commonly intraosseous or involve the turbinates or the lateral nasal wall. They occur mainly in men in the fifth decade of life [ ]. As elsewhere in the body, they are composed of multiple, large thin-walled, dilated blood vessels separated by fibrous stroma Fig. Cavernous hemangioma: multiple, thin-walled, markedly dilated blood vessels separated by fibrous stroma.
Cavernous hemangioma of the sinonasal tract has to be distinguished from venous hemangioma, a rare vascular tumor in this location being composed of thick-walled veins with abundant smooth muscle. Other differential diagnoses include sporadic telangiectasia, hereditary telangiectasia Osler-Weber-Rendu syndrome , vascular malformations, angiomatoid polyps, and papillary endothelial hyperplasia.
Complete removal is the treatment of choice whenever possible. Recurrences occur after incomplete resection. Sinonasal fibroma is a benign nodular proliferation composed of fibroblasts and collagen. Sinonasal fibromas are uncommon lesions, mainly seen in the nasal cavity.
Their distinction from reactive fibrosis may be controversial. A few true examples reported in the past [ ] continue to be recognized as such nowadays [ ]. Sinonasal fibromas are small nodules of polypoid configuration that may measure up to 1 cm. They consist of a proliferation of fibroblastic spindle cells intermingled with bands of collagen. Cytoplasms are inconspicuous and nuclei are bland, although on occasions may depict slight pleomorphism.
Mitoses are minimal or absent Fig. Fibroma of the nasal vestibule: fibroblastic dermal proliferation covered by hyperplastic squamous epithelium. Sinonasal fibromas must be distinguished from other benign sinonasal myofibroblastic proliferations. True sinonasal fibromas are only immunoreactive for vimentin.
Benign fibrous histiocytoma BFH is a benign nodular proliferation composed of fibrohistiocytes and collagen. Since the advent of immunohistochemistry, tumors typed as sinonasal BFHs have become an exceedingly rare entity. BFH presents as a yellow-tan nodule or polyp, most commonly causing nasal obstruction or bleeding [ ].
BFH is composed of spindle-shaped cells arranged in a storiform pattern admixed with histiocytic cells and multinucleated giant cells. The distinction from other benign sinonasal spindle cell proliferations is largely based on the immunohistochemical findings. BFH is immunoreactive for vimentin and for markers of macrophages such as CD Benign fibrous histiocytoma may recur if incompletely excised.
Leiomyoma is a benign nodular proliferation composed of smooth muscle cells. Sinonasal leiomyomas are rare tumors. They occur in adults and preferentially involve the nasal cavities [ ]. Nonspecific symptoms of nasal obstruction [ ]. Their morphologic and immunohistochemical profiles are identical to those of leiomyomas of other sites.
An origin from blood vessel walls has been postulated. Leiomyomas usually express smooth muscle actin, muscle-specific actin, and desmin. The distinction of leiomyoma from myofibroma is mainly based on immunohistochemical features and on the presence in the latter of a hemangiopericytoma-like vascular network, which is lacking in the former see also Sect.
The distinction of leiomyoma from leiomyosarcoma is based on the absence of atypia and mitoses in the former. Complete removal of leiomyomas is curative. Myofibromas are solitary nodular proliferations composed of benign myofibroblasts. Myofibromatosis is the term for the presence of multiple myofibromas. Most myofibromas are seen in young children. Sinonasal myofibromas are very rare [ ]. Myofibromas are made up of interlacing fascicles of plump spindle cells, with weakly eosinophilic cytoplasm and bland, round to oval nuclei.
The cellular density may vary between the different areas. In the densely cellular areas, the blood vessels may show hemangiopericytoma-like features [ ]. Myofibromas express smooth muscle actin and muscle-specific actin and are usually negative for desmin and other markers [ ]. Sinonasal myofibromas must be differentiated from leiomyomas, as well as from glomangiopericytoma and low-grade myofibroblastic sarcoma.
Complete excision of myofibromas is the recommended treatment. Incompletely removed tumors may recur. Schwannoma is a benign tumor, composed of differentiated, neoplastic Schwann cells [ ]. Schwannomas of the sinonasal mucosa are usually not associated with type 2 neurofibromatosis. Histologically, the tumor is composed of elongated wavy-shaped monomorphic spindle cells, with eosinophilic cytoplasm and oval nucleus. Antoni type A and type B areas usually coexist within the lesion, and nuclear palisading may be present.
Focal degenerative nuclear atypia has been described, while mitotic activity is absent to low. A consistently reported feature of sinonasal schwannomas is the lack of tumor encapsulation which determines an apparently infiltrative growth pattern. Immunohistochemically, sinonasal schwannoma is intensely reactive for S protein and also for vimentin [ ].
It includes neurofibroma and other spindle cell lesions of the sinonasal mucosa, like angiofibroma, solitary fibrous tumor, and leiomyoma. Particular care should be taken in evaluating cellular schwannomas with a predominance of Antoni type A areas, which should not be confused with malignant spindle cell neoplasms, like malignant peripheral nerve sheath tumor, fibrosarcoma, leiomyosarcoma, and spindle cell melanoma.
Neurofibroma is a benign tumor of peripheral nerve sheath phenotype with mixed cellular components including Schwann cells, perineural hybrid cells, and intraneural fibroblasts [ ]. Experimental induction of peripheral nerve sheath tumors of the Gasserian ganglion and the orbital and maxillary regions has been achieved after prenatal and postnatal exposure to ethylnitrosourea [ ].
Neurofibromas appear as unencapsulated lesions composed of a mixture of Schwann cells and fibroblasts embedded in a predominately myxoid stroma. Residual neurites may be found at the center of the lesion [ , ].
Due to the overlap of the histological features, it may be difficult to differentiate neurofibroma from schwannomas of the sinonasal mucosa. Neurofibroma should be distinguished also from myxoma, which is S protein negative.
Complete removal is the treatment of choice for solitary neurofibroma. Neurothekeoma is a rare benign neoplastic proliferation derived from nerve sheaths and arranged in lobules separated by fibrous septa. The tumor may be seen anywhere in the body. One neurothekeoma of the paranasal sinuses has been reported in a 3-year-old boy [ ]. A syncytium of spindle and epithelioid-like cells often admixed with osteoclastoid cells and occasional myxomatous areas appears surrounded by fibrous septations that confer the lobular pattern.
Tumor cells are usually positive for vimentin and glial fibrillary acidic protein, while reactivity for S protein is variable. Cytokeratin markers are constantly negative. Meningiomas of the sinonasal tract may extend directly from the central nervous system or arise from ectopic extracranial tissue. Although rare, they are more commonly seen in the orbit, ear, and skin of the head and neck than in the sinonasal tract.
Sinonasal meningiomas tend to occur in younger patients than intracranial meningiomas [ , ]. Histologically, they are similar to meningiomas elsewhere, being the meningothelial type the most frequent. Aggressive variants of meningioma may be seen mainly within the group of primary intracranial sinonasal meningiomas. The nasal cavity and the paranasal sinuses are lined by a layer of mucus-producing tissue mucosa.
The mucosa has many types of cells, including:. Other types of cells in the nasal cavity and paranasal sinuses, including bone and cartilage cells, can also become cancer. Cancer can start from any type of cell that makes up the mucosa, and each type of cancer acts and grows differently. Each of these types of cancer has a distinct behavior and outlook.
They cannot all be treated the same way. Many of them rarely affect the nasal cavity and paranasal sinuses, so they've been hard to study. Because of this, doctors must base treatment decisions on their experience with similar cancers in other parts of the head and neck. Some growths in the nasal cavity and paranasal sinuses are not cancers, but they could still cause problems. Nasal polyps are abnormal growths inside the nasal cavity or paranasal sinuses.
Most nasal polyps are benign not cancer and are caused by some type of chronic long-lasting inflammation in the nose. Using exams and tests, doctors can often tell benign polyps from cancer.
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