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Nasal Cavity and Paranasal Sinuses 2 Chapter 2 Nasal Cavity and Paranasal Sinuses 2 A. Cardesa · L. Alos · A. Franchi Contents 2.1 Introduction . 40 2.9.1.1 Squamous Cell Papilloma . 46 2.1.1 Embryology . 40 2.9.1.2 Exophytic Papilloma . 46 2.1.2 Anatomy . 40 2.9.1.3 Inverted Papilloma . 46 2.1.3 Histology . 40 2.9.1.4 Oncocytic Papilloma . 47 2.9.2 Salivary-Type Adenomas . 48 2.2. Acute and Chronic Rhinosinusitis . 40 2.9.3 Pituitary Adenomas . 48 2.2.1 Viral Infections (Common Cold) . 40 2.2.2 Bacterial Infections . 40 2.10 Benign Sinonasal Soft Tissue Neoplasms . 48 2.2.3 Allergic Rhinitis . 40 2.10.1 Haemangiomas . 48 2.2.4 Atrophic Rhinitis . 41 2.10.2 Haemangiopericytoma . 48 2.2.5 Hypertrophic Rhinitis . 41 2.10.3 Solitary Fibrous Tumour . 48 2.2.6 Non-Suppurative Chronic Sinusitis . 41 2.10.4 Desmoid Fibromatosis . 49 2.10.5 Fibrous Histiocytoma . 49 2.3 Sinonasal Polyps . 41 2.10.6 Leiomyoma . 49 2.3.1 Allergic Polyposis . 41 2.10.7 Schwannoma and Neurofi broma . 49 2.3.2 Polyposis in Mucoviscidosis . 41 2.10.8 Meningioma . 50 2.3.3 Polyposis in Immotile Cilia Syndrome 2.10.9 Paraganglioma . 50 and in Kartagener’s Syndrome . 41 2.10.10 Juvenile Angiofi broma . 50 2.3.4 Antrochoanal Polyps . 41 2.11 Malignant Sinonasal Tumours . 50 2.4 Sinonasal Hamartomatous 2.11.1 Keratinising Squamous Cell Carcinoma . 51 and Teratoid Lesions . 42 2.11.2 Cylindrical Cell Carcinoma . 52 2.4.1 Hamartomas . 42 2.11.3 Sinonasal Undiff erentiated Carcinoma . 53 2.4.2 Teratoid Lesions . 42 2.11.4 Small Cell (Neuroendocrine) Carcinoma . 54 2.5 Pseudotumours . 43 2.11.5 Primary Sinonasal Nasopharyngeal-Type 2.5.1 Mucocele . 43 Undiff erentiated Carcinoma . 54 2.5.2 Organising Haematoma . 43 2.11.6 Malignant Melanoma . 55 2.5.3 Amyloidosis . 43 2.11.7 Olfactory Neuroblastoma . 57 2.5.4 Myospherulosis . 43 2.11.8 Primitive Neuroectodermal Tumour . 58 2.5.5 Eosinophilic Angiocentric Fibrosis . 43 2.11.9 High-Grade Sinonasal Adenocarcinomas . 58 2.5.6 Heterotopic Brain Tissue . 43 2.11.9.1 Intestinal-Type Adenocarcinoma . 58 2.11.9.2 Salivary-Type High-Grade Adenocarcinoma . 60 2.6 Fungal Diseases . 44 2.11.10 Low-Grade Sinonasal Adenocarcinomas . 60 2.6.1 Aspergillosis . 44 2.11.10.1 Non-Salivary-Type 2.6.2 Mucormycosis . 44 Low-Grade Adenocarcinomas . 60 2.6.3 Rhinosporidiosis . 44 2.11.10.2 Salivary-Type 2.7 HIV-Related Infections . 44 Low-Grade Adenocarcinomas . 61 2.11.11 Sinonasal Malignant Lymphomas . 61 2.8 Mid-Facial Necrotising Granulomatous Lesions . 45 2.11.12 Extramedullary Plasmacytoma . 62 2.8.1 Wegener’s Granulomatosis . 45 2.11.13 Fibrosarcoma . 62 2.8.2 Lepromatous Leprosy . 45 2.11.14 Malignant Fibrous Histiocytoma . 63 2.8.3 Tuberculosis . 45 2.11.15 Leiomyosarcoma . 63 2.8.4 Sarcoidosis . 45 2.11.16 Rhabdomyosarcoma . 63 2.8.5 Rhinoscleroma . 45 2.11.17 Malignant Peripheral Nerve Sheath Tumour . 63 2.8.6 Leishmaniasis . 45 2.11.18 Teratocarcinosarcoma . 63 2.8.7 Cocaine Abuse . 46 2.8.8 Local Steroid Injections . 46 References . 64 2.9 Benign Epithelial Neoplasms . 46 2.9.1 Sinonasal Papillomas . 46 40 A. Cardesa · L. Alos · A. Franchi 2.1 Introduction paranasal sinuses, with the exception of the roof [261]. Numerous goblet cells are interspersed in the respira- tory-type epithelium. The lamina propria contains sev- 2 2.1.1 Embryology eral seromucous glands, lymphocytes, monocytes, and a well-developed vascular network, particularly evident The midface, or area between the upper lip and forehead, in the inferior and middle turbinate. The olfactory epi- develops at between 4 and 8 weeks’ gestation [219]. The thelium is predominantly made of columnar non-cili- frontal prominence forms during the 4th postovulatory ated sustentacular cells, with scattered bipolar sensory week and gives rise to the superior and middle portions neurons and basal cells. of the face. The maxillary and nasal swellings form be- neath the frontal prominence. At the end of the 4th week surface thickening of the nasal swellings forms the nasal 2.2 Acute and Chronic Rhinosinusitis placodes, which are of ectodermal origin and give rise to the epithelial lining of the nasal cavity and paranasal sinuses. The placodes invaginate, producing the nasal 2.2.1 Viral Infections (Common Cold) pits that become the anterior choanae (nostrils) and, less superficially, the primitive posterior choanae. The Infectious rhinitis is typically viral and is often referred medial nasal and frontal processes give rise to the nasal to as the “common cold”. It is more common in children septum, frontal bones, nasal bones, ethmoid sinus com- than in adults, and the most frequently identified agents plexes and upper incisors. The lateral nasal and maxil- are rhinovirus, myxovirus, coronavirus and adenovirus lary processes fuse to form the philtrum and columella. [67, 271]. Swelling of the mucosa may cause obstruction The cartilaginous nasal capsule forms deep to the nasal of a sinus ostium, with subsequent secondary bacterial and frontal bones from the chondrocranium (skull base) infection (acute bacterial sinusitis). The histologic find- during the 7th and 8th postovulatory weeks. The para- ings include marked oedema and a non-specific mixed nasal sinuses develop from the lateral nasal walls at the inflammatory infiltrate of the lamina propria. 6th foetal week, and their growth continues after birth, throughout childhood and adolescence. 2.2.2 Bacterial Infections 2.1.2 Anatomy Bacterial rhinosinusitis usually follows a viral infection or allergic rhinitis, and the most commonly involved The nasal cavities are separated by the nasal septum, agents are Streptococcus pneumoniae, Haemophilus and limited by a roof, which is formed by the cribriform influenzae and Moraxella catarrhalis [11, 34]. A dense plate of the ethmoid, and a floor, which is formed by the inflammatory infiltrate mainly made of neutrophils oc- hard palate [261]. The lateral walls have three turbinates cupies the lamina propria. Acute bacterial rhinosinusitis or conchae, and three horizontal spaces, or meatus, on usually resolves with antibiotic therapy. Complications each side. The nasolacrimal duct opens in the inferior are rare and include contiguous infectious involvement meatus, whereas the middle meatus receives drainage of the orbit or central nervous system. from the frontal, anterior ethmoid and maxillary sinus- es. Below the superior turbinate is the sphenoethmoid recess, with the openings of the sphenoid and posterior 2.2.3 Allergic Rhinitis ethmoid sinuses. Each nasal cavity communicates pos- teriorly with the nasopharynx through the choanae. Allergic rhinitis (hay fever) is part of an inherited syn- The paranasal sinuses are a group of cavities within the drome, which may also manifest as atopic eczema and corresponding craniofacial bones (maxilla, sphenoid, asthma. In allergic rhinitis, airborne particles, such as ethmoid and frontal) that communicate with the nasal grass pollens, moulds and animal allergens, are depos- cavities through an ostium. ited on the nasal mucosa giving rise to acute and chron- ic reactions. Allergens combine with the IgE antibod- ies produced by the plasma cells of the nasal mucosa, 2.1.3 Histology which are avidly bound to the Fc-epsilon receptors on mast cells. This triggers degranulation of mast cells and The nasal vestibule and skin share a similar histology. releases the inflammatory mediators of the type I hyper- At the level of the limen nasi, the keratinising squamous sensitivity reaction, causing rhinorrhoea and nasal ob- epithelium gradually changes first to cuboidal or colum- struction. Microscopically, the nasal mucosa shows nu- nar epithelium, and then to ciliated respiratory-type ep- merous eosinophils, abundant plasma and in some cases ithelium, which lines most of the nasal cavity and all the an increased number of mast cells. There is goblet cell Nasal Cavity and Paranasal Sinuses Chapter 2 41 hyperplasia of the respiratory epithelium and the base- sinophilic proteinaceous fluid and infiltrates of in- ment membrane, which is destroyed in the acute phase, flammatory cells [115]. They are covered by respira- appears considerably thickened in the chronic phase. tory epithelium with variable ulceration, goblet cell hyperplasia, squamous metaplasia and thickening of the basement membranes. Seromucous glands and 2.2.4 Atrophic Rhinitis mucin-containing cysts may also occur. They arise most frequently in the ethmoidal region and the upper Atrophic rhinitis is a chronic inflammation of the nasal part of the nasal cavity. Allergic polyps usually exhibit mucosa of unknown aetiology characterised by progres- heavy infiltration by eosinophils (Fig. 2.1a), marked sive nasal mucosal atrophy and by a thick, dense secre- thickening of the basement membranes and goblet tion, with a foetid smell and crusting [178]. Multiple cell hyperplasia. Most sinonasal polyps are of allergic factors may be involved in the pathogenesis, including origin. Epithelial dysplasia is present in a few cases. chronic bacterial infections and nutritional deficiencies. Granulomas may be present in polyps treated with Its incidence has markedly decreased in the last centu- intranasal injection, application of steroids or other ry, and nowadays most cases are secondary to trauma, oily medications. Atypical fibroblasts with abundant surgery, granulomatous diseases, infection and radia- cytoplasm, poorly defined cell borders and large pleo- tion exposure [178]. Histologically, there is non-specific morphic nuclei are present in a small proportion of chronic inflammatory infiltrate, squamous metaplasia cases [183]. These atypical cells occur individually of the surface epithelium and of glandular excretory and are more frequently found close to blood vessels ducts, and atrophy of mucoserous glands [1, 69]. (Fig. 2.1b) or near the epithelial surface. Such stromal atypia is a reactive phenomenon and it should not be confused with sarcoma.
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