Pathology of nasal polyp Jump to: navigation, search

From Otolaryngology Online


Macroscopically polyp appears to arise like a pedicled tissue from the nasal mucosa. Histopathology of these nasal polypi are rather diverse ranging from simple inflammatory polyp to benign / malignant neoplasm. Polyp due to chronic rhinosinusitis can be defined as non granulomatous inflammatory tissue projection arising from the nasal mucosa.

Histology of normal sinonasal mucosa:

For sake of convenience components of normal sinonasal mucosa can be categorized under two heads;

1. Structural components

2. Non structural components

Structural components – Include epithelium, basement membrane and submucosal tissue

Non-structural components – Include resident and Non resident cells of lymphoid and myeloid lineage.

Epithelium & Basement membrane:

The anterior 2 cms of the nasal cavity is lined by skin comprising of keratinized stratified squamous epithelium. It also contains fibrocollagenous dermis and adnexal glands. The rest of the nasal cavity is lined by respiratory type of epithelium which develops from ectoderm. This mucous membrane is also known as Schneiderian membrane.

The Schneiderian membrane is composed of four cell types:

1. Ciliated columnar / cuboidal epithelial cells

2. Interspaced between these cells are goblet cells

3. Non ciliated columnar cells with microvilli

4. Basal cells

The ratio of columnar to goblet cells is roughly 5:1. The normal nasal epithelium may show metaplastic changes i.e. presence of cuboidal / metaplastic squamous epithelium due to constant drying effects of inspired air. Metaplastic changes are commonly seen at the head of inferior turbinate. The columnar epithelium contains tight junctions and they rest on the basement membrane.

The basement membrane contains collagen fibres of types (I, III, IV, V, VI and VII). Other constituents of basement membrane are:

1. Heparan sulfate proteoglycan

2. Laminin

3. Nidogen

The basement membrane is rather thin and delicate in the whole of the nasalcavity. It is usually thick over the inferior turbinate area.

In comparison the lining mucosa of the paranasal sinuses are rather thin and less specialized in nature. This difference could be attributed to their different embryological origin and functional differences.

The superior turbinate, superior portion of nasal septum, roof of the nasal cavity, and superior and medial portions of the middle turbinate are lined by olfactory epithelium. The olfactory epithelium is also pseudostratified ciliated columnar epithelium containing bipolar olfactory cells, microvillar cells and supporting sustentacular cells. Due to increasing age / infections the olfactory epithelium may be replaced in patches by normal nasal mucous membrane.


This lies under the basement membrane overlying the cartilage / bony frame work of the nasal cavity. It is composed of loose fibrovascular connective tissue, numerous seromucinous and minor salivary glands. It also contains blood vessels, nerves, myeloid and lymphoid cells. The blood vessels include extensive arterial and venous anastomosis. These blood vessels communicate with venous erectile tissue. This erectile tissue is more prominent over the turbinates.

Non structural components:

Lymphoid tissue in the nasal mucosa comprises of:

1. single lymphocytes scattered among the epithelial cells and lamina propria

2. NALT – Nasal associated lymphoid tissue resembling payer's patches of the gut. These are not encapsulated.

NALT is not well formed like Payer's patches of the gut. They become enlarged and pronounced during nasal infections.

The lymphoid cells include:

1. T cells

2. B cells

3. Plasma cells

4. Natural killer cells

Conditions causing nasal polypi include:

1. Chronic rhinosinusitis

2. Samter's triad – This include bronchial asthma, aspirin sensitivity and nasal polyposis

3. Eosinophilic mucous chronic rhinosinusitis (including AFRS)

4. Cystic fibrosis

5. Young's syndrome

6. Churg – Strauss disease

Macroscopic features of nasal polypi:

1. Pale smooth shining and oedematous

2. Soft in consistency when compared to surrounding nasal mucosa

3. Long standing nasal polypi can be firm and white due to metaplasia of lining mucosa and presence of extensive fibrosis

Polypidue to chronic rhinosinusitis does not show surface mucosal ulceration.Presence of surface ulceration macroscopically in polyp tissue should arise suspicion of other pathologies. Presence of thick dark tenaceous secretions along with nasal polypi is caused due to Eosinophilicc mucous chronic rhinosinusitis / AFRS etc:

Microscopic changes:

Microscopic changes seen in polypoid tissue are:

1. Structural changes involving lining epithelium, submucosa and rarely underlying bone

2. Presence of inflammatory exudate

Typicalnasal polyp is lined by ciliated columnar epithelium. Their basement membrane is of varying thickness. The stroma contains lymphocytes.

Histological classification of nasal polypi:

1. Oedematous / allergic nasal polypi

2. Chronic inflammatory nasal polypi

3. Seromucinous / glandular polypi

Oedematous / allergic nasal polypi:

Is the commonest variety. This type is seen inpatients with allergy. The association between nasal allergy and polyposis still remains controversial. These polypi are lined by ciliated columnar epithelium with ulceration, mucositis, epithelial hyperplasia, squamous metaplasia. The basement membrane is thickened and the submucosa is oedematous. Mucous retention cysts may also be seen. Inflammatory cell infiltrate include eosinophils, plasma cells and lymphocytes. Polypi in patients with cystic fibrosis have thin basement membrane with less stromal eosinophilia and predominantly neutrophilic infiltrations. Hence cystic fibrosis polypi are termed as neutrophilic polyp. Mucous secretions in patients with cystic fibrosis are thick and densly eosinophilic in nature.

Chronic inflammatory polyp:

This is also known as fibroinflammatory polyp. Thistype of polypi are less common. This type of polypi may be caused when oedematous polypi are traumatized. Thee stroma may undergo secondary inflammatory change causing myofibroblastic proliferation. These polypi may mimic soft tissue neoplasm. The surface epithelium shows squamous metaplasia which is a manifestion of chronicity of the disease. The submucosa characteristically show fibrosis. This is a classic feature ofthis type of polyp.

Seomucinous polypi:

Hyperplasia of seromucinous glands are rare. These are considered to be true neoplasm.

Underlying bone shows remodelling. This is all the more true in long standing disorders.