Theories of nasal polyposis
Duringthe past century several theories have been proposed to explain the etiopathogenesis of nasal polyposis. The fact that so many theories havebeen proposed is the evidence of our poor knowledge of this topic. Majority of these theories are based on tissue oedema, increase in the number of tubulo-alveolar glands, presence of cysts of mucous glands.
Adenoma fibroma theory of Billroth:
Billrothin his studies found a large number of tubular glands in the nasal polypoidal tissue studied. He concluded that these glands were not normally seen in such large numbers in the nasal mucosa. He hence interpreted nasal polyp to be adenomas that began growing under the nasal mucosa pushing the epithelium and nasal glands outwards. However Hopmann disagreed with this hypothesis saying that the glandular tissue found in the tissue samples of nasal polypi studied contained only mucous glands normally found in the nasal mucosa and concluded that nasal polypi could be soft fibromas and used the term fibroma theory to explain this. These two theories are not currently accepted at present.
Necrotizing ethmoiditis theory of Woakes:
Thistheory suggests that ethmoiditis causes periostitis and ostitis of ethmoid bone causing bone necrosis. The necrotic bone initiates mucosal reaction leading on to mucosal oedema and polyp formation. This theory has been flawed from the very begining as no evidence of bone necrosis could be found in the polypoidal tissue studied so far.
Glandular cyst theory:
Evidentlythis theory is based on the presence of cystic glands and mucous filledcysts in the nasal polypoid tissue. The probable cause for the formation of these glandular cysts could be oedema of submucosa causing obstruction to the drainage of mucoid glands present in the nasal mucosa. These mucous cysts expands outwards pushing the nasal mucosa causing the polyp to occur. Taylor in his meticulous study has proved that mucous glandular cysts usually occur after the polyp has formed and hence he believed that glandular cysts could be caused by nasal polyposis and not vice versa.
Mucosal exudate theory of Hayek:
Hayekbeleived that nasal polyp formed due to accumulation of exudate localised deep in the mucosa. This accumulation of exudate causes the mucosa to bulge leading to polyp formation. Nasal mucosal glands and tubuloalveolar glands are also displaced outwards. These glands are hence found in the distal part of the polyp. Theory of cystic dilatation due to obstruction of excretory ducts of nasal glands and blood vessel obstruction:
In chronic inflammation involving nasal mucosa blocks the excretory ducts of nasal tubulo alveolar glands causing the glands to dilate due to pent up secretions within. The blood vessels (capillaries and veins) surrounding these distending glands are also stretched. Stretching of these blood vessels impedes blood circulation and causes tissue oedema due to transudation of fluid. This theory is not valid due to the fact that dilatation of mucous glands occur only after formation of nasal polypoidal tissue. Blockade theory of Jenkins:
This theory is based on the premise that development of nasal polypi is almost always preceded by certain degree of nasal mucosal inflammation. The inflammation could be the result of either infection / allergy. Histologically polyp itself is accumulation of intracellular fluid dammed up in a localized tissue. If this blockage persists polyp develop, if the blockage covers a large area then multiple polypi forms. This theory doesnt explain why nasal polyp prefers certain areas of nasal cavity.
Periphlebitis / perilymphangitis theory of Eggston and Wolff: This theory is based on the premise that recurrent infections of nasal mucosa blocks intercellular fluid transport mechanism in the mucosa. This is always associated with oedema of lamina propria. This theory is based on the demonstration of chronic vascular changes in the nasal mucosa in response to inflammation. Histologically these changes are supposed to be rather diffuse and hence cannot be used to explain the pathogenesis of nasal polypi which can always be localised to certain areas of nasal cavity.
Glandular hyperplasia theory of Krajina:
According to Krajina chronic inflammation of nasal mucosa cause local hyperplasia of nasal mucosal glands. These hyperplastic glands will cause bulging of nasal mucosa. In addition to glandular hyperplasia changes that occur in the blood vessels will cause oedema in the region of the middle meatus. This in turn increases nasal mucosal oedema. Studies have shown that the number of nasal mucosal glands are the same in polypoidal as in the normal tissue.
Epithelial rupture theory:
This is the currently proposed theory. In this theory the initial stage of nasal polyp formation startsof as epithelial rupture possibly due to inflammation and tissue oedema. This is followed by prolapse of lamina propria through the defect. The adjacent epithelium attempts to cover up the defect there byforming a lining for the polypoidal tissue. Ifthe defect in the epithelium is not covered up real fast the prolapsed lamina propria continues to grow and the polyp complete with its stalk develops. After epithelization of the polyp the characteristic new long tubular glands are formed.
Role played by mucous glands:
The glandular elements seen in the nasal polypoidal tissue are nasal glands. Commonly seen glands are degenerated long glands. The entire long duct along with their lateral branches are distended due to filled up secretions. Due to the pent up secretion and distention the secretory epithelium of the nasal gland become cuboidal and flat losing their secretory ability. This is followed by degeneration of the gland.
Role played by cellular infilatrates:
Eosinophilicinfiltration is an important feature in the pathogenesis of chronic rhinosinusitis and nasal polypi. Accumulation of eosinophils in the polyp stroma is basically caused by increased transendothelial migration, increased survival, and increased concentration of interleukin 5.