Theories of nasal polyposis
Dr T Balasubramanian
the past century several theories have been proposed to explain the
etiopathogenesis of nasal polyposis. The fact that so many theories
have been 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:
in 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.
Figure showing increasing number of nasal mucosal glands
Figure showing formation of nasal polyp due to increase in the number of mucosal glands (adenoma theory)
Necrotizing ethmoiditis theory of Woakes:
theory 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:
this theory is based on the presence of cystic glands and mucous filled
cysts 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:
beleived 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.
Figure showing exudate accumulating
Figure showing nasal polyp developing after formation of exudate
Theory of cystic dilatation due to obstruction of excretory ducts of nasal glands and blood vessel obstruction:
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:
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.
Figure showing cystic enlargement of nasal mucosal glands
Figure showing cystic enlargement of nasal mucosal glands prior to nasal polyp formation
Periphlebitis / perilymphangitis theory of Eggston and Wolff:
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 starts
of 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
by forming a lining for the polypoidal tissue.If
the 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.
Figure showing rupture of epithelium (rupture theory)
Figure showing formation of nasal polyp following rupture of epithelium
Role played by mucous glands:
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:
infiltration 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