4 DISCUSSION
We show that COVID-19 impairs the
epithelial structure and vascularization of both nasal and oral mucosa,
although the nasal mucosa seems to be altered to a less extent than the
oral mucosa is. We suggest that COVID-19 may cause multiple cranial
neuropathies of quite varying degree (i.e. mild to profound) involving
the nerves responsible for the innervation of fPap and the transmission
of the chemical stimuli. Most patients reported a concomitant loss of
smell and taste, and fewer patients reported only loss of either smell
or taste [15,17]. 65.71 % of the patients reported a total recovery
of both taste and olfaction within 4 weeks after the discharge from the
hospital, and 74.29 % had recovered within 6 weeks after hospital
discharge (both olfactory and gustatory function). However, the reported
recovery time (median: 17 days) was not as short as reported in previous
studies, probably because the hospitalized patients included in our
study had more severe disease [17].
A significant study limitation is the lack of objective data on taste
and olfaction in the study participants before hospitalization and even
before the infection. Although all participants reported no history of
gustatory or olfactory disorder in the past, any objective measurements
to compare are missing. Another limitation is the lack of subjective
methods for the evaluation of gustatory function. In our study
electrogustometry was preferred, because of its reliability and the
ability to take repeated results on the same loci. It should be
mentioned that the control group was not measured twice, as these
subjects remained healthy throughout the study the study, without
corresponding pneumonia or any other medication.
The nasal cavity plays an important role in COVID-19 infection; it is
probably the major entry point for SARS-CoV-2 and the site of intense
viral replication [17,18]. SARS-CoV-2 seems to have its own
mechanisms of aggression to the olfactory neuroepithelium, with a
greater predilection for neural structures’ involvement over the nasal
mucosa [19]. Subjective olfactory dysfunction in COVID-19 patients
has been extensively reported in a number of studies [1,4,8-9].
The exact mechanisms underlying olfactory and gustatory disorders among
patients with COVID-19 infection remain unclear. SARS-C0V-2 seems to
enter the central nervous system (CNS) via the olfactory or trigeminal
route. Initially, the CNS infection or inflammation could be mild and
cause olfactory damage [23-25]. However, olfactory impairment after
upper respiratory tract infection is a common occurrence in clinical
settings [21-24]. Another hypothesis is that COVID-19 infection
could be related to the involvement of the olfactory bulb or to
peripheral damage of the olfactory receptor cells in the nasal
neuroepithelium. This assumption is based on the potential neurotrophic
features of SARS-CoV-2 [17,18].
The role of innervation in the regeneration of the fungiform papillae
has been extensively studied. The impact of denervation on fungiform
taste buds appears to be less severe than on circumvallate; while the
former are reduced in number, many albeit smaller taste buds remain
[21,24]. Differentiated taste buds disappear or are reduced in
density in denervated taste epithelium. Progenitor taste cells also
require the trophic and / or electrical signals provided by the afferent
taste nerve fibres, in order to continue to provide immature taste cells
to the taste buds [24,25].