Dear Editor,
We read with great interest the article by Song et al
1
on the assessment of the expression of angiotensin‐converting enzyme 2 (ACE2) and
transmembrane serine proteases 2 (TMPRSS2) in salivary glands using publicly available
databases. Undiagnosed infections were reported to facilitate the rapid dissemination
of the coronavirus disease 2019 (COVID‐19)
2
caused by the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2). The SARS‐CoV‐2
depends on ACE2 and TMPRSS2 for cell entry and priming.
3
The salivary glands were suggested to act as reservoirs for COVID‐19 asymptomatic
infections and transmission since high expression of the ACE2 receptor was found in
minor salivary glands.
4
The Transcriptome data analysis by Song et al
1
showed that ACE2 and TMPRSS2 were expressed in salivary glands. Thus, the virus might
entry into the salivary glands. Corroborating this, in other communication,
5
ACE2 and TMPRSS2 were found to be expressed in the salivary glands.
The analysis carried out in available databases (Genotype‐Tissue Expression portal
and Human Protein Atlas repository) by Song et al,
1
Xu et al,
4
and Pascolo et al
5
are valid to reinforce the hypothesis of salivary gland infection by SARS‐CoV‐2.
6
However, we cannot forget that several factors, such as gene regulatory networks,
tissue pH, hormones, concentration of co‐factors and metabolic events change the expression,
concentration and activity of enzymes.
7
,
8
,
9
To the best of our knowledge, besides the higher number of available publications,
literature still lacks this information in the context of salivary glands infection
by SARS‐CoV‐2.
Even though saliva is important biological fluid for SARS‐CoV‐2 detection, the source
of virus in saliva has not been fully investigated in most studies. Chen et al
6
collected saliva directly from the submandibular salivary glands ducts of 31 confirmed
cases of patients with COVID‐19. Interestingly, the expression of SARS‐CoV‐2 was found
only in four patients (12.90%), being higher in severe cases (3/4). This suggested
SARS‐CoV‐2 coming directly from the salivary gland might be due to high viral loads
at the late stage of the disease
6
and not from individuals with mild, limited, or lack of symptoms. It is encouraged,
however, to carry on research on SARS‐CoV‐2 shedding from salivary glands to undersdand
their contribution to viral load in saliva given literature on this topic is still
scarce.
It has been widely reported that dental practice accounts for an increased risk of
SARS‐CoV‐2 infection due to the close contact with the patient's airways and performance
of aerosol‐generating procedures.
10
,
11
,
12
Dental activities worldwide were profoundly affected by the COVID‐19 pandemic.
13
,
14
Several dental care facilities closed or limited appointments to urgent and emergency
care. In addition, several recommendations were issued to provide dental care while
mitigating the disease spread.
15
,
16
,
17
Mild, limited and asymptomatic infections, from individuals who never experience noticeable
symptoms, have been widely reported for COVID‐19.
18
,
19
,
20
However, even if asymptomatic infections are common, transmission from asymptomatic
individuals was reported to be probably uncommon.
21
Overall, even though the current literature shows that salivary glands can be infected,
we cannot affirm that they act as reservoirs for COVID‐19 asymptomatic infections.
Despite the indication of mouthwashes might cause confusion among the practitioners,
along with other biosafety practices they would be able to decrease the risk of SARS‐CoV‐2
transmission by limiting viral load in saliva droplets and aerosols produced during
dental procedures.
12
,
22
The maintenance of oral healthcare is a serious problem that requires attention and
appropriate measures.
23
The adoption of the preventive measures in dental setting to reduce viral load in
mouth could be useful to provide elective care in asymptomatic patients in times of
COVID‐19. Studies are necessary to understand the real role of salivary glands in
COVID‐19 asymptomatic infections and transmission.
CONFLICT OF INTEREST
The authors declare that there are no conflict of interest.
AUTHOR CONTRIBUTION
MS Pedrosa CR Sipert and FN Nogueira conceived the study and discussed the results.
MS Pedrosa drafted the first manuscript. MS Pedrosa CR Sipert and FN Nogueira critically
read and revised the manuscript, and gave final approval for publication.
DISCLAIMER
The funding agencies had no role in the design and conduct of the study; collection,
management, analysis, and interpretation of the data; preparation, review, or approval
of the manuscript; or decision to submit the manuscript for publication.