Oral Health and Liver Function in Children and

Adolescents with Cirrhosis of the Liver

Low Tee Eng

160112142502

Supervisor:
Riani Setiadhi, drg, Sp.PM

Universitas Padjadjaran
Faculty of Dentistry
Bandung
2016
Title

Oral Health and Liver Function in Children and

Adolescents with Cirrhosis of the Liver

Name :

Low Tee Eng

NPM :

160112142502

Bandung, August 2016

Approved by:
Supervisor

Riani Setiadhi, drg, Sp.PM

CONTENT

CHAPTER 1 INTRODUCTION..1
CHAPTER 2 LITERATURE REVIEW..2
2.1 ORAL CANDIDIASIS.2
2.2 PETECIA AND GINGIVAL BLEEDING....4
2.3 ANGULAR CHEILITIS..5
2.4 MEMBRANE JAUNDICE..7
2.5 ATROPHIC GLOSSITIS....8
CHAPTER 3 DISCUSSIONS.10
CHAPTER 4 CONCLUSION.....22
REFERENCE LIST.....23

CHAPTER 1
INTRODUCTION

The oral cavity is an important anatomical location that carries out many
different physiologic processes, such as digestion, respiration, and speech
(Wadhawan, 2014). Furthermore, the oral cavity is also an important indicator of
the health of an individual. Oral lesions may manifest early, concomitant with a
systemic disease, disappearing with general health improvement, or later
persisting in spite of disease remission, and usually presenting developmental
abnormalities (Olczak-kowalczyk, 2014).
Manifestations of liver diseases include symptoms of malnutrition, ascites,
edema, esophageal varices and coagulation disorder. Medications such as
glucocorticoid or other immunosuppressant administered for autoimmune liver
disease maybe influence the oral health of the individual; it may disturb dental
development and may contribute to dental caries, periodontal disease and oral
mucosa lesions. Lesion type and severity depend on the age of the child when the
systemic disorders started, type and duration, as well as their impact (Olczakkowalczyk, 2014).

CHAPTER 2
LITERATURE REVIEW

There are many liver diseases that require professional care; the most
commonly known liver diseases are the hepatitis, liver cirrhosis, and liver fibrosis.
Results of a present studies indicate that a higher incidence of oral lesions is seen
with patient with cirrhosis of the liver, up-to-date publications suggest children
with liver failure are more prone to oral mucosa lesions than generally health
children, which might result from hypoproteinaemia, coagulopathy, malnutrition,
cholestasis or immunodeficiency. The most commonly seen oral manifestation in
liver disease patients is oral candidiasis, angular cheilitis, yellow or yellow-brown
hyperpigmentation, petechial, and atropic tongue (Bayless T & Deihl A, 2005).

2.1 Oral Candidiasis

Candida is a normal organism in the mouth, but the overgrowth of this
organism can lead to a condition known as oral thrush or oral candidiasis, in
which the fungal candida albican accumulates in the oral lining. It appears as
white patches known as plaques which resembles milk curds. Oral candidiasis
can be distinguished from milk curds by mechanically removing the plaque. In
oral candidiasis patients, edematous and erythematous surface, and sometimes
bleeding occur is observed after the plaque have been removed mechanically
(Jain et al, 2010).

Figure 2.1 Pseudomembranous oral candidiasis with plaques on the buccal and
sever thrush on tongue (Akpan & Morgan, 2002)

Oral candidiasis is normally found in babies, elderly patients, and

immunocompromised patients. Patients with liver disorder are also susceptible to
oral candidiasis, as liver disease can cause immunodeficiency due to the
immunosuppressive medications taken by the liver disease patients (Hassan et al,
2014).
Topical antifungal therapy is the recommended first line treatment for
uncomplicated oral candidiasis. Nystatin and amphotericin are not absorbed from
the gastrointestinal tract and are used by local application in the mouth.
Miconazole, an imidazole, can be used as a local application in the mouth but its
use in this way is limited because of potential side effects such as vomiting and
diarrhea. Other drugs belonging to this class are clotrimazole and ketoconazole.
Nystatin is the most widely used topical agent for the treatment of oral

candidiasis. It is available as an oral rinse, pastille, and suspension. It should be

used as a rinse four times a day for two weeks. It can cause nausea, vomiting, and
diarrhea (Akpan & Morgan, 2002).
Systemic antifungal therapy in oral candidiasis is appropriate in patients
intolerant of or refractory to topical treatment and those high at risk of developing
systemic infections. Both nystatin oral rinses and clotrimazole have a high sucrose
content and if tooth decay is a concern or the oral candidiasis is complicated by
diabetes, steroid use or an immunocompromised state, triazoles which include
itraconazole once per day has been found to be effective in these cases.
Ketoconazole is also as effective as fluconazole and troconazole but its use in
elderly patient is not recommended due to drug interactions and side effects,
which include hepatotoxicity (Roa, 2012).

2.2 Petechia and Gingival Bleeding

Oral petechia are round, red, pinpoint areas of hemorrhage. Oral petechias
are usually caused by trauma, viral infection, or a bleeding problem. Petechia can
also be found in patients with liver diseases, this is due to the fact that the liver
synthesizes many of the clotting factors necessary for hemostasis. In addition,
vitamin K, a fat-soluble vitamin, requires proper liver function to be adequately
absorbed from the intestines. In patients with liver disease, the resultant impaired
hemostasis can be manifested in the mouth as petechia or excessive gingival
bleeding with minor trauma (Bayless T & Deihl A, 2005).

Figure 2.2 Petechia located on the vestibulum in the oral cavity (Finkelstein M,
2013)

Treatment for petechia is not necessary as the petechia would resolve

within two weeks, but further investigation is required if systemic disease is
suspected from the patient (Finklestein, MW, 2013).

2.3 Angular Cheilitis

Angular cheilitis is a common inflammatory condition affecting the labial
folds of the mouth or the oral commissures. There are many causes of angular
cheilitis, the most commonly known causes of angular cheilitis include nutritional
deficiencies of folate, iron or vitamin B12, poor oral hygiene, fungal infection,
poorly maintained dentures, or immunosuppressant drugs. (Devani, 2007)
In the case of patients with liver diseases, the immunosuppressant drugs
taken by the patients may play a role in the manifestation of the angular cheilitis
in patients with liver diseases due to a fungal infection. On the other hand,

patients with liver disease may also experience a folate and iron deficiency due to
the liver disease, in which folate cannot be metabolizes completely by the liver
and iron cannot be stored completely in the liver as ferratin. Hence, this
nutritional deficiency is also a factor of angular cheilitis in patients with liver
disease (Halsted et al, 2002).

Figure 2.3 Angular cheilitis located on both borders of the vermillion

(Stoopler E, et al, 2013)

The treatment of angular cheilitis is highly dependent on the cause. For

idiopathic causes, the treatment could be as simple as applying petroleum jelly to
the affected area. But if Staphylococcus aureus is implicated, topical treatment
with combination of mupirocin or fusidic acid and 1% hydrocortisone cream
works effectively. If Candida is implicated, an antifungal ointment like
ketoconazole should be prescribed. For patients with underlying hematological
diseases, correcting nutritional deficiencies should reverse the inflammatory
process. For example, iron-replacement therapy for patients suffering from iron-

deficiency anemia can cause regression of the manifestation of angular cheilitis

(Devani, 2007).

2.4 Membrane Jaundice

Yellow pigmentation may be observed on the oral mucosa and may be
accompanied by scleral and cutaneous jaundice in patients with liver diseases.
This is due to the excess bilirubin in the blood results in the accumulation of
bilirubin in tissues, including the oral mucosa, inducing a yellow discoloration.
The severity of the yellow discoloration depends on the blood concentration of
bilirubin and the duration of the problem. Because bilirubin has an affinity of
elastin the mobile oral tissues with higher elastin content, such as lingual
frenulum and the soft palate, are more severely affected. A yellowish to greenish
pigmentation occurs in the teeth of children with hyperbilirubinemia during
calcification, as may be seen in the primary teeth of biliary artesia patients. This is
not seen in adults who develop liver disease after the enamel on the teeth has
already calcified (Daley & Armstrong, 2007).
Gastroenterologists may examine the oral tissues to help in the clinical
assessment of the extent of jaundice. However, care should be taken in assessing a
yellowish discoloration of the soft palate of patient receiving or eating large
amount of vitamin A, which is stored in the fat of the soft palate. (Daley &
Armstrong, 2007)

Figure 2.4 Jaundice at the junction between hard and soft palate (Gomez I, et al,
2007)

2.5 Atrophic Glossitis

The malabsorption of nutrients due liver diseases may have an effect on
the oral mucosa. The classical examples are iron malabsorption inducing iron
deficiency anemia. When the malabsorption is sufficiently severe, the first oral
manifestation is atropic glossitis, in which the filiform papilla and sometimes the
fungiform papilla of the dorsum of the tongue undergo atrophy, leaving a bald, red
tongue. In milder cases, the atrophy is patchy, but more severe cases show
involvement of the entire dorsum. In very severe cases, they may be shallow,
round to oval-shaped, persistent ulcers with bright red borders, clinically
resembling aphthous ulcers but often responsive to appropriate replacement
therapy. Overt tongue lesions are usually sore, but a more common complaint is
burning sensation (glossopyrosis) that may preceded clinically detectable oral
lesions. Other oral mucosa may also become involved with the atrophic zones,
with or without aphthous-like ulcers and the burning sensation, but these lesions

are not dramatic as the bald tongue and often go unnoticed. Affected patients are
predisposed to developing angular cheilitis. (Daley & Armstrong, 2007)

Figure 2.5 Picture of atrophic glossitis also commonly known as the smooth
tongue (Daley T and Armstrong J, 2007)

CHAPTER 3
DISCUSSION

Liver diseases can be classified into acute or chronic, and based on the
extent and origin of the damage, chronic liver disease ranges from steatosis or
fatty liver to hepatocellular carcinoma, and includes hepatitis, fibrosis and
cirrhosis. Liver diseases can also be further classified as infectious such as
hepatitis A, B, C, D, E and G viruses, infectious mononucleosis, or secondary
syphilis and tuberculosis, or non-infectious such as substance abuse such as
alcohol and drugs (Pamplona et al, 2011).
Liver disease are very common, and the main underlying causes are viral
infection, alcohol abuse and lipids and carbohydrates metabolic disorders. The
liver has a broad range of functions in maintaining homeostasis and health such as
synthesize most essential serum proteins, produce bile and its transporters,
intervene in the regulation of nutrients, and metabolize and conjugate lipophilic
compounds to facilitate their excretion in bile or urine. Liver dysfunction alters
the metabolism of carbohydrates, lipids, proteins, drugs, bilirubin and hormones.
Accordingly, liver disease is characterized by a series of aspects that must be
taken into account in the context of medical and dental professions (Pamplona et
al, 2011).
Liver diseases have extrahepatic manifestations that can be seen in the oral
cavity, which include symptoms such as oral petechia and gingival bleeding, oral
candidiasis, atrophic glossitis, yellow or yellow-brown hyperpigmentation of the

10

oral mucosa, coated tongue, and angular cheilitis. Theses symptoms should be
made known to all dental professions as the dental management for patients with
liver diseases would be different from those that do not have liver diseases
(Pamplona et al, 2011).
Hepatitis of viral origin comprises a heterogeneous group of diseases
caused by at least 6 different types of viruses: A, B, C, D, E and G. Hepatitis A is
caused by the hepatitis A virus (HAV), and is transmitted via the enteral route as a
result of the ingestion of contaminated water or food. The disease is normally
mild and self-limiting, and typically presents symptoms such as fever, fatigue,
abdominal discomfort, diarrhea, nausea and/or jaundice. Hepatitis B is transmitted
through sexual contact, intravenous drug use and blood transfusions. An important
consideration among dental professionals as dental professionals are three to four
times great at risk of percutaneous transmission through punctures or cuts with
instruments infected from HBV-positive patients, or absorption through the
mucosal surfaces (eyes, oral cavity). Transmission through saliva can occur as a
result of absorption from mucosal surfaces. Hepatitis C infection is the main cause
of chronic liver disease and of liver-related morbidity and mortality worldwide;
the hepatitis C virus is normally transmitted via the parenteral route from infected
blood. The source of contagion includes blood transfusion, percutaneous exposure
through contaminated instruments, and occupational exposure to blood (Pamplona
et al, 2011).
Alcoholic liver disease is one the 10 most common cause of death in the
industrialized world, in which the clinical spectrum of alcoholic liver disease

11

ranges from simple liver steatosis with alcoholic hepatitis to more sever
steatohepatitis or cirrhosis. The condition ranges from asymptomatic forms to
liver failure and life-threatening situations, and is usually accompanied by
febricula, jaundice, leukocytosis and liver enzyme elevations (Pamplona et al,
2011).
Non-alcoholic fatty liver is defined as the accumulation of fat in the liver,
representing over 5% of the weight of the organ. The observed liver damage
ranges greatly from simple steatosis to steatohepatitis, advanced fibrosis and
cirrhosis. This disorder is mainly associated with obesity, diabetes, hyperlipidemia
and insulin resistance and excessive triglyceride accumulation within the liver
cells (Pamplona et al, 2011).
Liver cirrhosis has very well defined morphological characteristics that
lead to destruction of the liver parenchyma. The disease is accompanied by a
series of extrahepatic manifestations in other body organs and system. Liver
cirrhosis is irreversible, and is characterized by the formation of fibrous scarring
in the liver; with the formation of regeneration nodules that increase resistance to
blood flow through organ (Pamplona et al, 2011).
The oral cavity can reflect liver dysfunction in the form of mucosal
membrane jaundice, bleeding disorder, petechia, increased vulnerability to
bruising, gingival bleeding (even in response to minimum trauma), cheilitis,
smooth and atrophic tongue, and oral candidiasis. The oral manifestation of liver
dysfunctions patients can be due to the drugs taken by the patient or due to the

12

nutrient deficiency cause by the malabsorption by the liver (Pamplona et al,

2011).
Patients with liver dysfunction can be normally seen with oral petechial,
bleeding disorder, or an increased vulnerability to bruising and even gingival
bleeding. This is due to the vitamin K deficiency as the liver synthesizes bile acids
and secretes them into the small intestines where they play a critical role in
absorption of lipids. Vitamin K, as a fat-soluble vitamin, requires proper lipids
absorption for its own absorption. Liver diseases that result in decreased bile salt
synthesis leads to impaired vitamin K absorption and deficiency (Hershline et al,
2010). Furthermore, majority of clotting factors are synthesized almost
exclusively in the liver, so liver disease can cause defects in blood clotting by
several mechanisms. Thus, patients with liver dysfunction would have oral
petechia and excessive gingival bleeding as a result of impaired hemostasis. On
the other hand, patients with liver dysfunctions should also be made known to the
dentist, as dental procedure that would cause excessive bleeding should also be
avoided as the clotting factors synthesize by the liver is also impaired. The
treatment of oral petechia is not required as the lesion is normally self-limiting
and should resolve within 2 weeks (Finkelstein M, 2013).
Mucosal jaundice can also be observed in patients with liver dysfunctions,
as the oral mucosa appears to be yellow and/or yellow-brown hyperpigmentation.
This is due to the accumulation of bilirubin in the tissue due to the excessive
bilirubin in the blood. Hence, inducing a yellow pigmentation of the oral mucosa.
Bilirubin is a by-product from the breakdown of the red blood cells, which is then

13

metabolize in the liver and excreted out of the body in the form of stool. If liver
dysfunction is present, the bilirubin is not properly excreted from the body, thus
resulting in an excessive bilirubin in the blood, which would then accumulate in
the tissue. Hence, causing a yellowish appearance on the skin, oral mucosa, and
sclera. The oral lesions are more commonly seen in the soft palate and the lingual
frenulum. Dentists should pay attention to the color of the oral mucosa as it can
determine the underlying systemic disease the patient is currently experiencing
(Daley & Armstrong, 2007).
Oral candidiasis and angular cheilitis are also oral manifestation of patient
with liver dysfunction. Oral candidiasis are caused by the opportunistic growth of
the oral fungal known as candidia albican, resulting in symptoms such as white
patches or plaque on the oral mucosa or tongue, erythematous gingival mucosa,
and sometimes burning sensation can also be felt by the patient. The cause of oral
candidiasis in patients with liver dysfunction are normally drug induced, which
immunosuppressive drugs such as prednisone and azathioprine are taken by the
patient to decrease inflammation of the liver in autoimmune hepatitis. Thus, the
immunosuppressive drug taken by the patient would be a factor in the
manifestation of oral candidiasis as the immune system of the host is suppressed.
On the other hand, angular cheilitis can also be due to a fungal infection, causing
the vermillion border to crack and slight edematous and erythematous can be seen
on the vermillion border as well (Hassan et al, 2014).
Last but not least, atrophic glossitis can also be seen in patients with liver
dysfunction. Atrophic glossitis is also known as smooth tongue because of the

14

atrophy of the filliform papillae. Nutritional deficiency of iron, folic acid, vitamin
B12, riboflavin, and niacin are common causes of atrophic glossitis (Reamy et al,
2010). Anemia is a condition normally seen in patient with liver dysfunction, this
can be due to the thrombocytopenia conditions due the hemorrhage from the
esophageal or gastric varices; the involvement of alcohol in which it has a
negative impact on the bone marrow, leading to the development of secondary
malnutrition of which the anemia may be caused by folic acid deficiency; the
treatment of chronic hepatitis C with a combination of interferon and ribavirin can
cause ribavirin-induced hemolysis. Hence, the anemic condition induced by the
liver dysfunction would manifest as atrophic glossitis in the oral cavity causing
the tongue to appear smooth and sometimes causes a painful sensation on the
tongue (Gonzales-C R, et al, 2009).
Atrophic glossitis is also known as smooth tongue because of the smooth,
glossy, appearance with a red or pink background. The smooth appearance quality
is caused by the atrophy of the filiform papillae. Atrophic glossitis is primarily a
manifestation of underlying conditions such as amyloidosis, drug reactions,
systemic infections, nutritional deficiencies and pernicious anemia, and warrants a
thorough diagnostic evaluation. Nutritional deficiencies of iron, folic acid, vitamin
B12, riboflavin, and niacin are common causes. Other etiologies include systemic
infections, localized infection, amyloidosis, celiac disease, protein-calories
malnutrition, and xerostomia triggered by some medications and Sjoren
syndrome. Atrophic glossitis caused by nutritional deficiency often causes a

15

painful sensation in the tongue. Treatment includes replacement of the missing

nutrients or treatment of the underlying disease (Reamy BV et al, 2010).
In order to find out the exact nutrient deficiency that causes atrophic
glossitis, a complete blood count can be carried out and the measurement of the
serum iron, ferritine, vitamin B12, and folic acid levels can be taken to make sure
that they are within the normal range (Pastore L & Muzio LL, 2007).
The normal range of serum iron found in adult men ranges from 65-175
g/dL, adult women ranges from 50-170 g/dL, children ranges from 50-120
g/dL, and the range of infants ranges from 100-250 g/dL, while the normal
range of ferritin for normal men: 20-250 ng/mL, women: 10-120 ng/mL, children:
7-140 ng/mL, and infants: 25-200 ng/mL. The normal value range of vitamin B 12
ranges from 200-835 pg/mL for adults, and 160-1300 pg/mL for newborns. The
normal range of folic acid in adult is found to be 2-20 ng/mL, children 5-21
ng/mL, and infants to be 14-51 ng/mL (Fischbach FT, 2003).
Angular cheilitis is the term used or an infection involving the lip
commissures. The majority of cases are Candida associated and respond promptly
to antifungal therapy. There is frequently a coexistent denture stomatitis, and
angular cheilitis is uncommon in patients with a natural dentition. Other possible
etiologic cofactors include reduced vertical dimension; a nutritional deficiency
(iron deficiency anemia and vitamin B or folic acid deficiency) sometimes
referred to as perleche; and (more rarely) diabetes, neutropenia, and AIDS, as well
as co-infection with Staphylococcus and beta-hemolytic Streptococcus. Moreextensive desquamative lesions affecting the full width of the lip and sometimes

16

extending to the adjacent skin are associated with habitual lip sucking and chronic
Candida infection (Greenberg MS and Glick M, 2003).
The treatment of angular cheilitis of fungal infection etiology is the topical
imidazole derivative such as 1% clotrimazole ointment, 2% ketoconazole gel, or
nystatin ointment are efficacious in treating angular cheilitis (Greenberg MS and
Glick M, 2003). Angular cheilitis can also result from a polymicrobial infection,
consisting of Candida and S. aureus or enteric bacteria, local application of
fusidic acid 2% ointment (Jenkinson HF and Douglas LJ, 2002). Miconazole
nitrate 2% gel can be applied to the affected area as well, because it is an
antifungal with some activity against gram-positive bacteria including
streptococci and staphylococci and is the treatment of choice for angular cheilitis
(Cross LD and Short L, 2009).
Dental plaque is the primary etiology for chronic gingivitis, which
typically develops within 10 to 21 days in the absence of plaque control.
Approximately 50% of the population over the age of 30 has some form of
gingivitis. Although mechanical plaque control can be an effective strategy for
preventing the progression of periodontal diseases, most individuals do not
adequately brush their teeth, and only 11% to 51% of the population admits to
using dental floss or some types of inter-dental cleaning device on a daily basis.
The daily use of an effective antiseptic mouthwash is generally considered a
simple strategy most patients can easily incorporate into their home care routine.
Thus, using an antiseptic mouthwash to supplement mechanical plaque removal
can produce an antimicrobial effect thorough the mouth (Osso & Kanani, 2013).

17

Besides plaque control, antiseptic mouthwashes are also indicated for oral
conditions such as oral sores, halitosis, xerostomia, and periodontal diseases
(Parashar A, 2015).
Bisguanides have a very broad antimicrobial spectrum effective with both
gram negative and gram positive bacteria. Chlorhexidine gluconate is a catonic
bisguanide and was presented to the market as a 0.2% mouthwash. The
mechanism of action of bisguanide is to bind strongly to bacterial cell membranes,
increasing the cell permeability, this initiating leakage and/or precipitating
intracellular components. Furthermore, it binds to salivary mucins, reducing
pellicle formation, thereby inhibiting subsequent colonization. It also hinders the
adsorption of bacteria onto the tooth surface (Asadoorian J, 2006).
The advantage of chlorhexidine gluconate over other catonic agents is that
it can bind strongly to many sites in the oral cavity and is released slowly over 7
to 12 hours after rinsing, thus providing considerable substantivity and a sustained
antimicrobial effect restricting bacterial proliferation. Chlorhexidine gluconate
binds strongly with anionic glycoproteins and phosphorproteins on the mucosa
and tooth pellicle, but it can also bind to cell surfaces of bacteria affecting the
cells ability to adhere. Unfortunately, chlorhexidine gluconate has several
clinically significant disadvantages including brown staining of the teeth, tongue,
and restorations, particularly on composites, requiring professional removal;
alterations of taste perception of up to four hours after rinsing; and potentially
increased supra-gingival calculus build-up. Hypersensitivity of mucosa and hairy
tongue are less common side effects (Asadoorian J, 2006).

18

Quaternary ammonium compounds, which are generally cationic agents,

interact with the cell membrane of bacteria affecting their permeability and
subsequently resulting in loss of cell contents. Quaternary ammonium compounds
are bactericidal to both gram positive and gram negative bacteria. These
compounds have the ability to bind strongly to oral tissues, but they are released
at a more rapid rate than chlorhexidine gluconate (Asadoorian J, 2006).
Cetylpyridium chloride usually at 0.05% with or without domiphen
bromide or benzethonium chloride also at 0.05% have been used in mouthwash
for many years. It has been shown that cetylpyridium chloride control supragingival plaque and calculus, but it is significantly less effective than
chlorhexidine gluconate. On the other hand, cetylpyridium chloride shares some
of the adverse effect of chlorhexidine gluconate, such as tooth staining, burning
and increased calculus formation (Asadoorian J, 2006).
Phenols, either alone or in combination, have been used in mouthrinses or
lozenges for a considerable time. Essential oils refer to over the counter antiseptic
mouthwash containing 2 phenol related essential oils, thymol and eucalyptol
mixed with menthol and methyl salicylate in a hydro-alcoholic vehicle. Most
essential oils contain alcohol (as a solvent) at a concentration of approximately
22%, which is contraindicated for young children and patients who are immunecompromised, have mucosities, a history of alcohol abuse and/or undergoing
radiation therapy for head and neck (Osso D & Kanani N, 2013). Essential oils are
fragrant component of plants and contain phenolic compounds. These essential
oils kill microorganisms by disrupting their cell membrane and inhibiting enzyme

19

activity. The essential oils prevent bacteria from aggregating with gram positive
pioneer species, slows bacterial multiplication, and extract endotoxins from gram
negative pathogens, thus reducing bacterial load. The essential oils also reduces
plaque maturation time and decrease plaque mass and pathogenicity (Asadoorian
J, 2006).
Povidone-iodine is a water-soluble combination of molecular iodine and
the solubilizing agent polyvinyl-pyrrolidone. This iodophor has a bacterial effect
similar to that of pure iodine; is effective against most of the bacteria, including
putative periodontal pathogens, fungi, mycobacteria, viruses, and protozoa.
Previous studies have showed that povidone iodine, as a mouthwash exerts only
an immediate antibacterial effect and unlike chlorhexidine, is not retained at
antibacterial levels within the oral cavity after expectoration (Venkataraghavan K
et al, 2014).
Oxygenating agents such as hydrogen peroxide, sodium peroxyborate and
peroxycarbonate act by liberating nascent oxygen to loosen debris, remove stains
and kill anaerobic microorganisms. They have a broad spectrum of antimicrobial
properties. Oxygenating agents containing mouthwashes are recommended for
acute ulcerative conditions, to relieve soreness caused by dentures, orthodontic
appliances and stain removal (Parashar A, 2015).
The incorporation of ethanol into mouthwashes serves several purposes: it
is a solvent for other active ingredients, has antiseptic properties and acts as a
preservative. Ethanol is easy to produce and relatively cheap (Werner & Seymour,
2009). Additionally, ethanol has antimicrobial activity against various bacteria,

20

fungi and viruses by causing protein denaturation and dissolution of lipids

(Parashar A, 2015).
Mouthwashes containing significant amount of alcohol have number of
disadvantages as well. Furthermore, correction between xerostomia and the usage
of high alcohol containing mouthwashes have been implicated (Asadoorian J,
2006). Alcohol containing mouthwashes have shown to reduce the hardness of
composite and hybrid resin restorations and may also alter the color of composite
restorations. Therefore, the use of alcohol containing mouthwashes should be
restricted to short term (Parashar A, 2015).

21

CHAPTER 4
CONCLUSION

In conclusion, a dentist should be well aware of the oral manifestation

such as mucosal jaundice, atrophic glossitis, oral candidiasis, oral petechial and
gingival bleeding, and angular cheilitis, as these are signs and symptoms of a
patient with liver dysfunction. Dentist should also pay close attention to the
treatment plan for patients with liver dysfunction, traumatic procedures such as
extraction and root planing should be avoided; this is due to the vitamin K
deficiency experience by patients with liver dysfunction. Hence, a traumatic
procedure might cause a bleeding disorder. On the other hand, the dentist should
take precautionary care as well because dentist have a 4 to 5 times higher rate of
contracting the Hepatitis B virus through puncture wounds or cuts from
instruments and through mucosal surface. Furthermore, the drugs prescribed for
patients with liver dysfunction have to be taken into consideration, as the liver is
the main organ that metabolizes drug.

22

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Cross DL and Short L, (2009). Angular Cheilitis Occurring during Orthodontic
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