-~---------- 
----- 
CLINICO-PATHOLOGICAL AUDIT OF ORAL MUCOSAL 
LESIONS AMONG PATIENTS AT THE MUHIMBILI NATIONAL 
HOSPITAL IN TANZANIA 
By 
Sira Stanslaus Owibingire (DDS) 
A Dissertation Submitted in Partial Fulfillment of the Requirements for the Degree 
of Master of Dentistry (Oral Surgery) of the Muhimbili University of Health and 
Allied Sciences. 
Muhimbili University of Health and Allied Sciences 
October, 2007 

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11 
CERTIFICATION 
The undersigned certify that they have read and hereby recommend for acceptance a 
dissertation entitled: Clinico-pathological Audit of Oral Mucosal Lesions Among 
Patients at the Muhimhili National Hospital in Tanzania, in fulfillment of the 
requirements for the degree of Master of Dentistry in Oral Surgery of the Muhimbili 
University of Health and Allied Sciences. 

Dr. E. N. M. Simon 
(SUPERVISOR) 
~ cr·, I 0' ~€){).1- 
	Date 	. 

(SECOND SUPERVISOR) 
.J9· /0 . ;)00'1 
	Date 	. 

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111 
DE CLARA TION 
AND 
COPYRIGHT 
I, Dr Sira Stanslaus Owibingire, declare that this dissertation is my own original work 
and that it has not been presented and will not be presented to any other University for a 
similar or any other degree award. 
Signature ... k.t..~'>.c .... 
This dissertation is copyright material protected under the Berne Convention, the 
Copyright Act 1999 and other international and national enactments, in that behalf, on 
intellectual property. It may not be reproduced by any means, in full or in part, except 
for short extracts in fair dealings, for research or private study, critical scholarly review 
or discourse with an acknowledgement, without a written permission of the Directorate 
of Postgraduate Studies, on behalf of both the author and the Muhimbili University of 
Health and Allied Sciences. 
-~- 

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ACKNOWLEDGEMENT 
First and foremost, I thank The Almighty God, the origin of every wisdom and 
understanding, Alfa and Omega, for granting me, strength, health and the living. 
I am greatly indebted to my supervisors Dr. E. N. M. Simon and Dr. B. M. Kalyanyama 
for their relentless sacrifice, challenging guidance and constructive criticism. They used 
much of their invaluable time to read my drafts, correct and direct me several times. 
I am grateful to Dr. Shubi who worked together with my supervisors not only to teach 
me the practice of oral and maxillofacial surgery but also to correct, advice, and 
encourage me throughout this study. 
I am indebted to all doctors and nurses and their assistants working at Muhimbili 
National Hospital (MNH) dental clinic and wards 19 and 20 who assisted me with data 
collection exercise. I thank Ms C. Mushiro who together with other academic' staff in her 
department enlightened me on research methodology and data management. I am also 
thankful to Dr. Hamza Omar for assistance in some technical issues on data analysis. 
I sincerely thank the Ministry of Health and Social Welfare for the financial support. 
I extend my gratitude to the Dean of School of Dentistry and the Director of 
Postgraduate Studies and the rest of the management at Muhimbili University of Health 
and Allied Sciences (MUHAS) for timely guidance and logistic support. 

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t : 
I am sincerely thankful to Dr. Mwakyoma of the Department of Histopathology and 
Morbidy Anatomy for his criticism, advice and guidance especially on histopathology 
aspect, and to post-graduate students (Dr W. Muller and Dr L. Mtango) and other 
members of the department for assistance in laboratory aspect of this study. 
Lastly, to my beloved wife Georgia, for her constant encouragement and moral support. 
She strove to make the atmosphere more conducive for my study. My family, relatives 
and friends who encouraged and prayed for me and all those who have not been 
mentioned here, I say THANK YOU VERY MUCH! 

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VI 
DEDICATION 
This work is dedicated to the memory of my beloved and caring father Stanslaus Simon 
Owibingire and mother Theresa Kanyambo who died consecutively within an interval of 
100 days. Their deaths came when I was at the vital stages of this work. It is God's will 
that they died at that particular time. May their souls rest in eternal peace, Amen. 

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vii 
ABBREVIATIONS 
AIDS - Acquired Immunodeficiency Syndrome 
CD4+ - Cluster of differentiation - 4 
HAART - Highly active antiretroviral therapy 
HHV - Human Herpetic Virus 
HIV - Human Immunodeficiency Virus 
HSV - Human Simplex Virus 
KS - Kaposi's sarcoma 
MNH - Muhimbili National Hospital 
MUHAS - Muhimbili University of Health and Allied Sciences 
OMLs - Oral mucosal lesions 
OPD - Out patient department 
OPG - Orthopantomogram 
OSCC - Oral squamous cell carcinoma 
pH - Negative logarithm of Hydrogen Ion concentration 
PHGS - Primary herpetic gingivostomatitis 
RAU - Recurrent aphthous ulcer 
RR - Relative Risk 
SPSS - Statistical Programme for Social Sciences 
UK - United Kingdom 
USA - United States of America 
WHO - World Health Organization 

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LIST OF TABLES 
Table Page 
	Table 1. Distribution of the study population by age and sex 	.42 
	Table 2. Sociodemographic characteristics of the study population 	.43 
	Table 3. Major presenting symptoms 	44 
Table 4. Categories of oral mucosal lesions and proportion of 
	malignant lesions in each category 	.44 
Table 5. Distibution of study subjects with malignant oral mucosal 
	lesions by age and sex 	45 
Table 6. Distribution of study subjects with squamous cell 
	carcinoma by age and sex 	: 	.46 
Table 7. Distribution of study subjects with oral Kaposi's sarcoma 
	by age and sex 	47 
	~-------------- 	eJ

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IX 

LIST OF FIGURES 
Figure Page 
	Figure 1. Location of oral mucosal lesions 	32 
	Figure 2. Clinical photograph of patient with squamous cell carcinoma 	33 
	Figure 3. A photomicrograph of oral squamous cell carcinoma 	34 
	Figure 4. Clinical photograph of patient with oral Kaposi's sarcoma 	35 
	Figure 5. A photomicrograph of oral Kaposi's sarcoma 	36 
	Figure 6. Clinical photograph of patient with oral malignant melanoma 	39 
	Figure 7. A photomicrograph of oral malignant melanoma 	.40 

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ABSTRACT 
Background: Oral mucosal lesions (OMLs) are common in adult population although 
not as frequently reported as for traditional oral health problems. These lesions include; 
ulcerative/vesiculobullous, white/red, pigmented lesions, benign mucosal swellings and 
tongue mucosal lesions. Some OMLs are either malignant, premalignant or benign while 
others are caused by common infectious agents. Some of them may result from 
autoimmune reaction while others may be associated with systemic diseases including 
HIV/AIDS. Lesions suspected to have pre-malignant properties need close follow-up, 
early recognition and management. Due to the variation in clinical presentation and the 
uncertainty as to whether a lesion is malignant or benign, OMLs pose a challenge with 
regard to diagnosis and management. The burden of OMLs in Tanzanian populations 
has hardly been documented. 
Objective: The objective of this study was to determine the Occurrence and clinico- 
pathological presentation of oral mucosal lesions in patients presenting for treatment in 
the Oral Surgery department of the MNH. 
Study Design: This was a prospective cross sectional descriptive study. 
Study Setting: The study was done at the MNH at the oral surgery out patient clinic and 
in wards where oral surgical patients were admitted. 
Study Duration: The study was conducted over an 8-month duration. 
Methods: The subjects who consented to participate in the study were interviewed using 
a pre-tested questionnaire. Oral examination was done and the details of findings, and 

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Xl 

investigations results including biopsy were recorded. The data were analyzed using the 
SPSS programme version 12.0.1 and interpretation of the results done. 
Results: The prevalence of OMLs was 4.6%. The age of subjects ranged from 1 to 86 
years with mean 41.5 +/- 19.9 years and the male to female ratio was 0.72:1. Majority 
(56.3%) had primary education only while 17.5% had no formal education. 76 (47.5%) 
subjects indicated they drank alcohol, 23(14.4%) smoked tobacco and 15 (9.4%) used 
snuff. 34 types of OMLs were observed from the 172 lesions and these were 
categorized into; white/red OMLs 24 (14.0%), ulcerative lesions 64 (37.2%), pigmented 
OMLs 37 (21.5%), mucosal swellings 34 (19.8%) and tongue mucosal lesions 13 
(7.6%). Out of the oral ulcerative OMLs 34 (53.1 %) were malignant and for pigmented 
OMLs and oral mucosal swellings the proportion of malignant OMLs was 56.8% and 
23.5% respectively. Squamous cell carcinoma (See) was the most frequent OMLs 
observed in 34 (21.3%) of the subjects followed by Kaposi's sarcoma (KS) in 19 
(11.9%) subjects. More females were found to have had see and "(S than males and the 
most affected age was 60 years and above for see and 20-49 years for KS. All patients 
with KS were HIV positive and 94.1 % with see presented with clinical stage IV 
lesions. Other OMLs with a relatively higher frequency included; peripheral granuloma 
(7.5%), traumatic ulcer (5.8%), haemangioma (5.2%), adenocarcinoma (4.7%), 
pseudomembraneous candidiasis (4.6%), aphthous ulcer (4.1%), geographic tongue 
(3.5%) and fissured tongue (2.3%). The most common site for occurrence of OMLs was 
the lower lip followed by the hard palate and anterior 2/3 of the tongue. 

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Conclusion: Results indicate that OMLs is a problem in Tanzania. The malignant 
lesions constituted the large proportion of OMLs observed. The most common lesion 
type was see followed by KS. The most common site for the OMLs was the lower lip 
followed by the hard palate. 

TABLE OF CONTENTS 

Xlll 

Page 

Front page -------------------------------------------------------------------------------------- i 
Certification ---------------------------------------------------------------------- ------------ ii 
Dec larati on and co pyri gh t ----- ----- ---- - --- ---- -- - ---- ---- ---- ---------------------- ---- ---- iii 
Ackno wledgem ent --------------------- ---------- ---------------------------------- ----------- i v 
Dedication ------------------------------------------------------------------------------------- vi 
Abbreviations--------------------------------------------------------------------------------- vii 
List of tables. --------------------------------------------------------------------------------- viii 
List of figures --------------------------------------------------------------------------------- ix 
Abstract. ---------------------------------------------------------------------------------------x 
Table of contents. ----------------------------------------------------------------------------xiii 
1. Introduction and Literature review------------------------------------------------------1 
1.1. Background--------------------------------------------------------------------- 1 
1.2. General epidemiology of oral mucosal lesions -------------------------- 2 
1.2.1. Prevalence of oral mucosal lesions ---------------------------- 2 
1.2.2. Age ----------------------------------------------------------------- 4 
1.2.3. Sex ----------------------------------------------------------------- 5 
1.2.4. Geographical location ------------------------------------------ 6 
1.2.5. Occupation -------------------------------------------------------- 7 
1.2.6. Intra-oral site -------------------------------------------------------7 
1.2.7. Denture wearing -------------------------------------------------- 7 
1.2.8. Tobacco smoking ------------------------------------------------- 8 

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1.2.9. Alcohol consumption---------------------------------------------- 9 
1.2.10. Use of snuff, chewing of tobacco and betel nuts ------------ 9 
	1.3. 	Specific types of oral mucosal lesions --------------------------------- 11 
1.3.1. Premalignant and malignant lesions -------------------------- 11 
1.3.2. Ulcerative and vesculobullous lesions ------------------------- 12 
1.3.3. White and red mucosal lesions ---------------------------------- 16 
1.3.4. Oral mucosal benign swellings ----------------------------------17 
1.3.5. Pigmented oral mucosal lesions ---------------------------------17 
1.3.6. Tongue mucosal lesions ------------------------------------------ 18 
2.	Statement of the problem ------------------------------------------------------------ 20 
3.	Rationale of the study -----------------------------------------------------------------21 
4.	0 bj ecti ves ------ --- ------ ----------------------- ------- -- ---- ---------- ------- ---------- 22 
4.1. Broad objective ---------------------------------------------------------------- 22 
4.2. Specific objectives ------------------------------------------------------------ 22 
	5. 	Materials and methods --------------------------------------------------------------- 23 
		5.1. 	Study setting ----------------------------------------------------------------23 
		5.2. 	Study design ---------------------------------------------------------------- 23 
		5.3. 	Study duration ------------------------------------------------------------- 23 
		5.4. 	Study population ---------------------------------------------------------- 23 
		5.5. 	Inclusion and exclusion criteria ------------------------------------------ 24 
		5.6. 	Sample size ----------------------------------------------------------------- 24 
		5.7. 	Sampling procedures ------------------------------------------------------ 24 

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	5.8. 	Data collection ------------------------------------------------------------- 24 
5.8.1. Examination procedures ----------------------------------------- 25 
5.8.2. Locating mucosal lesions -----------------------------------------25 
5.8.3. Description ofthe lesions ---------------------------------------- 25 
5.8.4. Histopathological investigation ----------------------------------25 
5.9. Data handling and analysis ------------------------------------------------26 
5.10. Ethical considerations ----------------------------------------------------- 27 
	6. 	Ftesults ---------------------------------------------------------------------------------- 28 
		6.1. 	Age and sex distribution -------------------------------------------------- 28 
		6.2. 	Socio-demographic characteristics -------------------------------------- 28 
		6.3. 	Risk factors for oral mucosal lesions ----------------------------------- 29 
		6.4. 	Major presenting symptoms and reason for attendance -------------- 30 
		6.5. 	Types and categories of oral mucosal lesions diagnosed ------------ 30 
		6.6. 	Location of oral mucosal lesions ---------------------------------------- 31 
		6.7. 	Oral mucosal lesions with relatively high frequencies --------------- 32 
		6.8. 	Co-existence of oral mucosal lesions ----------------------------------- 40 
		6.9. 	Association of OMLs with HIV I AIDS --------------------------------- 41 
7.	Discussion ----------------------------------------------------------------------------- 48 
8.	Co n c I usi ons --- --------- - -- ------ ----- --------- - - ------------ ----------------- --- ---- ---- 59 
9.	Limitation of the study --------------------------------------------------------------- 60 
10.	Recommendations --------------------------------------------------------------------- 61 
11.	References -------------------------------------------------------------------------------62 

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XVI 
12. Appendix -------------------------------------::-------------------~------------------------77 
12.1. Questionnaire -----------------------------------------------------------------77 
12.2. Clinical form/check list----------------------------------------------------- 85 
12.3. Topography of oral mucosal sites---------------------------------------- 91 
12.4. Distribution of specific type of OMLs according to sex-----------------92 
12.5. Informed Consent ------------------------------------------------------------93 
12.6. Informed Consent [Swahili version] ---------------------------------------95 

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1. INTRODUCTION AND LITERATURE REVIEW 
1.1. Background 
Traditionally oral health problems have been sighted to be mostly dental canes, 
periodontal diseases, oro-facial trauma, congenital anomalies and neoplasms. However, 
oral mucosal lesions (OMLs), although not as frequently mentioned, are also a common 
problem in the adult population I. As a group, OMLs are more common than conditions 
like tension headaches, phlebitis or arthralgias 2 and include both surgically treatable and 
non-surgical conditions that are not always easy to differentiate. There is a wide range of 
OMLs including ulcerative, vesicular and bullous, white/red, pigmented lesions, benign 
mucosal growths and oral cancer 1,3.4. In this context, therefore, even their symptoms 
and presentation vary very much with some causing pain and discomfort while others 
are symptom-free and follow an indolent course. 
The significance of understanding and managing OMLs is documented and highly 
encouraged by the World Health Organization (WHO) 5. There is a close relationship 
between general health and OMLs and some general disease conditions may to a good 
extent be mirrored in the oral mucosa 6. Actually, some of the OMLs, such as lupus 
erythematosus are important indicators of severe underlying systemic diseases 2. Some 
lesions like lichen planus or pemphigus are caused by autoimmune reaction 7 and others 
like leukoplakia or erythroplakia may be indicators of the possibility of developing oral 
cancer 8,9,10. Of current concern is the prevalence of HIV infection, in which a great 
	. 	fill' 	b 	11-13 
	vanety 0 ora mucosa eSlOns may e seen 		. 

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There have been a number of studies that have documented the epidemiology of oral 
mucosal lesions worldwide 14-22. Among these, there are studies that concentrated on a 
single lesion like the herpes labialis 23, leukoplakia 24 or oral lichen planus 25 and some 
that were specific to one intra-oral site, for example the tongue 26,27. Also, some of the 
studies dealt with special community groups like the child population 28-32 and old 
people 33-36. The findings of these studies, however, vary and seem to depend on many 
factors including, the geographical location, ethnicity, habits and practices, age and sex 
distribution of the population studied. Very few population-based studies on the 
epidemiology of OMLs have been documented in Africa and so far hardly any has been 
carried out in Tanzania. 
	1.2. 	General epidemiology of OMLs 
1.2.1 Prevalence of OMLs 
Various studies have documented the prevalence of OMLs. The pioneering studies of 
large samples done in adult populations are those of Axell (1976) in Sweden 17 and 
Bouqout (1986) in the USA 15. In Axell' s study the most frequently reported lesions 
included; leukoedema (48.9%), a history of recurrent aphthous ulcers (17.7%) and 
geographic tongue (8.45%) 17. Bouqout (1986) revealed that the overall prevalence of 
OMLs was 14.8% and the most prevalent lesion was leukoplakia (2.9%). The overall 
prevalence of OMLs in Malaysia was found to have been 9.7%, with denture stomatitis 
having been the most prevalent lesion 18. Among studies that registered low prevalences 
of OMLs were those ofIkeda et al. (1995) 19 and Ikeda et al. (1991) 21 who documented 

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prevalences of 4.9% and 5.2% respectively. In Sweden, however, Salonen et al. (1990) 
found the prevalence of OMLs to have been as high as 64.7% 37. In the USA, Shulman 
et al. (2004) reported a prevalence of27.9% whereby denture-related lesions (stomatitis, 
hyperplasia, ulcers, inflammation and angular cheilitis) together composed 8.4 % 16. 
There are studies that documented higher prevalences of OMLs. In Kenya, Macigo et al. 
(1995) found that among the individuals they examined 48.6% had at least one oral 
mucosal lesion, the most common having been leukoedema (26%) followed by 
melanosis (12.7%) and leukoplakia (10.6%) 22. Pearson et al. (2001) found that 40% of 
Bangladeshi descendants living in the UK aged 40 years and above, and who were users 
of medical care had OMLs with leukoplakia having been the most prevalent 38, Kovac- 
Kavcic et al. (2000) in Slovenia documented a prevalence of 61.1% with Fordyce's 
spots observed most frequently 20. In Germany among individuals aged 35-44 and 65-74 
years only 33.8% and 33.9% respectively had no OMLs 39. 
Most studies involving elderly populations found high prevalences of OMLs. For 
example, in Mexico, Chile, Israel and Hong Kong the prevalence of OMLs ranged from 
36% to 55.6% 33,36,40,41. High prevalences have also been reported by studies that dealt 
with special groups at risk for some specific OMLs. Campisi and Margiotta in Italy 
reported 81.3% prevalence of OMLs in a group of men aged 40 years and above, among 
. whom 73% were alcohol drinkers, 58.5% were smokers, 25% edentate and only 3% had 
good oral hygiene 42. However, Salonen et al. (1990) reported a 64.7% prevalence of 
OMLs in a population where two-thirds were using neither tobacco nor snuff 37. 

4 
Rioboo-Crespo et al. (2005) reviewed data of recent epidemiological studies of oral 
mucosal lesions in children and found a wide variability in the prevalences of OMLs in 
different regions of the world 28. They found out that the percentage of children with 
OMLs in different communities in the world ranged from 4.1 % to 52.6%. They revealed 
that the prevalence of most commonly occurring OMLs in different studies included 
recurrent aphthous stomatitis (0.9-10.8%), labial herpes (0.8-5.2%), fissured tongue 
(1.49-23%), geographic tongue (0.6-9.8%), oral candidiasis (0.1-37%) and traumatic 
injuries (0.1-22.1 %). Kleinman et al. (1994) reported that 4% of schoolchildren aged 5- 
17 years had one or more OMLs while 33% and 37% of the children reported a history 
of recurrent herpes labialis and recurrent aphthous ulcers respectively 29. Bessa et al. 
(2004) reported a prevalence of 27% of oral mucosal changes in children aged 0 -12 
years 32. 
1.2.2. Age 
Generally, age is a significant risk factor for the occurrence of some of OMLs. Shulman 
et al. (2004) found that, the risk of having a mucosal lesion increased steadily with 
age 16. They noted that people aged 70 years and above had almost double the risk of 
having a lesion compared to those aged between 17 and 29 years. It was also found by 
do Santos et al. (2004) that 52.6% of children aged 12 years old and 73.4% of 
individuals aged 13 years or older presented with at least one oral mucosal condition 43. 
Mumcu et al. (2005) reported that being 65 years old or above was found as a 
statistically significant risk factor for the occurrence of pigmentation, fissured tongue, 

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varices, hairy tongue, denture stomatitis and petechiae 44. In studies where middle aged 
(35-44 years) and elderly (65-74 years) age groups were compared for prevalences of 
OMLs; Lin et al. (2001) in China and Micheelis et al. (1999) in Germany found that the 
overall prevalence increased with age 14,39. Some of the studies done in elderly people 
appreciated that increased age was related to the development of OMLs 45 while others 
found the opposite to be true 40. Espinoza et al. (2003) in their study in the elderly 
reported that age had no effect to the occurrence of OMLs 40. Some of the studies 
involving children and adolescents also noted that the prevalence of some OMLs 
increased with increasing age 32. Looking at individual oral mucosal lesions/group of 
lesions, Kovac-Kavcic et al. (2000) found that the prevalence of white mucosal lesions, 
denture related lesions, fissured tongue, varices and mucocele has been found to 
increase with increasing age 20. 
1.2.3. Sex 
Statistically significant difference in the overall prevalence of OMLs between males and 
females is not a common finding although in some of the lesions there are differences 
reported. Micheelis et al. (1999) in their study where 35-44 and 65-74-year age groups 
were studied found no statistically significant differences in the overall prevalence 
between males and females 39. Looking at individual lesions, however, statistical 
differences between males and females were noted for the prevalence of Fordyce's 
spots, a history of herpes labialis, aphthous ulcers and lip/cheek biting which were more 
common in females than males. Similarly, Corbet et al. (1994) found no statistically 

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significant difference in the prevalence of OMLs between men and women among the 
65-74-year-old Chinese in Hong Kong 36. Contrary to this, Lin et al. (2001) found that in 
the 65-74-year age group there were statistically significant higher prevalences of OMLs 
in males compared to females for both urban (male 22% and female 12%) and rural 
(male 26% and female 19%) subgroups 14. Kovac-Kavcic et al. (2000) documented that 
lichen planus, denture stomatitis and herpes labialis occurred more frequently in the 
female population 20 while Neville et al. (2002) found that oral squamous cell carcinoma 
and leukoplakia were more common in males 8. 
1.2.4. Geographical location and place of residence 
Geographical location has an indirect influence on the prevalence of oral mucosal 
lesions. For instance, habits and practices of people in one location if different from 
another location may lead to the difference in the prevalence of OMLs. Other factors 
that are likely to differ from one geographical location to another include racial 
predilection, environment, climate, economic and living standards. 
Roberto et al. (2003) reported the prevalence of OMLs to have been higher in the urban 
community (76.9%), followed by the marginal-urban community (56.8%) and finally the 
rural community (51.7%) 41. While studying the association of OMLs and dentures, 
Mikkonen et al. (1984) found no significant difference in the geographical location 46. 

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1.2.5. Occupation 
An outdoor occupation leads to excessive exposure to actinic radiation and this is 
associated with the development of SCC of the lip 8,47. A study by Vianna et al. revealed 
a positive association between acid mists and gases and ulcerative lesions of the oral 
mucosa but only in the absence of lip sealing 48. Exposure to lead results in a bluish red 
or deep blue linear pigmentation of the gingival margin (Burtonian line) while exposure 
to silver causes a violet marginal line often accompanied by a diffuse bluish-grey 
discoloration throughout the oral mucosa 49. 
1.2.6. Intra-oral site 
OMLs can involve any part of the oral cavity. In their study Shulman et al. reported that 
most lesions occurred in the hard palate (25.9 %), followed by the gingiva (20.4 %), lips 
(15.4 %) and dorsum of the tongue (14%) 16. Ulcerative lesions are likely to be found on 
non-keratinized mucosal sites (e.g. labial and buccal mucosa). However, primary 
herpetic gingival stomatitis most often occurs on keratinized mucosal sites 4. Oral SCC 
occurs most often on the lips and lateral borders of the tongue, followed by the floor of 
the mouth and gingiva 8,47, while the hard and soft palates, followed by the maxillary 
gingiva, are the most common sites for oral mucosal melanomas 50. 
1.2.7. Denture wearing 
In Chile the prevalence of OMLs in the elderly population was found to have been 53% 
predominated by denture stomatitis 22.3% 40. Similarly, Mikkonnen et al. (1984) in 

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Finland reported a 50% prevalence of OMLs in removable denture wearers 46. Denture 
stomatitis is the most common mucosal problem encountered in elderly removable 
denture wearers. Corbet et al. (1994) reported 10% denture stomatitis lesions in the 65- 
74 years-old Hong Kong Chinese population 36 and Micheelis et al. reported a 18.3% 
prevalence in a similar age group 39. Kovac-Kavcic et al. (2000) in Slovenia found out a 
prevalence of 14.7% of denture stomatitis in denture wearers 20 and Axell found 16% of 
subjects with denture stomatitis in a Swedish population 17. 
1.2.8. Tobacco smoking 
A wide variety of mucosal changes have been noted in habitual users of smoked and 
smokeless tobacco. These changes most likely result from the many irritants, toxins, and 
carcinogens found naturally in cured or burned tobacco leaves. The significant mucosal 
changes noted in tobacco users have been identified as oral cancer, leukoplakia, nicotine 
palatinus stomatitis, smokeless tobacco keratosis, smoker's melanosis, submucous 
fibrosis, leukoedema and hairy leukoplakia 51. Kovac-Kavcic et al. (2000) found two 
tobacco-related lesions (leukoplakia and smoker's palate together) to have been more 
prevalent in men than women (5.7% and 1.7% respectively) 20. Prout et al. (1977) 
documented a 13% prevalence of OMLs among tobacco users while oropharyngeal 
squamous cell carcinoma was found in 3% of these patients 52. When Salonen et al. 
(1990) analyzed the relationship between tobacco habits and mucosal lesions, a positive 
correlation between tobacco use and leukoplakia, frictional white lesion, coated tongue, 

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hairy tongue and excessive melanin pigmentation were demonstrated while a negative 
correlation was observed for geographic tongue and aphthous ulcers 37. 
1.2.9. Alcohol consumption 
Excessive alcohol has little impact on the prevalence of oral carcinoma, but it is a 

\ 
\ 
\ 

powerful "promoter", capable of altering mucosal cells to make them much more 
susceptible to malignant transformation by tobacco carcinogens 51. It has been found that 
most of the alcohol drinkers are also heavy smokers and hence the total effects become 
greater. Sankaranarayanan et al. (1990) assessed the risk factors for oral cancer and 
noted that the duration of tobacco chewing and smoking was a better predictor of risk 
than either daily frequency or total lifetime exposure 53. Harris et al. (2004) studied 
OMLs alcohol abusers in South London where it was found that 28.1 % had oral mucosal 
lesions 54. Frictional keratosis (8.8%), scar tissue of the lips (4.8%), candidiasis and 
angular cheilitis were the lesions with the highest frequency. 
1.2.10. Use of snuff, chewing tobacco and betel nuts 
The association between the use of snuff and the prevalence and severity of oral lesions 
has been documented in various descriptive studies. Mucosal change is found in almost 
all snuff users at the site where the snuff is placed. In Sweden for example, studies done 
on the effects of Swedish snuff on the oral mucosa showed that the degree of 
development of an oral lesion positively correlates with the daily duration of stay of 

10 

snuff in the area, daily consumption frequency and the number of years of active snuff 
use 55-57. The degree of lesions seems to increase with increasing pH as well as 
increasing nicotine content 56-58. Oral lesions caused by snuff are reversible following 
quitting 59. A recent review, however, has found that the use of chewing tobacco and 
moist snuff is associated with low risks for oral cancers (relative risks [RR] from 0.6 to 
1.7) while dry snuff is associated with higher RRs, ranging from 4 to 13 60. 
There are data from a study by Tomar et al. (1997) that suggested that snuff may be a 
stronger risk factor than chewing tobacco for smokeless tobacco users, but the use of 
either of these forms of tobacco exhibits a dose-response relationship with the 
occurrence of lesions 61. In another report, Tomar and colleagues found out that in the 
USA men more commonly switched from snuff use to smoking than the opposite and 
that those who use snuff to quit smoking had less success than non-snuff users 62. 
There is significant evidence in the literature concerning the development of oral see 
and its precursors including leukoplakia and submucous fibrosis in betel nut/quid 
chewers 63,64. The habit is more prevalent in Southeast Asia and corresponds to the fact 
that in places like India oral see is the commonest malignant neoplasm accounting for 
20-30% of all cancers 65. 

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1.3. Specific types of OMLs 
1.3.1 Pre-malignant and malignant oral mucosal lesions 
The importance of understanding pre-malignant OMLs lies in the fact that some can 
transform into oral cancers. Approximately, 90% of oral cancers are primary see 
arising from the lining mucosa of the mouth, most commonly the tongue and the floor of 
the mouth 66. Despite the fact that oral cancer is largely preventable it has remained the 
gravest oral mucosal lesion 67. It is the sixth most common cancer in the world 68 and is 
the commonest malignant neoplasm, in India 69. It accounts for approximately 2% of all 
cancer deaths worldwide 65. The mean UK annual incidence rate for both sexes is 
approximately 4.5: 100,000 70 while in the USA it was estimated that in 2002 these 
tumors could account for 28,900 new cases and 7,400 deaths 71. The most popularly 
documented oral pre-malignant lesions are leukoplakia and erythroplakia, others being 
lichen planus, submucous fibrosis, oral hairy leukoplakia, nicotine stomatitis, tobacco 
pouch keratosis and syphilis 8,47. Leukoplakia is a white lesion involving the oral 
mucosa that cannot be removed by rubbing and cannot be classified as any other lesion 
following histopathologic examination 47. According to the WHO, it is defined as "a 
white patch or plaque that cannot be characterized clinically or pathologically as any 
other disease" 72. Most cases of leukoplakia are a hyperkeratotic response to an irritant 
and are asymptomatic, but about 20% of leukoplakic lesions show evidence of dysplasia 
or carcinoma at first clinical recognition 73. Silverman et al. (1984) in a prospective 
follow-up study documented a 17% malignant transformation of leukoplakia 74. 
Extensive reviews have shown that different studies have given varying proportions of 

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12 
malignant transformation of leukoplakia ranging from 3 to 20% 75, however, there are 
subtypes of leukoplakia which have been associated with rates as high as 40% 74. 
Various studies have documented prevalences of leukoplakia. Bouqout (1986) recorded 
leukoplakia to have been the most frequent oral mucosal lesion with a prevalence of 
2.9% 15, while in Axell's study the prevalence was 3.1 % 17. Ikeda et al. (1995) in 
Cambodia found a prevalence of 1.1 % 19 and Macigo et al. (1995) in Kenya reported 
10.6% 22. 
Erythroplakia, presents as red patches, with a surface that is frequently velvety in 
texture and margins that may be sharply defined. Erythroplakia is less common but 
when compared to other mucosal lesions it carries the highest risk of malignant 
transformation 76. Erythroplakia lesions may be malignant in up to 80% of tissue 
biopsies 77,78. 
Lichen planus is a complex immunologically mediated mucocutaneous disease primarily 
seen in adults and more commonly in women 47. The premalignant or malignant 
potential of lichen planus is in dispute, however, there is a low but measurable risk of 
malignant transformation 78,79 which has been reported to range between 0.4% and 
2.5%47. 

, 

1.3.2 Ulcerative and vesiculobullous oral mucosal lesions 
There are various types of oral lesions presenting with ulcers which mayor may not be 
preceded by vesicles and bullae formation. Most infections of the oral mucosa (majority 

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being viral) fall under ulcerative and vesicular groups':". Non-infective recurrent ulcers 
including recurrent aphthous ulcers and chronic multiple lesions such as pemphigus also 
constitute this group. The most common viral infections are caused by viruses of the 
Human Herpetic virus (HHV) group. Eight types of HHV have been linked to oral 
diseases. These types have different disease patterns in their hosts 80. Primary herpetic 
gingivostomatitis (PHGS) represents the clinically apparent pattern of primary herpes 
simplex virus (HSV) infection, since the vast majority of other primary infections are 
symptomless. PHGS is caused predominantly by HSV -1 and affects mainly children 81. 
The actual frequency of oral herpes infection decreases with age, increases with 
increasing socioeconomic status and is related to race 82. Up to 80% of the population 
are asymptomatic carriers of the virus and 20-40% of the people have experienced cold 
sores some time in their life 4,76,82. Factors that may trigger a recurrence of oral herpes 
simplex include; immunosuppression, upper respiratory tract infections, fatigue, 
emotional stress, physical trauma, exposure to sun (ultraviolet light), and menstruation 
82", Berker et al. (1988) while investigating the seroprevalence level of human 
herpesviruses in the 1-15-year-old children found a high (73%) prevalence of antibodies 
to the herpes simplex virus type 1 and also noted that, from the medical records, 30% of 
the children had suffered from herpetic gingivostomatitis prior to the study 83. 
Bessa et al. (2004) determined the prevalence of oral mucosal alteration in children and 
found-that primary herpetic gingivostomatitis had a prevalence of 0.3% and recurrent 
herpes 0.8%, the former showed an increase with increasing age 32. In Bouqout's study 

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herpes labialis was found in 0.2% of the adult population 15. The history of herpes 
labialis was found in 21.9% in the study of Kovac-Kavcic et al. (2000) in which after 
excluding subjects with no recurrence within 1-2 years the prevalence was found to be 
16% 20. Micheelis et al. (1999) found 31.3% and 20% of the 35-44 and 65-74-year age 
groups respectively to have had a history of herpes labialis 39. In this survey females 
showed significantly higher rates of recurrent herpes labialis than males. Lowhagen et 
al. (2002) assessed the level of self-reported herpes labialis in the Swedish population 
where 26.6% reported that they had herpes in past while 19.4% had had herpes in the 
	. 2 	84 
prevIous years . 
Other causes of infective stomatitis could be the Coxsakie virus (causing herpangina, 
foot and mouth disease), the Epstein Barr virus causing infectious mononucleosis, and 
Varicella zoster viruses 4. Tuberculosis and syphilis, also, may present with some forms 
of ulcerative lesions mainly on dorsum of the tongue for tuberculosis and lips and tip of 
the tongue for syphilis 76. Deep chronic ulcers with destruction of the adjacent tissues 
are common with malignant ulcer/carcinoma, bacterial (tuberculosis, syphilis), and 
fungal infections (cryptococosis, aspergillus). Non-infectious ulcerative lesions can also 
affect the oral mucosa. Traumatic ulcers are the commonest, ranked first with a 
prevalence of 1.8% in Mexico 85. In children, Bessa et al. (2004) determined the 
prevalence of cheek biting to have been 6.11 % and other traumatic lesions 2.33% 32. In 
the general population the prevalence of cheek biting as reported by Bouqout was 0.12% 
15 while Kovac-Kavcic et al. (2000) registered 2.7% 20 and Macigo et al. (1995) 1.3% 22. 

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Recurrent aphthous ulcers (RAU), or recurrent aphthous stomatitis, represent a chronic 
inflammatory disease characterized by painful oral ulcers recurring with varying 
frequency. The categories of RAU lesions are as follows; minor aphthous ulcers (80- 
85% ofRAU cases) are 1-10 mm in diameter and heal spontaneously within 7-10 days. 
Major aphthous ulcers constitute 10-15% of RAU cases. These lesions are greater than 
10 mm in diameter, take 10-30 days or more to heal, and may leave scars. Herpetiform 
ulcers (5-10% of RAU cases) are multiple, clustered; 1 to 3 mm lesions that may 
coalesce into plaques and usually heal within 7-10 days 86. The actual cause ofRAU is 
not straightforward but factors predisposing patients to RAU may include trauma, 
emotional stress, malabsorption, celiac disease, regional enteropathy, menstruation, food 
hypersensitivity, allergic reaction, and exposure to toxins such as nitrates in drinking 
water 4,86,87. Between 5% and 25% of the general population experience RAU 87. In the 
USA, although RAU is commonly believed to occur in approximately 20% of the 
general population, a study of medical and dental students revealed a prevalence ranging 
from 31 % to 66% 86. 
There are chronic ulcerative and vesiculobullous lesions that affect the skin but can also 
occur in the oral cavity and are mainly associated with autoimmune reaction and 
sometimes can occur as oral manifestations of systemic diseases 4,88. These include 
pemphigus vulgaris, paraneoplastic pemphigus, bullous pemphigoid, cicatricial 
pemphigoid, dermatitis herpetiformis and linear IgA dermatosis. The prevalence of these 
lesions is low, for instance, it is estimated that pemphigus has an incidence rate of 0.5 to 

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16 
3.2 per 100,000 population and one of every 15,000 to 40,000 patients treated in an eye 
clinic may have ocular pemphigoid 88. 
1.3.3.White and Red mucosal lesions 
Apart from the red and white lesions with defined precancerous potential there are other 
red and white lesions without precancerous potential. They range from variations of 
normal mucosa such as leukoedema and Fordyce granules to infections including oral 
candidiasis, and from keratotic white lesions such as nicotine palatinus, frictional 
keratosis to non-keratotic white lesions including lesions due to burn and cheek 
biting3,89. These lesions are widely documented in most population studies. For example, 
Kovac-Kavcic et al. (2000) obtained a 49.7% prevalence of the Fordyce's condition 
while the prevalences of frictional keratosis and smokers' palate were 2.2% and 0.5% 
respectively 20. In Kenya Macigo et al. (1995) found leukoedema in 26%, palatal 
keratosis 6.4%, frictional keratosis 5.5%, and the snuff dippers lesion in 0.4% of the 
studied population 22. In Turkey, the study by Mumcu et al. (2004) documented 
frictional keratosis in 1.3% among 765 subjects, leukoedema in 0.4% and Fordyce's 
spots 1.3% 44. Ikeda et al. (1991) observed 0.3% prevalence for candidiasis and 
smoker's palate each 21. In Germany, Micheelis et al. (1999) reported Fordyce's spots in 
26.6%, leukoedema 1.0% and candidiasis in 0.4% 39. 

17 

1.3.4. Oral mucosal swellings 
Oral warts or papilloma and epulides/granulomas are among the commonly reported oral 
mucosal swellings. Bouqout (1986) 15 registered prevalences of such mucosal swellings 
as follows: papillary hyperplasia 0.3%, papilloma 0.5% and irritation fibroma 1.2%. 
Ikeda et al. (1991) noted that in their study fibroepithelial hyperplasia had a prevalence 
of 0.5% while papilloma and gingival hyperplasia were seen in less than 0.1 % of the 
study population each 21. Bessa et al. (2004) in children obtained a prevalence of 0.1 % 
for oral warts and 0.2% for eruption cysts 32. Diaz-Guzman et al. (1994) reported a 
prevalence of 1.4% for irritation fibroma, 0.3% papillary hyperplasia and 
papillomaepulis fissuratum each and 0.1 % gingival hyperplasia 85. 
1.3.5. Pigmented oral mucosal lesions 
Pigmented lesions are commonly found in the oral cavity. Such lesions represent a 
variety of clinical entities ranging from physiologic changes such as racial pigmentation 
to manifestations of systemic illnesses including Addison's disease and malignant 
neoplasms such as melanoma and Kaposi's sarcoma 90. Oral pigmentation occurs in all 
races 91 and there is no significant difference in oral pigmentation between males ttnd 
females 92. Bouqout (1986) found the prevalence of oral melanotic macule and amalgam 
tattoo to have been 0.09% each 15 and Ikeda et al. (1991) registered a prevalence of 0.1 % 
each for excessive melanin pigmentation and haemangioma 21. Corbet et al. (1994) 
found the prevalence of haemangioma and excessive melanin pigmentation in the 
elderly of Hong Kong to be 11.2% and 1% respectively 36. In Kenya Macigo et al. 

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(1995) observed melanosis in 12.7% of people aged 15 years and above 22. In the survey 
by Micheelis et al. (1999) the 35-44-year-old group had a prevalence of 0.4% and 3.5% 
for haemangioma and amalgam tattoo respectively while in the 65-74-year-old group 
these lesions were observed in 2.6% and 5.1 % respectively 39. 
1.3.6. Tongue mucosal lesions 
The lesions affecting the lingual mucosa include those generally affecting other parts of 
the oral mucosa including candidiasis, traumatic ulcers and recurrent aphthous ulcer. 
However, there are some lesions specific to the lingual mucosa such as the geographic 
tongue, hairy tongue, median rhomboid glossitis, fissured tongue, lingual varicosities, 
glossitis and foliate papillitis 93. Lin et al. (2001) found that tongue lesions and white 
lesions were relatively common 14. Their findings included the fissured tongue, hairy 
tongue, atrophic tongue and lingual varicosities. The most frequently seen lesion was the 
fissured tongue which had a prevalence of 12.5% among the rural people aged 65 -74 
years 14. A recent review documented the prevalence of fissured tongue in children to be 
between 1.5% and 23% while that of geographic tongue was 0.6 - 9.8% 28. In children, 
Shulman et al. (2005) obtained a prevalence of geographic tongue of 1.8% 94. In 
Bouqout's study the recorded tongue lesions included black hairy tongue (0.1 %), 
median rhomboid glossitis (0.1 %), enlarged lingual tonsils (0.2%), geographic tongue 
(0.3%) and fissured tongue (0.3%) 15. Kovac-Kavcic et al. (2000) in Slovenia registered 
2.2% and 21.1 % prevalences for geographic and fissured tongue respectively 20. Yarom 
et al. (2004) documented the prevalence of fissured tongue to have been 30.5% while 

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•••••••••... •••.•......... ------------- 
19 
geographic tongue and median rhomboid glossitis were found in 12.7% and 2.4% of the 
study population, respectively 95. A gradual increase in the prevalence of the fissured 
tongue and geographic tongue was noted with advancing age while median rhomboid 
glossitis decreased similarly. 

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2. STATEMENT OF THE PROBLEM 
OMLs can occur in a wide range of patterns and pose diagnostic and management 
challenges. The prevalence, occurrence pattern and clinico-pathological presentation of 
OMLs have been found to differ from country to country based on culture, practices and 
habits. Tanzania is a country with a mixture of cultures especially in the urban areas and 
hence a multitude of behaviour pattern and practices. Worldwide, there are several risk 
habits and practices that have been documented that could be the cause or predisposing 
factors of the OMLs, especially the cancerous and pre-cancerous oneS. There has been 
no study executed in Tanzania to determine the prevalence or clinico-patholigic features 
of OMLs or the relationship between risk habits and the occurrence of these lesions. It is 
important, therefore, to carry out a study to compare the epidemiological picture of 
OMLs with that found elsewhere in the world. 
.• In the current era of HIV / AIDS there has been a changing pattern of OMLs. Majority of 
patients who are infected with HIV present with oral lesions, most of which are found 
affecting the mucosa. It is, therefore, most important to get a further insight into such 
changing patterns. Some of the OMLs present with an innocent clinical appearance and 
course but are cancerous or may transform into oral cancer later hence they need close 
follow-up, early recognition and management. In Tanzania, patients report late for 
treatment of most oral diseases including oral cancers. Some of the factors contributing 
to this may include inadequate understanding of clinicians regarding the diagnosis and 

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management of oral mucosal conditions, lack of awareness of oral mucosal diseases 
including cancers; and the existence of a bureaucratic referral system. There is no 
guideline so far issued by the ministry of health on the management of OMLs. There are . 
no well-established initiatives to raise awareness of the general population on at least the 
most important oral mucosal conditions such as oral cancer. 
	3. 	RATIONALE OF THE STUDY 
There is no local study that has been done in Tanzania to document lesions affecting the 
oral mucosa. The findings of this study may, therefore, provide an insight on the 
magnitude, pattern of occurrence and clinico-pathological features of oral mucosal 
diseases and conditions in a Tanzanian population. These findings may also serve as the 
basis for planning and improving both preventive;. and curative care of OMLs in the 
country. The findings of this study will be submitted to the ministry of health where they 
could be used to prepare guidelines for the management of oral mucosal conditions and 
to some extent develop a scientific basis for the population awareness strategy. On the 
other hand, the results will contribute to the improvement of care of the HIV infected 
patients and other immunocompromised patients as far as the mucosal lesions are 
concerned. The study forms a part of the requirements for degree of Master of Dentistry 
in Oral Surgery at the Muhimbili University College of Health Sciences of the 
University ofDar es Salaam (currently MUHAS). 
'!" 

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	4. 	OBJECTIVES. 
- 
	4.1. 	BROAD OBJECTIVE: 
To determine the -occurrence and clinico-pathological presentation of OMLs among 
patients presenting for treatment at the Oral Surgery department of the MNH. 
	4.2. 	SPECIFIC OBJECTIVES: 
1. To determine the frequency of occurrence of OMLs among patients presenting 
for treatment at the Oral Surgery department of the MNH. 
2. To determine the socio-demographic features of patients with OMLs presenting 
for treatment at the Oral Surgery department of MNH. 
3. To determine the associated major risk factors with the occurrence of OMLs 
among patients presenting for treatment at the Oral Surgery department of the 
MNH. 
4. To determine the types and anatomical sites of the OMLs among the patients 
presenting for treatment at the Oral Surgery department of the MNH. 
5. To determine the histological and cytological types of OMLs among the patients 
presenting for treatment at the Oral Surgery department of the MNH. 

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	5. 	MATERIALS AND METHODS 
	5.1. 	Study settings 
The study was conducted at the MNH, which is the largest referral and University 
teaching hospital in Tanzania. The hospital has the largest dental clinic in the country 
and is the only hospital in the country currently with an Oral and Maxillofacial centre. It 
provides surgical services to the residents of Dar es Salaam (a city with over 3.6 million 
people) and those from allover the country. The study was carried out at two settings of 
patient care; the oral surgery out-patient clinic and on the wards. 
	5.2. 	Study design 
This was a descriptive prospective cross-sectional study. 
	5.3. 	Study duration 
The study was conducted over an 8-month duration (July 2006 to February 2007 
inclusive). 
	5.4. 	Study population 
The study population included all admitted and outpatient oral surgical patients during 
the duration of the study. 

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24 
5.5. Inclusion and exclusion criteria 
	5.5.1. 	Inclusion criteria 
All patients presenting at the Oral Surgery department and found with oral mucosal 
lesions were included in the study after they gave their consent. 
	5.5.2. 	Exclusion criteria 
All patients presenting at the Oral Surgery department with OMls who did not 
consent for various reasons were not included in the study. 
5.6. Sample size 
A total of 160 study participants qualified for the inclusion criteria and were recruited in 
the study. 
5.7. Sampling procedures 
All patients who were examined and found with OMLs and who consented were 
included in the study. The subjects meeting the inclusion criteria were being enrolled in 
the study as they were received at the OPD clinic and in the admitting wards. 
5.8. Data collection 
The subjects were interviewed using a pretested questionnaire. Then thorough oral 
examination was done and details of examination findings and investigation results were 
recorded on the clinical form. 

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5.8.1. Examination procedures 
Oral examination was carried out with a patient seated in a dental chair using artificial 
light. The identification of OMLs through clinical examination using diagnostic 'criteria 
as recommended by WHO 5 was adopted with minor modifications. All examinations 
were done by the same examiner (the investigator) hence consistence in diagnosis. 
5.8.2. Locating mucosal lesions [Topographical classification]. 
A systematic and standardized method for recording oral mucosal conditions was 
observed. The topographical classification of the oral mucosa as per the WHO 5 criteria 
which were adopted from Petersen & Renstrup 96 was used (Appendix ll). 
5.8.3. Description of the lesions 
Depending on the type of observed lesion, the clinical description was given to aid in the 
diagnosis. This was in accordance with the WHO guidelines'. 
5.8.4. Histopathological investigation. 
The major means of diagnosing the OMLs were clinical and histopathological 
examination. In the few lesions where biopsy was not indicated diagnosis was based on 
clinical features. For most of the lesions a definitive diagnosis was reached after 
histopathological or cytological analysis of tissue or cell specimens respectively. Tissue 
biopsy was either incisional by taking a small wedge shaped specimen from the lesion or 
excisional where the entire lesion was excised. Taking of tissue biopsy was done by the 
author at the clinic under local anesthesia at the outpatient clinic. hnmediately after 
obtaining the tissue it was put into a special container with 10% formalin and 
immediately transferred to the laboratory together with a form with details of the 

I - 

26 
particulars of the patient including clinical notes. At the laboratory the tissue specimens 
were registered followed by the take-in exercise whereby the tissue was macroscopically 
inspected and sampled ready for processing. The tissues were secondarily fixed with 
formalin first, then dehydrated in alcohol in ascending concentration of 70%, 90% then 
100%. Washing the tissue with xylene to remove alcohol then followed. The tissue was 
then embedded in paraffin wax to prepare blocks. Cutting of slices was done with a 
microtome machine at 3-5 microns then slices were mounted on the microscope slides 
labeled with accompanying identification numbers. The sections were deparaffinized 
with xylene, then washed with alcohol, followed by dionized water. Staining was done 
using routine haematoxylin and eosin followed by coating and placing cover slip for 
protection. For lesions where cytology was indicated, fine needle aspiration was done by 
the pathologist in the laboratory. The aspirated cells/materials were suspended in 70% 
alcohol for 20 - 40 minutes then mounted on slides and stained with the Papanicolaou 
stain. The slides (of both tissue and fine needle aspiration biopsy) were then examin~- 
under a light microscope at magnifications of 4 xlO, 10x10, then 40xlO. The 
histological and cytological examination and reporting was done by experienced 
pathologists. 
5.9. 	Data handling and analysis. 
Data were entered in the computer on the same day of collection. Analysis of data was 
done using the SPSS software version 12.0.1 (Chicago, II: SPSS Inc; 2004). The 
investigator consulted a biostatistician regarding the data analysis and interpretation. 
-- -- ~ ~-, ----~- - -~-- ,- 

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Statistical significance testing was done using the chi-square test; p-value of less than 
0.05 was considered statistically significant. 
5.10. Ethical consideration 
The patients were given explanation on what the study was about before they were 
asked to participate in the study. Only those who freely consented were enrolled. All 
information was handled confidentially. To enhance confidentiality, identification 
numbers were used in the questionnaire and clinical forms instead of each patient's 
name. Patients who were found having OMLs were managed per the existing hospital 
and ministry of health protocols. 
5.10.1 Ethical clearance 
The proposal was presented in the department of Oral Surgery and Oral Pathology of the 
Muhimbili University College of Health Sciences. Thereafter, ethical clearance was 
obtained from the Research and Publication committee of the Muhimbili University 
College of Health Sciences (currently MUHAS). 

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6. RESULTS 
During the study period, out of 3486 patients who received treatment in the Oral Surgery 
department 160 (4.6%) had OMLs. 
6.1. Age and sex distribution 
A total of 160 patients aged between 1 and 86 years with OMLs were recruited in the 
study. These comprised of 67 (41.9%) males and 93 (58.1 %) females with a male to 
female ratio 0.72:1. The most affected age group was 20 - 29 years with 31 (19.4%) of 
the subjects. The age group 0 - 19 yeas was least affected by OMLs with 9 (5.6%) of the 
subjects. More females were found at older ages than males (Table 1). 
6.2. Socio-demographic characteristics of the study population 
Table 2 summarizes the socio-demographic characteristics of the study subjects. 
6.2.1. Education: Twenty eight (17.5%) of the subjects had no any formal education, 97 
(60.6%) had a maximum of primary education and 28 (17.5%) had secondary school 
education and above. Among females 23 (24.7%) had no formal education compared to 
5 (7.4%) among males. 
6.2.2. Marital status: Eighty four (52.5%) study subjects were married, 34 (21.3%) 
were single while there were more females in divorced and widowed groups than males. 
6.2.3. Occupation: Nearly one third (31.9%) of study subjects were peasants, 13 
(19.4%) were small-scale traders and 25 (15.6%) were employed personnel. 
6.2.4. Place of residence: Majority (51.9%) of the subjects were residing in the Dar es 
Salaam urban areas followed by those from upcountry rural settings 61(38.1%), 
- - - -- ---- -- ~ --- ~ 

29 
upcountry urban (6.9%) and 5 (3.1%) of subjects were from the Dar es Salaam peri- 
urban. 
6.3. Risk factors for oral mucosal lesions. 
6.3.1. Smoking 
Twenty three (14.4%) subjects comprising 19 (82.6%) males and 4 (17.4%) females had 
once smoked tobacco in their lives. Six were still smoking while 17 (73.9%) had 
stopped due to various reasons. Of the six who were current smokers, 3 smoked 10 - 20 
cigarettes per day while the other 3 smoked less than 10 cigarettes per day. Three (50%) 
out of the six who were still smoking had smoked for between 10 and 19 years, the other 
3 had smoked for over 20 years. All reported to have smoked factory made cigarettes. 
Among those who had stopped smoking, 11 (64.7%) had done so within the previous 1 
year, 4 (23.5%) in the previous 1 - 4 years and 3 (17.6%) more than 10 years. On 
average, nine (52.9%) had smoked 1 - 10 cigarettes per day and 8 (47.1%) used to 
smoke 11 - 20 cigarettes a day. Twelve (70.6%) had smoked for more than 20 years and 
12 (70.6%) of those who had stopped did so after being sick. 
6.3.2. Use of snuff 
Among 15 (9.4%) subjects (all females) who used snuff 13 (86.7%) had used snuff for 
20 years. Majority, 12 (80%) used it 6-10 times a day but generally the frequency ranged 
between 1 and 20 times per day; and the snuff was left on site of placement for less than 
30 minutes in 14 (93.3%) subjects. Sites of placement were reported to have been the 
labial sulcus by 7 (46.7%) subjects, buccal sulcus 5 (33.3%), under the tongue by 2 
(13.3%) subjects and one (6.7%) subject used to inhale snuff through the nose. 
-.~ - --~-----~-~- 

l

30 
6.3.3. Alcohol drinking 
Seventy six (47.5%) subjects including 9 (51.3%) males and 37 (48.7%) females used to 
take alcohol. More than half (57.9%) consumed factory-made beer while 26 (34.2%) 
consumed local brew and the consumption of spirits was reported by 6 (7.9%) subjects. 
Twenty nine (38.2%) drunk alcohol on average of less than one day per week, 33 
(43.4%) one to three days, 12 (15.8%) 4 - 6 days and 2 (2.6%) drunk alcohol 7 days a 
week. A high frequency of more than 3 days alcohol consumption per week was 
reported by 12 (30.8%) males while among females only 1 (2.7%) reported such a 
frequency. 
6.4. Major presenting symptoms and reasons for attendance 
Most subjects presented with pain 90 (56.3%), followed by ulceration (53.8%) and 
swelling (51.8%) [Table 3]. In 126 (78.8%) patients OMLs were the primary reason for 
attendance, in 7 (4.4%) they were the secondary problem while in 27 (16.9%) of 
subjects the finding of OMLs was coincidental (Fig. 6). 
6.5. Types and categories of OMLs diagnosed. 
One hundred and seventy two OMLs were found in the 160 subjects, 12 (7.5%) of 
whom had two types of lesion each. There were 34 types of OMLs which were 
categorized into white/red 24 (14.0%) lesions, ulcerative 64 (37.2%), pigmented OMLs 
37 (21.5%), mucosal swellings 34 (19.8%) and tongue mucosal lesions 13 (7.6%). There 
were 63 (36.6%) malignant lesions. Among these, 34 (53.9%) were oral see which 
presented as ulcerative lesions, 21 (33.3%) were pigmented lesions among which 19 
----~-- 

31 
were Kaposi's sarcoma and 2 malignant melanoma while 8 (12.7%) were mucosal 
swellings of malignant minor salivary glands (Table 4). 
6.6. Location of OMLs 
The oral cavity was divided into 39 small sites (see appendix Ib) and the overall scores 
of presence of mucosal lesions on the particular sites were analyzed. There were no 
statistically significant difference between the left and right sides. Sites were merged 
into 12 locations, the scores are displayed in Fig. 1 below. The most affected site was 
the lower lip (28.8%) followed closely by the hard palate (26.3%) and anterior two 
thirds of the tongue in 37 (25.0%). The oropharynx was the least affected site by OMLs. 
- 
-----~-~,~ 

32 
1
Oropharynx ~ ~.(3.8) 
	Floor of oral cavity ~ ,., 	._	:.(10.6) 
	TOngUeposterio~ ! 	"""""'.,,; 	.........,.~~ 	_. (12.5) 
•• 1II!!!IlIJ •.•••••••••••• 1IIII!I!!II.,...~.1(15.6) 
Tongue lateral borders 	IT 	? . ,0; 	• 
Soft palate ••.. "r....;', .(16.3) 
	Upper lip - ~. 	.(1 ~.5) 
 .: 
•••••• --~IIIiIIIIIIIII ••••••••••••• I--~ (20.6) 
	Mandibular ging' 	• 
Maxillary gingiv ~~m~~,~~.·.<:·,~~ 
Buccal mucosa 
Tongue anterior 21 
!!III",I!II!I!I!!I,. yW.:>II,!I{ ••• " ••• :.II!!I! •.••••.• IIIII .•• (21.3 
) 
.............-.""'!I!I!!I!I;.:";IIII!!I.!!II.~.; •• '(_IlIIIII •••••••.•••••• (22.1) 
••••••••••• ~IIIIIIIIJIIIII.....,IIII!.........II!III!IIIIII! •••• !IIIIII!III: ..•• , (25.0) 
•.••• 1!III'IIIIlI~ •••••• IIW!I!II __ •.••••••• IIIIII!II! ••••••••••• (26.3) 
	;:, 	"'0': 	• 
- 
~ - -- ---~---- - -----------_. 
Hard palat 
/' 

Lower ltp ; 
Location 
- 
/' 
/' 
/' 
10 
20 
30 
40 
50 
o 
Frequency(%) 
Figure 1. Location of OMLs in the oral cavity. 
6.7. OMLs with relatively high frequencies 
6.7.1. Oral see 
Thirty four (21.3%) subjects comprising 11 (32.4%) males and 23 (67.6%) females had 
oral sec. All subjects except 2 presented with clinical stage IV oral see (Table 7). 
Twenty two (64.7%) of the patients with oral see were aged 60 years and above. 
Seventeen (50%) had no formal education among whom 13 (76.5%) were females. The 
t
l
i

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association of low level of education and oral see was found to have been statistically 
significant (P < 0.001). Most, (70.6%) of the subjects with oral see were peasants. 
Nine (26.9%) subjects had smoked tobacco, 10 (29.4%) had used snuff and 24 (70.6%) 
reported to have consumed alcohol. Among those who consumed alcohol 20 (83.3%) 
had used alcohol for more than 20 years and 3 (12.5%) drank more than 3 days a week. 
Oral see was found in almost all intraoral sites including the dorsum of the tongue 
(Fig. 1), however, the most affected intraoral site was the mandibular gingiva (44.1 %) 
followed by the lateral borders of the tongue (41.2%) and the floor of oral cavity 
(26.5%). 

Figure 2. see of the tongue in a male patient aged 63 years. 

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Figure 3. Photomicrographic appearance of oral see showing 
hyperchromatism, nuclear pleomorphism and keratin formation 
and invasion of stroma. [Hematoxylin and Eosin (H & E) stain, original 
magnification X40) 
6.7.2. Oral Kaposi's sarcoma 
Oral Kaposi's sarcoma was found in 19 (11.9%) subjects among whom 7 (36.8%) 
were males and 12 (63.2%) were females. Seventeen (89.5%) were aged 20 - 49 years 
[Table 8]. Generally, females with oral KS were younger compared to males. All 
subjects with oral KS were HfV positive, 17 (89.5%) had skin KS lesions and 8 (42.1%) 
were already on highly active antiretroviral therapy (HAART). Fifteen (78.9%) Oral KS 
lesions presented as nodular lesions while the rest presented as reddish brown lesions. 
Eleven of the subjects were in stage III of the IllV disease (WHO classification) and the 
rest were in stage IV. The mean CD+ 4 count was 158 +/- 14 cells mm". 

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Figure 4. Kaposi's sarcoma on the tongue (nodular stage) in a 23-year-old 
HIV positive female patient who was already on HAART for 13 
months. 
	- - -------- 	--~-- 

36 

Figure 5. Photomicrographic appearance of oral Kaposi's sarcoma showing 
spindle shaped cells, vascular slits and extravasated red blood cells. 
(H & E stain, original magnification xlOO) 
6.7.3. Peripheral granuloma 
There were 12 (7.5%) subjects with peripheral granulomas. Eleven (9l.7%) 
were pyogemc and reparative/reactionary granulomas, one (8.7%) was a 
pregnancy-associated tumour. Among subjects with granulomas 5 (4l.7%) were males 
and 7 (58.3%) were females. The most common site of occurrence of peripheral 
granuloma lesions was the maxillary gingiva 4 (33.1%) followed by the hard palate 3 
(25.0%), mandibular gingiva 2 (16.7%), anterior two thirds tongue 2 (16.7%), lower lip 
1 (8.3%) and soft palate 1 (8.3%). 
- ~~-- ----------- 

37 

6.7.4. Haemangioma 
There were 9 (5.6%) subjects with haemangioma. Hemangiom accounted for 5.2% of all 
observed lesions. Most (77.8%) of the subjects were females all aged below 40 years 
and 2 (22.2%) were males aged 40 - 59 years. 
6.7.5. Traumatic ulcer. 
Traumatic ulcerations were diagnosed in 10 (6.3%) of the subjects and constituted 5.8% 
of all the lesions. The distribution was equal among males and females. The cause in 6 
(60%) was repetitive trauma from sharp/ragged teeth and in 4 (40%) ulcers were due to 
ill-fitting removable partial dentures. 
6.7.6. Pseudomembraneous candidiasis 
Pseudomembranous candidiasis was diagnosed in 8 (5%) subjects compnsmg of 3 
(37.5%) males and 5 (62.5%) females. Most of the patients, 7 (87.5% ) with 
pseudomembranous candidiasis had other types of OMLs and of these, 4 had aphthous 
ulcer, one had Kaposi's sarcoma, one had a ranula and another one had depigmentation 
of lips as the second lesion. In this group, 5 (71.4%) subjects were known to have been 
HIV positive. 
6.7.7. Adenocarcinoma 
Adenocarcinoma of minor salivary glands was diagnosed in 8 (5%) of the subjects with 
an equal number of males and females. Only one subject among those with 
adenocarcinoma had education beyond primary school level and only two reported to 
have smoked cigarettes. The hard and soft palates were the commonest sites having been 
affected in 5 (62.5%) subjects. 
	- - - - ---- 	- - -~- 

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38 
6.7.8. Aphthous ulcer 
Recurrent aphthous ulcers (RAU) constituted 7 (4.1%) ofOMLs observed. Among these 
subjects with aphthous ulcers 4 (57.1 %) were HIV positive. Co-existence of aphthous 
and pseudomembraneous candidiasis occurred in 3 (42.9%) of the subjects. The lesions 
were found on the anterior two thirds of the tongue 4 lesions, tongue lateral borders 3, 
posterior 1/3 of the tongue 3 lesions, and upper lip, lower lip buccal mucosa and 
maxillary gingival each with one lesion. 
6.7.9. Geographic tongue. 
Geographic tongue occurred in 6 (3.5%) subjects with equal numbers of males and 
females. Most of the subjects with geographical tongue were aged 10 - 29 years and 
only one (female) was aged 71 years. Geographic tongue was the reason for attendance 
in half of the affected subjects. 
6.7.10. Adenoma. 
Adenoma of the minor salivary glands was diagnosed in 5 (3.1 %) subjects Comprised of 
2 males and 3 females. Three of these subjects were aged 20 - 49 and two aged 70 years 
and above. 
6.7.11. Desquamative cheilitis. 
Desquamative cheilitis was diagnosed in 6 (3.8%) subjects. These lesions were equally 
distributed among males and females with 5 (83.3%) of the subjects aged 10 - 39 years 
and one (female) aged 53 years. Four (66.7%) subjects had attended due to the primary 
complaint related to this condition. 

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6.7.12. Fissured tongue. 
Fissured tongue was recorded in 4 (2.5%) subjects among whom one was a male aged 
25 years and 3 were females aged above 50 years. None of the subjects mentioned 
fissured tongue to have been the primary complaint which necessitated attendance for 
care. 
6.7.13. Oral malignant melanoma 
Malignant melanoma was diagnosed in 2 (l.25%) subjects, both were females one aged 
45 years and the other 73 years. In the first patient the lesion was found in the anterior 
part of the maxillary gingivae and hard palate while in the second it was located in the 
mandibular gingiva. 

Figure 6. Malignant melanoma on the maxillary gingiva and 
hard palate in a 45 years female patient. 

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Figure 7. Photomicrographic appearance of oral malignant melanoma 
showing abundant pigmented and atypical melanocytes. (H&E stain, 
original magnification XIOO). 
6.8. Co-existence of oral mucosal lesions 
Among the 160 study subjects, 12 (7.5%) had two types ofOMLs. The co-existence was 
observed between aphthous ulcers and pseudomembranous candidiasis in 4 patients, 
ranula and angular cheilitis in 2 patients, ranula and pseudomembraneous candidiasis in 
one patient. Other co-existing lesions included adenocarcinoma and desquamative 
cheilitis, Kaposi's sarcoma and pseudomembraneous candidiasis, depigmentation of 
lower lip and pseudomembraneous candidiasis, peripheral granuloma and 
depigmentation of lips; and denture stomatitis and median rhomboid glossitis with each 
pair diagnosed in a single subject. 

41 
6.9. Association of OMLs with HIV/AIDS 
Twenty seven (16.7%) of the subjets of whom 11(40.7%) were males and 16 (59.3%) 
females had highly suggestive HIV oral manifestations and when screened tested 
positive to HIV antibodies. All subjects with oral KS had HIV while 5 out of 8 subjects 
with aphthous ulcers also had HIV. Others with HIV were 4 out of 8 with 
pseudomembraneous candidiasis and 1 out of 4 subjects with angular cheilitis. About 
half, (51.9%) were already on HAART. 
-- - ~- --- ------ --- 

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Table 1. Distribution of the study population according to age and sex 		
Age group 		Sex 		Total 		
	Male 		Female 				
	N 	0/0 	N 	0/0 	N 	0/0. 	
0-9 	5 	55.6 	4 	44.4 	9 	5.6 	
10 -19 	7 	58.3 	5 	41.7 	12 	7.5 	
20-29 	14 	45.2 	17 	54.8 	31 	19.4 	
30-39 	11 	42.3 	15 	57.7 	26 	16.3 	
40-49 	8 	40.0 	12 	60.0 	20 	12.5 	
50-59 	11 	47.8 	12 	52.2 	23 	14.4 	
60-69 	8 	34.8 	15 	65.2 	23 	14.4 	
70+ 	3 	18.8 	13 	81.3 	16 	10.0 	
Total 	67 	41.9 	93 	58.1 	160 	100.0 	
• Column percents. 							
X2 = 6.521, p= 0.48 							
) 							

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Table 2. Sociodemograpic characteristics of the study population. 		
Characteristics 		Male 	Female 	Total 		P value 	
	N 	% 	N 	% 	N 	0/0· 		
Education level: 								
No formal education 	5 	17.9 	23 	82.1 	28 	17.5 		
Primary education 	41 	42.3 	56 	57.7 	97 	60.6 	0.001 	
Secondary education 	12 	52.2 	11 	47.8 	23 	14.4 		
Tertiary education 	5 	100.0 	0 	0.0 	5 	3.1 		
Children below 								
school-age 	4 	57.1 	3 	42.9 	7 	4.4 		
Marital status: 								
Single 	22 	57.1 	16 	42.9 	35 	23.8 		
Married 	32 	38.1 	52 	61.9 	84 	52.5 	0.050 	
Widowed 	3 	16.7 	15 	83.3 	18 	11.3 		
Divorced 	1 	25.0 	3 	75.0 	4 	2.5 		
Cohabiting 	1 	50.0 	1 	50.0 	2 	1.3 		
Below 14 years 	8 	58.8 	6 	41.2 	14 	8.8 		
Occupation: 								
Peasant 	11 	21.6 	40 	78.4 	51 	31.9 		
Pet trading 	16 	51.6 	15 	48.4 	31 	19.4 		
Business 	4 	80.0 		20.0 	5 	3.1 	0.001 	
Employed 	14 	56.0 	11 	44.0 	25 	15.6 		
Self employed 	7 	70.0 	3 	30.0 	10 	6.3 		
House wife 	0 	0.0 	10 	100.0 	10 	6.3 		
Not applicable 1 	15 	53.6 	13 	46.4 	28 	17.5 		
Key: • Column percent 								
1 = below 18 years and schooling and above 75 years were subjects. 		
- - ----------- 

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Table 3. Major presenting symptoms 		
Presenting symptoms 	N 	%1 	
Swelling 	83 	51.8 	
Irritation 	32 	20.0 	
Ulceration 	86 	53.8 	
Pain 	90 	56.3 	
Bleeding 	7 	4.4 	
Discolouration 	8 	5.0 	
Key: 	1 = Multiple responses were allowed 		

Table 4. Categories of OMLs and their proportions. 			
Category of OMLs 	Out of total OMLs 	Malignant OMLs 	
	N 	0/0 	N 	0/0 	
White / red OMLs 	24 	14.0 	0 	0 	
Oral ulcerations 	64 	37.2 	34 	53.1 	
Oral mucosal swellings 	34 	17.2 	8 	23.5 	
Pigmented OMLs 	37 	17.8 	21 	56.8 	
Tongue lesions 	13 	7.6 	0 	0 	
TotalOMLs 	172 	100 	63 	36.6 	
~- ------- -.- -------- 

45 
Table 5. Distribution of subjects with malignant OMLs according to age and 
sex 

Age group 	Male 		Female 	Total 	
(years) 	N 	% 	N 	0/0 	N 	% 	
0-9 	0 	0.0 	0 	100.0 	0 	0.0 	
10 - 19 	0 	0.0 	1 	100.0 	1 	1.6 	
20-29 	2 	25.0 	6 	75.0 	8 	12.7 	
30-39 	5 	45.5 	6 	54.5 	11 	17.4 	
40-49 	3 	30.0 	7 	70.0 	10 	15.9 	
50- 59 	3 	50.0 	3 	50.0 	6 	9.5 	
60-69 	6 	37.5 	10 	62.5 	16 	25.4 	
70+ 	3 	27.3 	8 	72.7 	11 	17.5 	
Total 	22 	34.9 	41 	65.1 	63 	100.0 	
-- ----- ----- ------- 

46 

Table 6: Distribution of subjects with squamous cell carcinoma by age and sex 		
Age group 		Sex 			Total 		
	Male 		Female 				
	N 	% 	N 	% 	N 	0/0- 	
0-9 	0 	0.0 	0 	0.0 	0 	0.0 	
10 - 19 	0 	0.0 	1 	100.0 	1 	2.9 	
20-29 	0 	0.0 	0 	0.0 	0 	0.0 	
30-39 	1 	25.0 	3 	75.0 	4 	11.8 	
40 -49 	1 	33.3 	2 	66.7 	3 	8.8 	
50- 59 	2 	50.0 	2 	50.0 	4 	11.8 	
60-69 	4 	28.6 	10 	71.4 	14 	41.2 	
70+ 	3 	37.5 	5 	62.5 	8 	23.5 	
Total 	11 	32.4 	23 	67.6 	34 	100.0 	
Key: - Column percent 
	- - 	-----~- .. - .---~--.--- 

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Table 7. Distribution of study subjects with oral Kaposi's sarcoma according to age 	
and sex 							
Age group 		Sex 			Total 		
	Male 		Female 				
N 	% 	N 	% 	N 	%* 	
0-9 	0 	0.0 	0 	0.0 	0 	0.0 	
10 - 19 	0 	0.0 	0 	0.0 	0 	0.0 	
20-29 	1 	14.3 	6 	85.7 	7 	36.8 	
30-39 	3 	50.0 	3 	50.0 	6 	31.6 	
40-49 	1 	25.0 	3 	75.0 	4 	21.1 	
50-59 	0 	0.0 	0 	0.0 	0 	0.0 	
60-69 	2 	100.0 	0 	0.0 	2 	10.5 	
70+ 	0 	0.0 	0 	0.0 	0 	0.0 	
Total 	7 	36.8 	12 	63.2 	19 	100.0 	
Key: * Column percent 							

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7. Discussion 
This study was done with the aim of determining the occurrence and 
clinico-pathological presentation of OMLs among patients presenting for treatment in 
the Oral Surgery department of the MNH. It is the first study in Tanzania that attempted 
to characterize the clinico-pathological features of OMLs. It provided an insight on the 
extent of the burden of OMLs among the highly selected group of population, which 
constituted patients who presented for treatment in the department during the study 
period of 8 months. The findings of this study may assist in improving the care of 
patients suffering from OMLs. 
7.1. Age and sex distribution 
In this study, OMLs were found to occur in a wide range of ages (1 to 86 years). This is 
in agreement with observations by other authors 15,44. The highest frequency of 
occurrence of OMLs was observed in the age group 20 - 29 years and the peak 
incidence of OMLs in the 20 - 39-year age group. This could indicate that at these ages 
people care about their health and so are more aware of OMLs; and are more likely to 
seek treatment. In this study there were few (13.1 %) subjects aged below 20 years while 
on the other hand slightly over half 82 (51.3%) were aged 40 years and above. 
Generally, the trend showed that the occurrence of most of the OMLs tends to increase 
with increasing age of the subjects which was similar to findings in previous 
studiesI6,32,41. Malignant lesions like oral see were more commonly found in subjects 
aged 40 years and above, which could have been explained by the fact that these people 

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»; 

49 
had been exposed to risk factors for relatively longer periods before the occurrence of 
the lesions. Most studies have not been able to document statistically significant 
differences in the prevalences of OMLs among males and females 15-20. In this study, 
generally more females were affected by OMLs than males although this was not 
statistically significant (p=0.42). The predominance of females can be explained by the 
fact that there were more female patients who presented for treatment in the department 
of oral surgery at MNH during the time of this study. Also it could be due to the reason 
that females care more about their health compared to males. Majority of OMLs being 
painless and males being busy with social and economic activities they may not attend 
for treatment and hence the smaller number of male subjects. 
Oral SCC, KS and haemangioma predominantly manifested more in females than 
males. This is contrary to the Neville and Day's (2002) 8 and Cawson and Odell's (1998) 
76 reports which documented SCC and Kaposi's sarcoma to have occurred more in males 
than females. However, this study was in agreement with that of Mumcu et al. (2004) 
who found more females with haemangioma compared to males 44. SCC has been 
	D.J~~{> 	7 
documented by others to occur more in males than females 8,9 while. this study 
documented the contrary. 
- - ------~- 

50 
7.2. Associated risk factors 
Considering individual lesions, in this study oral SCC was found most often among 
subjects from the upcountry rural compared to the urban areas. This difference was 
found to be statistically significant (p<O.OOl). Since it is possible that some patients 
came from up country and stayed with their relatives in the city while seeking medical 
care, the number of patients from up country rural may be even higher than that reported. 
Majority (56.3%) of the subjects had a maximum level of primary education and 
possibly with no employment which could lead to an assumption that OMLs affected 
subjects with low socioeconomic status (who were mostly peasants and small scale 
traders) more often than those with a higher status. Very few of the subjects reported to 
have worked in hazardous occupational conditions and none were working in areas with 
mist/acidic fumes, in the textile or tobacco processing factories. In Tanzania peasants 
are engaged in subsistence farming which may not pose much of the occupational risks. 
However, the risk of prolonged exposure to the sun which might lead to lip carcinoma 
was a high possibility because most of the subjects such as peasants and pet traders had 
out-door occupations. Nevertheless, this study could not find any association between 
the different types of OMLs and the occupation of the subjects. 
Tobacco usage in various forms, alcohol consumption and betel quid/nuts chewing have 
been identified as potential risk factors for the development of OMLs 8,47,97. However, in 
the present study there were relatively few subjects (14%) who either smoked or had 
	~ 	--- ----- ~- 

	.. -"-------- 	- ._--"" - ------ ... " 	-- 	- - 	-- 	- 
51 
smoked tobacco in their lives. This study showed that while tobacco smoking has been 
documented as being a risk factor for the development of OMLs there may exist an 
interplay with other factors. The majority of smokers were males but they had fewer 
OMLs compared to females among whom only a few were smokers. In Tanzania, 
females use tobacco in the form of snuff and this has been revealed in this study that all 
snuff dippers were females. Alcohol drinking was reported by a significant proportion 
(47.5%) of subjects. None of the subjects had used betel quid or areca-nuts and the 
possible reason is that this study managed to recruit only one subject of Asian origin. In 
Tanzania people of Asian origin are known to be the common users of these two 
products. 
7.3. Overall prevalence 
The findings of 4.6% prevalence of OMLs in this study corresponds with those ofIkeda 
et al. (1995) in Cambodia and Ikeda et al. (1991) in Japan who registered a prevalence 
of 4.9% and 5.2% respectively 19,21. However, this prevalence is lower than those of 
most population based studies 15-17. Most OMLs studies recruited adult subjects 16,18,20,21 
and only a few included subjects aged 15 years 17,19. The inclusion of children in the 
present study, therefore, might have influenced the low prevalence observed. The 
variations in prevalence of OMLs depends on many factors including the geographical 
location, ethnicity, habits and practices, age and sex distribution of the population 
studied. Lack of knowledge on OMLs on the part of the patients and health care workers 
at primary centres might have led to non-referral of some of the cases of OMLs, a fact 
	- - 	--~---=~----~------------- 

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52 
which might have lowered the prevalence. The study revealed that majority (56.3%) of 
the subjects with OMLs presented to hospital primarily for relief of pain. Although some 
of these lesions do present without symptoms, infection may cause some of them to 
become painful and hence the reason for presenting to hospital. This was true for 
ulcerative lesions like SCC. 
7.4. Mucosal lesions diagnosed, types and categories. 
This study included both adults and children of all ages unlike most other studies which 
dealt with either adults 14 -22, children 28-32, the elderly 33-36 separately or a special group 
of people at risk 52,54 . In this study 34 types of OMLs were observed. This supports the 
fact that OMLs form a broad spectrum ranging from those which needed urgent 
measures to those needing observation only. The number of types of OML observed in 
this study was more than that observed by Kovac-Kavcic et al. (2000) who observed 25 
types among adults 20 but lower than that observed by Bouquot (1986) who observed 64 
types 15 • 
l- 
The first 12 lesions in order of frequency constituted about three quarters of the total 
number of lesions seen in this study. This corresponds with findings of some previous 
prevalence studies 15,17,18 meaning that although there are many types of OMLs, a good 
number of them occur with very low frequencies. Bouquot (1986) for example, found 
that the first 30 commonest lesions constituted 93.3% of the total lesions in 64 diagnoses 
~5. In 7.5% of the subjects there was existence of more than one lesion in one individual, 
-~------- 

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53 
which suggests that there is a possibility of exposure to more than one risk factor. 
However, this could also have occurred just as a coincidence. Generally, out of all the 
OMLs seen in this study 36.6% were malignant, the majority (>50%) belonged to 
pigmented and ulcerative categories. This underscores the importance of a careful and 
thorough examination whenever the clinician encounters pigmented and ulcerative 
lesions in the orofacial region. 
The proportion of subjects with oral see in this study was high [19.8%] compared to 
that found in population and hospital based studies in the USA, Sweden, Cambodia, 
Malaysia and Thailand 15,17-19,97. Some previous OML studies did not register any 
seeI4,20. The high proportion of subjects with see in this study is most possibly due to 
the fact that this study was done at the national referral hospital which is the only centre 
in the country where patients with oral see and other complicated conditions are 
referred to for appropriate management. 
About two thirds (64.7%) of the subjects with oral see were aged 60 years and above. 
This corresponds to previous reports which also showed advanced age among patients 
suffering from oral see 8,97,99. This may be explained by the fact that exposure to risk 
factors should be persistent and for long periods of time for cancer to develop. The only 
subject below 30 years of age with squamous cell carcinoma was a female aged 12 
years. Although it is rarely found in young individuals, oral see has been found to 
occur in children as young as 3 years 100. A previous study done in the same setting as 
this one reported the youngest patient with oral see to have been 13 years 101. 

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54 
The risk of oral cancer among tobacco smokers and alcohol drinkers is well documented 
8,47,99,102. In this study, 27% of the subjects with oral see were tobacco smokers, 29% 
used snuff and 71 % consumed alcohol. This may seem to be a clear indication that 
tobacco and alcohol could be the key risk factors for the development of oral sec. 
There is evidence for synergism between alcohol and tobacco smoking in causation of 
oral cancer 8,103-105. One of the reasons behind this fact is that penetration of tobacco 
carcinogens across the oral mucosa is enhanced in the presence of ethanol so that greater 
quantities of tobacco carcinogens are present locally in the tissues 104. In this study there 
was a considerable proportion of subjects who had oral see but were non-smokers and 
non-drinkers. This may be an indication of the existence of other risk factors as 
documented in the literature 106-110. 
Almost all (94%) of the patients with oral see presented with clinical stage IV lesions. 
Similar findings were reported by Mumena 101. This shows that delays in reporting to 
hospital by patients suffering from oral see is a serious problem, which underscores the 
need for concerted efforts in the health sector to educate the society on the importance of 
early reporting that shall lead to early diagnosis and management. 
Treatment of oral see depends on the stage of the disease. Stage I oral see may be 
treatable by surgery alone but stages II and III require radiotherapy prior to or after 
surgery with an intention for cure. Stage IV oral see is palliatively managed by 
chemotherapy/radiotherapy and sometimes combined with extensive surgery depending 
on the extent of the tumour and condition of the patients 47,99,103. However, radiotherapy 

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55 
is usually accompanied by several complications including mucositis, xerostomia, 
cervical caries and osteoradionecrosis, conditions which severely affect the quality of 
life ofpatients47,99,lo3. 
Kaposi's sarcoma (KS) was the second most prevalent OML observed in this study. This 
is in contrast to other studies where no KS was observed among the OMLs 15-22. In this 
study, majority ofKS patients were females contrary to other studies which found males 
more affected 111-113. Most of the subjects with KS were aged 20 - 39 years which 
corresponds with the peak age of patients infected with HIV 114. Another study 
conducted in the same setting as this one sighted KS as having been the most prevalent 
and most important pathognomonic feature to HIV infection 115. Results in this study 
revealed that all subjects who had KS were infected with HIV. The findings were similar 
to other studies which found KS to have been associated with HIV infection 111-113. KS 
was present even before the AIDS epidemic in the form of classic, endemic and 
iatrogenic types which are not related to HIV. Following HIV/ AIDS epidemic KS cases 
increased and these were mainly ofthe HIV-associated KS type 103. Occurrence ofKS in 
HIV negative people has been documented in the literature 116-118. One study done in 
Tanzania documented that out of77 patients with KS, 66(85.7%) were HIV positive and 
11(14.3%) were HIV negative. Among HIV positive individuals the male to female 
ration was 1.5:1 but all HIV-seronegative KS patients were males 116. 
In this study, a considerable proportion (42%) of the subjects with KS was already on 
HAART. A study previously done in the same hospital involving HIV positive patients 

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56 
documented a high number of KS cases among HIV positive patients who were not on 
HAART compared to those on this medication 119. Studies have documented a reduction 
in the incidence of other oral manifestations including KS among HIV positive subjects 
during the HAART era compared to the era before 120,121. 
It is interesting to note that this study registered oral malignant melanoma in two 
subjects whereby in the first patient the lesion was located in the anterior maxillary 
gingivae and palate (Fig. 8) and the second patient in mandibular gingivae. Both patients 
were females aged above 40 years. Oral malignant melanoma is rare but a very 
aggressive disease. It was not found in most of the studies even in those which recruited 
very large samples 15,17. Its aggressiveness, rapid growth and poor survival rate might 
explain why it is unlikely to be found in such population studies. The site of oral 
malignant melanoma in one subject was in line with documented findings that this lesion 
is common in the maxillary gingivae and hard palate anteriorly 50 • In the second case the 
lesion was located in the mandibular gingivae, however, which is a rare location. 
Treatment of malignant melanoma requires wide excision. When it occurs intraorally it 
poses a great challenge regarding management. 
7.5. Other lesions with relatively high frequencies 
The prevalence of clinically detected recurrent aphthous ulcers (RAU) in this study was 
0.2% which was lower than that obtained by most authors. Axell (1976) in a Swedish 
population registered 2.0%, Micheelis et al. (1999) registered 1.4% with RAU lesions 

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57 
and 18% with history of RAU 17,39. In the study by Zain et al.(1997) RAU was not 
among the prevalent lesions observed 18. RAU is one of the most common diseases 
affecting the oral mucosa and despite its painful affliction it is transient and it clears 
spontaneously within a few days 4,122. That may explain why few subjects with this 
condition attended for care at this tertiary health facility. 
After oral KS, haem angioma was the second most commonly encountered pigmented 
OML (22.3%). This lesion was most often found in rather young individuals which is 
consistent with the fact that haemangioma is congenital and presents in young ages. In 
the current study the prevalence of haem angioma (0.26%) was higher than that obtained 
by Ikeda et al.(1991) who registered 0.1 % 21. Considering that haemangioma is not a 
painful lesion and occurs insidiously it is likely that there are many people with 
haemangioma who do not present to hospital. Most of the patients with haemangioma in 
this country present to hospital when the lesion is big or when there is bleeding and/or 
ulceration. 
Peripheral granuloma featured in this study as one among the most prevalent lesions and 
the most probable explanation was related to the incidental finding of poor oral hygiene 
among the subjects. It was not the objective of this study but sharp edged and carious 
teeth in association with calculus and plaque were observed. Traumatic ulceration 
observed also to a large extent were related to sharp edged teeth (most likely as a result 
of dental caries) and also ill-fitting removable dentures. 

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58 

Geographical tongue and fissured tongue were some of the major tongue lesions 

encountered in this study. The prevalence of geographical tongue (0.17%) observed was 

lower than that observed by Bouquot (1986) 3.1%, Axell (1976) 8.45% and Kovac- 

Kavcic et al (2000) 2.2% but higher than that of Ikeda et al. (1991) <0.1% 15,17,20,21. 

Fissured tongue was also recorded in low prevalence compared with most of the 

previous studies 15,17,20 and the co-existence of geographical and fissured tongue was not 

observed as was seen by some previous authors 20,123. In this study, although there were 

no enough cases, the general trend did not contradict other authors who found that 

geographical tongue occurred at relatively young ages but the occurrence of fissured 

	. 	d wi h . 	. 	f h . divid 1 93 123 
tongue mcrease WIt mcreasmg age 0 t em IVI ua s ' . 

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8. CONCLUSIONS 
From the findings of this study, it can be concluded that: 
•	Large proportion of malignant OMLs was observed in this study. 
•	Among subjects with OMLs, oral see was the most common lesion and causing 
significant morbidity. 
•	KS was the second most common oral mucosal lesion observed whereby all 
patients with KS were HIV positive. 
•	The lower lip was the most commonly affected site by OMLs followed by hard 
palate. 
•	The age group most affected by OMLs was 20 -29 years while oral see and KS 
affected mostly subjects aged above 60 and 20 - 49 years respectively. 
•	Most patients with OMLs reported late for treatment as exemplified by see and 
this is mainly caused by lack of knowledge and awareness ofOMLs. 

-, 

60 
9. LIMITATIONS OF THE STUDY 

• 

The duration of the study was short and this caused this study to have relatively 
fewer cases and limited types of oral mucosal lesions. Considering that some of 
OMLs are rarely found, large sample and/or extended study duration would have 
been required. 

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61 
10. RECOMMENDATIONS 
There is a need to carry out a comprehensive study to determine the prevalence 
of OMLs in the Tanzanian general population. 
Emphasis should be given that in every examination of the oral cavity the 
clinician should search for the presence ofOMLs despite of the primary 
complaint of the patient, this will help in early detection of OMLs. 
The interplay of other risk factors for the development of OMLs apart from 
tobacco and alcohol need to be studied in detail among the Tanzanian 
population. 
There is a need to raise the awareness of the population at large on the 
importance of early health seeking behaviour as this will improve the early 
detection and management of malignant OMLs especially see. 
The Ministry of Health and Social Welfare should prepare a guideline on the 
management of OMLs and encourage clinicians at health facilities to help in 
early detection and referral (where necessary) of cases ofOMLs. 
•	Intensification of oral health care for people living with HIV/AIDS should be 
• 
• 
• 
• 
• 
done as this will have paramount effect on OMLs among these patients and 
hence improve their quality of life. 

•••••• • •......... --------------------~l 
62 
11. REFERENCES 
1. Yeatts D, Burn JC. Common oral mucosal lesions in adults. American Family 
	€ 	Physician Dee, 1991. Available at: http://www.findarticles.com/p/ articles 
(Accessed on 26/02/06). 
2. Marsland DW, Wood M, Mayo F. Content of family practice. Part I: Rank of order 
, 
of diagnoses by frequency. Part II: Diagnoses by diseases category and age/sex 
distribution. J Fam Pract 1975;3:37-68. 
3. Cawson RA, Langdon JD, Eveson JW (eds). White, red and pigmented lesions of the 
	1> 	oral mucosa. In: Surgical pathology of the mouth and the jaws. I st edition 1996. 
London, Elsevier. PP 166-188. 
4. Greenberg MS. Ulcerative, vesicular and bullous lesions. In: Lynch MA, Brightman 

I 
!) 

	5. 	
e) 		
\ ·f 	6. 	
(: 		
	7. 	
c?1 		
J 		
	8. 	

VJ, Greenberg MS. (eds). Burket's Oral Medicine: Diagnosis and treatment. 9th 
edition, 2001. Philedephia. Lippincott-Raven. PP 11- 50. 
WHO: Guide to epidemiology and diagnosis of oral mucosal diseases and 
conditions. Community Dent Oral Epidemiol 1980;8: 1-26. 
Axell T. The oral mucosa as a mirror of general health or disease. Scand J Dent Res. 
1992; 1 00:9-16. 
Neinberg MA, Insler MS, Campen RB. Mucocutaneous features of autoimmune 
blistering diseases. Oral Surg Oral Med Oral Pathol Oral Radiol & Endod 1997;84: 
517-534. 
Neville BW, Day TA. Oral cancer and precancerous lesions. CA Cancer J Clin 2002; 
52:195-215. 

'. 
63 
9. Pindborg JJ, Murti PR, Bhonsle RB, Gupta PC, Daftary DK, Mehta FS. Oral 
e) 	submucous fibrosis as a precancerous condition. Scand J Dent Res. 1984;92 :224-9. 
10. Frame JW. The management of oral premalignant lesions. Br J Oral Maxillofac Surg 
e) 1992;30:71. 
11. Clearinghouse EC. On Oral problems related to HIV infection and WHO 
Collaborating Centre on oral manifestation of immunodeficiency virus: 
Classification and diagnostic criteria for oral lesions in HIV infection. J Oral Pathol 
I 
Med 1993 ;22 :289-91. 
\ 
12. Ranganathan K, Reddy BVR, Kumarasamy N, Solomon S, Viswanathan R, Johnson 
N W. Oral lesions and conditions associated with human immunodeficiency virus. 
Oral Dis 2000;6:152-157. 
13. Eyeson JD, Wamakulasuriya KA, Johnson NW. Prevalence and incidence of 
oral lesions - the changing scene. Oral Dis 2000;6:267-273. 
shapeType75fBehindDocument1pWrapPolygonVertices8;6;(21499,0);(18485,0);(18485,19242);(0,19242);(0,21497);(21499,21497)posrelh0posrelv0pib
14. Lin HC, Corbet EF, Lo EC. Oral mucosal lesions in adult Chinese. J Dent Res. 
2001;80:1486 - 1490. 
, 15. Bouqout JE. Common oral lesions found during a mass screening examination. J 
e \ Americ Dent Assoc. 1986;112:50-57. 
16. Shulman JD, Miles B, Francisco R. The prevalence of oral mucosal lesions in U.S 
adults: Data from the Third National Health and Nutrition Examination Survey, 
1988 -1994. J Am Dent Assoc, 2004;135:1279-1286. 
17. Axell T. A prevalence of oral mucosal lesions in an adult Swedish population. 
\ 

e 
) 
Thesis. Odontol Revy 1976;27: suppl.(36). 

64 
18. Zain RB, Ikeda N, Razak lA, Axell T, Majid ZA, Gupta PC, Yaacob M. A national 

\ 
\ 
\ 
20. 
19\ 
) 
21. 
22. 

epidemiological survey of oral mucosal in Malaysia. Community Dent Oral 
Epidemiol. 1997;25:377-383. 
19. Ikeda N, Handa Y, Khim SP, Durward C, Axell T, Mizuno T, Fukano H, Kawai T. 
Prevalence study of oral mucosal lesions in selected Cambodian population. 
Community Dent Oral Epidemiol. 1995;23:49-54. 
Kovac- Kavcic M, Skaleric U. The prevalence of oral mucosal lesions in a population 
in Ljubljana, Slovenia. J Oral Pathol Med 2000;29:331-335. 
Ikeda N, Ishii T, Lida S, and Kawai T. Epidemiological study of oral leukoplakia 
based on mass screening for oral mucosal diseases in a selected Japanese population. 
Community Dent Oral EpidemiolI991;19:160-163. 
Macigo FG, Maniki DL, Guthua SW. Prevalence of oral mucosal lesions in a 
Kenyan population with special reference to oral leukoplakia. East Afr Med J. 1995; 
72:778-782. 

, 23. Y ong TB, Rimm EB, D' Alessio DJ. Cross-sectional study of recurrent herpes 
	9) 	labialis: Prevalence and risk factors. Am J Epidemiol 1988;127:612-625. 
.•. 24. Axell T. Occurance of leukoplakia and some other white lesions among 20333 
	€J 	adult Swedish people. Community Dent Oral Epidemiol. 1987;15:46-51. 
25. Axell T, Runquist 1. Oral lichen planus - a demographic study. Community Dent 
e\ 
	) 	Oral Epidemiol1987;15:52-56. 
26. Banoczy J, Rigo 0, Albrecht M. Prevalence study of tongue lesions in a Hungarian 
, 
	C?J 	population. Community Dent Oral Epidemiol1993;21:224-226. 

Community Dent Oral Epidemiol. 1987;15:309-313. 
shapeType75fBehindDocument1pWrapPolygonVertices8;4;(21500,0);(0,0);(0,21484);(21500,21484)posrelh0posrelv0pib

65 
27. Darwazeh AMG, Pillai K. Prevalence of tongue lesions in 1,013 Jordanian dental 
	C) 	outpatients. Community Dent Oral Epidemiol 1993;21 :323-324. 
, 28. Rioboo-Crespo MR, Planells-del PP, Rioboo-Garcia R. Epidemiology of the most 
common oral mucosal diseases in children. Med Oral Patol Oral Cir Bucal. 
2005; 1 0:376-387 
, 29. Kleinman DV, Swango P A, Pindborg JJ. Epidemiology of oral mucosal lesions in 
e ~ United States schoolchildren: 1986-87. Community Dent Oral Epidemiol. 1994; 22: 
243-253 . 
... 30. Skinner RL, Davenport WD, Weir JC, Carr RF. A survey of biopsed oral lesions in 
S paediatric dental patients. Pediatr Dent J. 1986;8:163-167. 
, 31. Arendrorf TM, van Der Ross R. Oral soft tissue lesions in a black pre-school African 
ej population. Community Dent Oral Epidemiol. 1996;24:296-297. 
32. Bessa CFN, Santos PJB, Aquiar MCF, do Carmo MAV. Prevalence of oral 
mucosal alterations in children from ° to 12 years old. J Oral Pathol Med. 
2004;33: 1722. 
33. Fleishman R, Peles DB, Pisanti S. Oral mucosal lesions among elderly in Israel. J 
e ) Dent Res. 1997;76: 1277-1286. 
34. Pindborg JJ, Glenert U, Andreasen JO. Holmstrup P, Schiodt M, Hansen HJ. 
Condition of oral mucosa in 478 inhabitants in Danish old age home. Dan Dent J. 
1985;89:223-227. 
35. Vigild M. Oral mucosal lesions among institutionalized elderly in Denmark. 
, 
ej 

shapeType75fBehindDocument1pWrapPolygonVertices8;4;(21498,0);(0,0);(0,21493);(21498,21493)posrelh0posrelv0pib

66 
36. Corbet EF, Holmogren CJ, Phillipsen HP. Oral mucosal lesions in 65-74-year-old 
	'E) 	Hong Kong Chinese. Community Dent Oral Epidemiol 1994;22:392-395. 
37. Salonen L, Axell T, Hellden L. Occurrence of oral mucosal lesions, the influence of 
tobacco habits and an estimate of treatment time in an adult Swedish population. J 
Oral Pathol Med 1990;19: 170-176. 
38. Pearson N, Croucher R, Marcenes W, O'Farrell M. Prevalence of oral lesions among 
	t J 	a sample of Bangladeshi medical care users aged 40 years and over living in Tower 
Hamlets, UK. Int Dent J 2001; 51:30-34. 
\ 39. Micheelis W, Reich E. The Third German Oral Health Study (DMS III), 
e Institute of German Dentists (IDZ), Deutschen Ante - Verlag, Koln, 1999. At: 
http://www.whocollab.odmah.se/euro/germany/ data/germanymucos. html. (Accessed 
on 26.02.2006). 
40. Espinoza I, Rojas R, Aranda W, Gamonal J. Prevalence of oral mucosal lesions in 
! 
~J elderly people in Santiago, Chile. J Oral Pathol Med. 2003;32:571-575. 
41. Roberto RG, Merchant R, Borges SA, Aldape BC, Gutierrez-Robledo LM. 
e y Prevalence of oral mucosal lesions in older people from three Mexican communities. 
From; http://iadr.con{ex.com/iadr/2003SanAntonitechprogram/abstract 27374.htm 
(Accessed on 7.3.06). 
42. Campisi G, Margiotta V. Oral mucosal lesions and risk habits among men in an 
	e J 	Italian study population. J Oral Pathol Med 2001 ;30:22-28. 

shapeType75fBehindDocument1pWrapPolygonVertices8;4;(21500,0);(0,0);(0,21462);(21500,21462)posrelh0posrelv0pib

67 
43. do Santos PJB, Bessa CFN, de Aguiar MCF, Carmo MAV. Cross-sectional 
study of oral mucosal conditions among a central Amazonian Indian community. 
Brazil. J Oral Pathol Med. 2004;33:7-12. 
44. Mumcu G, Cimilli H, Sur H, Hayran 0, Atalay T. Prevalence and distribution of oral 
	\: ) 	lesions: a cross-sectional study in Turkey. Oral Dis. 2004; II : 81 -87. 
45. Hand JS, Whitehill JM. The prevalence of oral mucosal lesions in elderly 
population. J Am Dent Assoc. 1986;112:73-76. 
46. Mikkonen M, Nyyssonen V, Paunio I, Rajala M. Prevalence of oral mucosal lesions 
associated with wearing removable dentures in Finnish adults. Community Dent 
Oral Epidemiol. 1984;12: 191-194. 
\ 47. Epstein J. Oral cancer. In: Lynch MA, Brightman VJ, Greenberg MS.(eds). Burket's 
	t..? 	Oral medicine. 9th edition. Philadelphia, J. B. Lippincott Co. 2001. PP 203-239. 
48. Vianna MI, Santana VS, Loomis D. Occupational exposures to acid mists and gases 
I 
-p 
\.., \ and ulcerative lesions of the oral mucosa. Am J Ind Med. 2004;45:238-245. 
49. Systemic and local cause of pigmentation. At; 
( http://www.thejcdp.com/isssue015/cicek/06cicek.shtml (Accessed on 16.03.06). 
50. Hicks MJ, Flaitz CM. Oral mucosal melanoma: epidemiology and pathobiology. 
	J 	OraIOncoI2000;36:152-169. 
51. Oral effects of tobacco abuse. At: 
nttp://www.maxillofacialcenter.comiTobaccoEfJects. html. (Accessed on 03/03/06). 

68 
e,(52. Prout MN, Sidari IN, Witzburg RA, Grillone GA, Vaughan CWo Head and neck 
cancer screening among 4611 tobacco users older than forty years. Otolaryngol 
Head Neck Surg 1977;116:201-208. 
53. Sankaranarayanan R, Duffy SW, Padmakumary G , Day NE and Nair MK. Risk 
factors for cancer of the buccal and labial mucosa in Kerala, southern India. J 
Epidemiol Community Health, 1990;44:286-292. 
54. Harris CK, Warnakulasuriya KAAS, Cooper DJ, Peters TJ, Gelbier S. Prevalence of 
oral mucosal lesions in alcohol misusers in south London. J Oral Pathol Med. 

2004;33:253-259. 
55. Andersson G, Axell T, and Larsson A. Clinical classification of Swedish snuff 
dippers lesions supported by histology. J. Oral Pathol. Med. 1991 ;20:253-257. 

. 56. Mornstad H, Axell T, and Sundstrom B. Clinical picture of snuff dipper's lesion in 
E{ 
	I 	Swedes. Community Dent. Oral Epidemiol. 1989; 17 :97 -101. 
57. Hirsch JM, Heyden G, and Thilander H. A clinical, histomorphological and 
histochemical study of snuff-induced lesions of varying severity. J. Oral Pathol. 
1982;11 :387-398. 
58. Andersson G, Axell T, and Curvall M. Reduction in nicotine intake and oral mucosal 
	r J 	changes among users of Swedish oral moist snuff after switching to a low-nicotine 
product. J. Oral Pathol Med. 1995;24:244-250. 

shapeType75fBehindDocument1pWrapPolygonVertices8;4;(21498,0);(0,0);(0,21495);(21498,21495)posrelh0posrelv0pib

-, 

69 
59. Larsson A, Axell T, and Andersson G. Reversibility of snuff dippers lesion in 
Sweedish moist snuff users: A clinical and histologic follow-up study. 1. Oral 
Pathol. Med. 1991 ;20:258-264. 
60. Rodu B, Jansson C. Smokeless tobacco and oral cancer: A review of the risk and 
	t:.::>\ 	determinants. Crit Rev Oral BioI Med 2004;15:252-263. 
61. Tomar SL, Winn DM, Swango PA, Giovino GA, Kleinman DV. Oral mucosal 
smokeless tobacco lesions among adolescents in the United States. J Dent Res 1997; 
76:1277-1286. 
, 62. Tomar SL. Snuff use and smoking in U.S. men: implications for harm reduction. Am 
e ) J Prey Med 2002; 23:143-149. 
63. Zain RB, Gupta PC, Warnakulasuriya S, Shrestha P, Ikeda N, Axell T. Oral lesions 
e \ associated with betel quid and tobacco chewing habits. Oral Dis 1997;3:204-205. 
) 
64. Johnson NW, Ramasinghe AW, Warnakulasuriya KA. Potentially malignant lesions 
and conditions of mouth and oropharynx: natural history cellular and molecular 
markers of risk. Eur J Cancer Prevo 1993; 2(suppl2):31-51. 
\ 65. Boring CC, Squires TS, Tong T. Cancer Statistics, 1993. Californian J 
C j Clinical Cancer 1993;43:7-26. 
66. Park BZ, Kohn WG, Malvitz DM. Preventing and controlling oral and pharyngeal 
eJ 	cancer - recommendations from a national strategic planning conference. Morbidity 
& Mortality Weekly report. 1998;47:1-12. 
" 67. Parkin SM, Laara E, Muir CS. Estimates of the worlwide frequency of sixteen major 
e) cancers. Int J Cancer 1988;41:184-197. 

shapeType75fBehindDocument1pWrapPolygonVertices8;4;(21499,0);(0,0);(0,21488);(21499,21488)posrelh0posrelv0pib

, 68. Raubenheimer EJ, De Villiers PIA. Clinical manifestations of oral pre cancer and 

e) 

cancer. J Dent Assoc S Afric.1989; 11-14. 

69. Nair UJ, Friesen M, Richard I, MacClennan R, Thomas S, Bartsch H. Effect oflime 

composition on the formation of reactive oxygen species from the areca nut extract 

in vitro. Carcinogenesis 1990; 11 :2145-2148. 

transformation. A follow-up study of 257 patients. Cancer 1984;53 :563-568. 
shapeType75fBehindDocument1pWrapPolygonVertices8;6;(21498,0);(18991,0);(18991,18346);(0,18346);(0,21499);(21498,21499)posrelh0posrelv0pib
, 70. Waterhouse J, Muir C, and Correa P. Cancer incidence in five continents. 1976. 
	C:j 	Lyon, IARC Scientific Publications. 

\ 71. American Cancer Society. Cancer facts and figures 2002. Atlanta, GA: American 
	\ 	Cancer Society; 2002. 
72. Kramer IR, Lucas RB, Pindborg, JJ. WHO Collaborating Centre for Oral 

Precancerous Lesions. Definition of leukoplakia and related lesions: An aid to 

studies on oral precancer. Oral Surg Oral Med Oral PathoI1978;46:518-539. 

73. Axell T, Pindborg JJ, Smith CJ, van der Waal 1. Oral white lesions with special 
	t>j 	reference to precancerous and tobacco-related lesions: conclusions of an 
international symposium held in Uppsala, Sweden, May 18-21 1994. J Oral Pathol 

Med 1996;25:49-54. 

r 74. Silverman S Jr, Gorsky M, Lozada F. Oral leukoplakia and malignant 
tj 

	75. Leukoplakia 	At: 
f V http://www.maxillofacialcenter.com/BondBook/mucosa/leukoplakia. html. (Acessed 

on 03/03/200). 

shapeType75fBehindDocument1pWrapPolygonVertices8;4;(21498,0);(0,0);(0,21500);(21498,21500)posrelh0posrelv0pib

", 

71 
76. Cawson RA and Odell EW (eds). Diseases of the oral mucosa. In: Essentials of oral 
k pathology and oral medicine. 6th edition. 1999. London. Churchill Livingston. 
PP 170-237. 
77. Mashburg A, Samit AM. Early detection, diagnosis and management of oral and 
C
or 
oropharyngeal cancer. CA Cancer J Clin 1989;39:67-88. 
78. Eversole LR. Lichen planus. Erythroplakia. Leukoplakia. Squamous cell carcinoma. 
In: Millard HD, Mason DK (eds). 1988 World Workshop on Oral Medicine. 
Chicago: Year Book Publishers; 1989. PP 60-65, 99-122. 

79. Silverman S Jr. Oral lichen planus: A potentially premalignant lesion. J Oral 
Maxillofac Surg 2000;58:1286-88. 
80. Viral Infections of the Mouth. At: www.emedicine.com. (Accessed on 3/3/2006) 
81. Kolokotronis A, Doumas S. Herpes simplex virus infection, with particular reference 

e)	to the progression and complications of primary herpetic gingivostomatitis. Clin 
Microbiol Infect 2006;12:202-211. 
82. Epidemiology of Herpes Simplex Viruses infection. 
At: http://virology-online.com/viruses/HSV3.htm. (Accessed on 12/3/06) 
83. Becker TM, Magder L, Harrison HR, Stewart JA, Humphrey DD, Hauler J and 
Nahmias AJ. Epidemiology of infection with the human herpesviruses in Navajo 
children. Amer J Epidemiol. 988;127:1071-1078. 
, 84. Lowhagen G, Bonde E, Ericksson B, Nordin P. Self-reported Herpes labialis in a 
e.	J Swedish population. Scand J Infectious Dis 2002;349:664-667. 

m

shapeType75fBehindDocument1pWrapPolygonVertices8;6;(21498,0);(18660,0);(18660,20432);(0,20432);(0,21499);(21498,21499)posrelh0posrelv0pib
72 
85. Diaz-Guzman L, Castellanos J L. Lesions of the oral mucosa: Epidemiological study 
y( of7,297 patients. Rev ADM 1991;48:75-80. At: 
www.maxillofacialcenter.com/epid/diazguzman.html (Accessed on 4/3/2006) 
el 86. Aphthous ulcers. www.emedicine.com (Accessed on 12/3/06) 
87. Ship I 1. Epidemiologic aspect of recurrent aphthous ulcerations. Oral Surg Oral 

Med Oral Pathol 1972:33:406-409. 
88. Bickle KM, Roark TR, Hsu S. Autoimmune bullous dermatoses: Review. J Americ 
e ) 	Fam Physician 2002;65:1861-1970. 
89.	Brightman VJ. Red and white lesions of the oral mucosa. In: Lynch MA, Brightman 
VJ, Greenberg MS. (eds). Burket's Oral Medicine: Diagnosis and treatnment. 9th 
edition, 2001. Philedephia. Lippincott-Raven. PP 51-120. 
90. Kauzman A, Pavone M, Blanas N, Bradley G. Pigmented lesion of the oral cavity: 
e \ review, differential diagnosis and case presentations. J Can Dent Assoc 
2004;70:683-693. 
) 
91.	Perlmuutter S, Tal H. Repigmentation of gingival following surgical Injury. J 
Periodontol 1986;57:48-50. 
92. Steigmann S. Treatment of melanin-pigmented gingival and oral mucosa by Co2 
laser. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000;90:14-15. 

93.	Brightman VJ. Diseases of the tongue. In: Lynch MA, Brightman VJ, Greenberg 
MS. (eds). Burket's Oral Medicine: Diagnosis and treatment. 9th edition, 2001. 
Philedephia. Lippincott-Raven. PP 241-300. 

73 
'. 
94. Shulman JD. Prevalence of oral mucosal lesions in children and youths in the USA. 
@..J 	lnt J Paediatr Dent 2005;15:89-97. 
95. Yarom N, Cantony U, Gorsky M. Prevalence of fissured tongue, geographic tongue 
shapeType75fBehindDocument1pWrapPolygonVertices8;6;(21499,0);(18586,0);(18586,19980);(0,19980);(0,21499);(21499,21499)posrelh0posrelv0pib
and median rhomboid glossitis among Israeli adults of different ethnic origins. 
DermatoI2004;209:88-94. 
96. Roed-Petersen B, Renstrup G. A topographical classification of oral mucosa suitable 
for electronic data processing: its application to 560 leukoplakias. Acta Odontol 
Scand. 1969; 27:681-695. 
97. 
Axell T, Zain RB, Siwamongstham P, Tantiniran D, Thampipit J. Prevlence of 
oral soft tissue lesions in out-patients at two Malaysian and Thai dental schools. 
Community Dent Oral Epidemiol. 1990; 18 :95-99. 
" 98. 
Parkin DM, Pisan P, Ferlay J. Estimates of the worldwide incidence of eighteen 
e\ 
j 
major cancers. lnt J cancer 1998;54:594-606. 
99. 
Cawson. RA, Langdon JD, Eveson JW (eds). Epithelial tumours and cancer of 
the mouth. In: Surgical pathology ofthe mouth and jaws. Oxford: Wright, 1996; 
190-214. 
100. 
Guan XF, Li WR, Wang YX, Ge SF, Li JL, Lan XJ, Zhong BM. The clinical 
analysis of oral squamous cell carcinoma under age of 40 years old. 
Shanghai Kou Qiang Yi Xue. 1996;5:189-191. 
101. 
Mumena CH. Clinico-pathological features of oral squamous cell carcinoma and 
relation to conventional prognostic parameters and nucleolar organizer regions. 
Dissertation. University ofDar es Salaam 2005. 

shapeType75fBehindDocument1pWrapPolygonVertices8;4;(21498,0);(0,0);(0,21492);(21498,21492)posrelh0posrelv0pib
74 
102. Rosenquist K, Wennerberg J, Schildt EB, Bladstrom A, Hansson BG, 
Andersson G. Use of Swedish moist snuff, smoking and alcohol consumption 
in the aetiology of oral and oropharyngeal squamous cell carcinoma. A 
population-based case-control study in southern Sweden. Acta Otolaryngol 
2005;125:991-998. 

103. 
104. 
105. 
106. 

Regezi JA, Scuibba JJ, Jordan JCK (eds). Ulcerative conditions. In: Oral 
Pathology: Clinical pathologic correlations. 4th Ed. Saunders. 2003. PP 23 -77. 
Du X, Squier CA, Kremer MJ, Wertz PW. Penetration ofN- 
nitrosonornicotine (NNN) across oral mucosa in the presence of ethanol and 
nicotine. J Oral Pathol Med 2000;29:80-85. 
Boyles P, Macfarlane GJ, Maisonneuve P, Zheng T, Scully C, Tedesco B. 
Epidemiology of mouth cancer in 1989: a review. J R Soc Med 
1990;83:724-730. 
Rosenquist K, Wennerberg J, Schildt EB, Bladstrom A, Hansson BG, 
Andersson G. Oral status, oral infections and some lifestyle factors as risk 

fJ 
factors for oral and oropharyngeal squamous cell carcinoma. A population-based 

107. 

case-control study in southern Sweden. 2005;125:1327-1336. 
Llewellyn CD, Johnson NW, Warnakulasuriya KA. Risk factors for 
squamous cell carcinoma of the oral cavity in young people - a 

comprehensive literature review. Oral OncoI2001;37:401~18. 
108.	McGregor GI, Davis N, Robi RE. Squamous cell carcinoma of the tongue and 
	G~ 	lower cavity in patients under 40 years of age. Am J Surg 1983;146:88-92. 

shapeType75fBehindDocument1pWrapPolygonVertices8;8;(21499,0);(0,0);(0,17916);(12122,17916);(12122,21493);(12535,21493);(12535,17916);(21499,17916)posrelh0posrelv0pib
	•... 	. .. 

109. Koch WM, Lango M, Sewell D, et al. Head and neck cancer in nonsmokers: 
e 	a distinct clinical and molecular entity. Laryngoscope 1999;109:1544-51. 

110. Scully C, Wrd-Booth RP. Detection and treatment of early cancer of oral 

111. 

cavity. Crit Rev Oncol HematoI1995;21:63-65. 
Ziegler JL, Newton R, Katongole-Mbiddle E, Mbulataiye S, De Cock K 

	e 	Wabinga H et al. Risk factors for Kaposi's sarcoma in HIV-positive subject 

in Uganda. AIDS 1997;11:1619-1626. 

112. Amir H, Kaaya EE, Manji KP, Kwesigabo G, Biberfeld P. Kaposi's 

	e' 	sarcoma before and during a human immunodeficiency virus epidemic in 
Tanzanian children. Pediatr Infect Dis 2001;20:518-521. 

113. Ziegler JL, Katongole-Mbiddle E. Kaposi's sarcoma in childhood: an analysis 
	e 	of 100 cases from Uganda and relationship to HIV infection. Int J Cancer 1996; 

65:200-203. 

C 114. TACAIDS. HIV/AIDS in Tanzania. At: http://www.tanzania.go.tz/hiv aids.html 
(Accessed February, 2007). 

115. Matee MI, Moshy J, Kalyanyama. Oro-facial lesions occurring in HIV-infected 
	~ 	individuals in Dar-es-Salaam. East Afr Med J 1996;73 :813-815. 
	116. 	Wamburu G, Masenga EJ, Moshi EZ, Schmid-Grendelmeier P, KempfW, 

Orfanos CEo HIV -associated and non HIV -associated types of Kaposi's 

sarcoma in an African population in Tanzania. Status of immune suppression 

and HHV-8 seroprevalence. Eur J Dermatol. 2006;16:677-682. 

shapeType75fBehindDocument1pWrapPolygonVertices8;8;(21499,0);(0,0);(0,698);(18652,698);(18652,20800);(0,20800);(0,21499);(21499,21499)posrelh0posrelv0pib

76 
117. Santarelli R, De Marco R, Masala MV, Angeloni A, Uccini S, Pacchiarotti R, 
Montesu MA, Satta R, Cerimele D, Faggioni A, Cottoni F. Direct correlation 
between human herpesvirus-8 seroprevalence and classic Kaposi's sarcoma 
incidence in Northern Sardinia. 1 Med Virol. 2001;65:368-372. 
118. 
Masala MV, Montesu MA, Cottoni F. A rare observation: Kaposi's 
sarcoma in HIV -negative spouses. 1 Eur Acad Dermatol Venerol 
2006;20: 1355-1356. 

Hamza 01M, Matee MIN, Simon ENM, Kikwilu E, Moshi Ml, Mugusi F, Mixk 
FHM, Verweij PE, van der ven lAM. Oral manifestations of HI V infection in 
e ) children and adults receiving highly active anti-retroviral therapy [HAART] in 
Dar es Salaam, Tanzania. BMC Oral Health 2006;6:12 
120. Schmidt-Westhausen AM, Priepke F, Bergmann Fl, Reichart PA. Decline in 
the rate of oral opportunistic infections following introduction of highly active 
antiretroviral therapy. 1 Oral Pathol Med 2000,31 :336-341. 
121. 
Greenspan D, Gange sr, Phelan lA, Navazesh M, Alves ME, MacPhail LA, 
Mulligan R, Greenspan lS. Incidence of oral lesions in HIV -I-infected 
women: reduction with HAART. 1 Dent Res 2004;83:145-150. 
122. 
~ 
Rogers RS. Recurrent aphthous stomatitis: clinical characteristics and 
associated systemic disorders. Semin Cutan Med Surg. 1997; 16:278-283. 
123. 
lainkittivong A, Langlais RP. Geographic Tongue: Clinical characteristics of 188 
(2J 
cases. J Contemp Dent Pract 2005;1 :123-135.