This document discusses premalignant lesions and conditions of the oral cavity. It begins with an introduction and historical perspective on oral cancer and premalignant disorders. It then covers definitions and classifications of premalignant lesions and conditions. Specifically, it discusses potentially malignant disorders (PMDs), which is the current term used. It covers clinical features, diagnosis, treatment and prognosis of oral leukoplakia, a common premalignant lesion. Histopathological grading of leukoplakia and differential diagnosis are also summarized.
Premalignantlesions and conditions by Dr. Amit T. Suryawanshi, Oral Surgeon,...All Good Things
Hi. This is Dr. Amit T. Suryawanshi. Oral & Maxillofacial surgeon from Pune, India. I am here on slideshare.com to share some of my own presentations presented at various levels in the field of OMFS. Hope this would somehow be helpful to you making your presentations. All the best.
Premalignantlesions and conditions by Dr. Amit T. Suryawanshi, Oral Surgeon,...All Good Things
Hi. This is Dr. Amit T. Suryawanshi. Oral & Maxillofacial surgeon from Pune, India. I am here on slideshare.com to share some of my own presentations presented at various levels in the field of OMFS. Hope this would somehow be helpful to you making your presentations. All the best.
AIDS is a lethal viral infection caused by human immunodeficiency virus (HIV) and is characterized by severe depletion of T4 lymphocytes with associated opportunistic infections.
Oral and perioral lesions are common in patients infected with human immune deficiency virus (HIV), are often the presenting feature, and may predict deterioration in general health and a poor prognosis.
Due to multiple oral conditions and periodontal involvement, periodontists are in a unique position to recognize possible HIV infection in its early stage and to be involved in the oral care of these patients.
This PowerPoint presentation demonstrate a useful review of Oral candidiosis, including its different types, clinical presentations, differential diagnosis, and treatment options.
Cancer of the oral cavity accounts for approximately 3% of all malignancies diagnosed annually in 270,000 patients world-wide. Oral cancer is the 12th most common cancer in women and the 6th in men. Many oral squamous cell carcinomas develop from potentially malignant disorders (PMDs). Lack of awareness about the signs and symptoms of oral PMDs in the general population and even healthcare providers is believed to be responsible for the diagnostic delay of these entities.
Differential diagnosis of white lesions in the form of a combination of various journals.
For easy diagnosis of various white lesions which we usually encounter in our clinics. A diagnosis tree along with various white lesions along with the lesions to which they resemble.
By:
Dr. Sunbul Tabrez
Oral cancer has been identified as Significant publec health threat. So its very important to know how to diagnose which is the first step in the treatment...
Hope you find it beneficial and rich .
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
AIDS is a lethal viral infection caused by human immunodeficiency virus (HIV) and is characterized by severe depletion of T4 lymphocytes with associated opportunistic infections.
Oral and perioral lesions are common in patients infected with human immune deficiency virus (HIV), are often the presenting feature, and may predict deterioration in general health and a poor prognosis.
Due to multiple oral conditions and periodontal involvement, periodontists are in a unique position to recognize possible HIV infection in its early stage and to be involved in the oral care of these patients.
This PowerPoint presentation demonstrate a useful review of Oral candidiosis, including its different types, clinical presentations, differential diagnosis, and treatment options.
Cancer of the oral cavity accounts for approximately 3% of all malignancies diagnosed annually in 270,000 patients world-wide. Oral cancer is the 12th most common cancer in women and the 6th in men. Many oral squamous cell carcinomas develop from potentially malignant disorders (PMDs). Lack of awareness about the signs and symptoms of oral PMDs in the general population and even healthcare providers is believed to be responsible for the diagnostic delay of these entities.
Differential diagnosis of white lesions in the form of a combination of various journals.
For easy diagnosis of various white lesions which we usually encounter in our clinics. A diagnosis tree along with various white lesions along with the lesions to which they resemble.
By:
Dr. Sunbul Tabrez
Oral cancer has been identified as Significant publec health threat. So its very important to know how to diagnose which is the first step in the treatment...
Hope you find it beneficial and rich .
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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2 Case Reports of Gastric Ultrasound
1. Premalignant lesions and
conditions of oral cavity
Dr. Amit T. Suryawanshi
Oral and Maxillofacial Surgeon
Pune, India
Contact details :
Email ID - amitsuryawanshi999@gmail.com
Mobile No - 9405622455
3. Oral cancer constitutes an important entity
in the field of Oral and Maxillofacial surgery . The global
incidence of oral cancer is 5,00,000 cases per year with
mortality of 2,70,000 cases. The incidence of oral cancer
In India is 40 % among all cancer and about 1,00,000
patients suffer from oral cancer in any year.Oral cancer is
responsible for 7% of all cancer deaths in males while it is
3 % in females.
Some oral cancers initiate as a De Novo lesion while
some are preceded by Oral premalignant lesions and
conditions.
Introduction
4. Introduction
Various premalignant lesions,
particularly red lesions(erythroplasias) and some
white lesions (leukoplakias) have a potential for
malignant change. In that, risk of erythroplasias
is exceedingly high.
Practitioners will see many oral white
lesions but few carcinomas. However they must
be able to recognize lesions at particular risk
and several features which help to assess the
likelihood of malignant transformation.
5. The accuracy of such predictions
about premalignant lesions and conditions is
low but the process of identifying “at risk”
lesions is fundamental for diagnosis and
treatment planning.
6. • Currently confusion came up between these two
terminologies and many opinioned that the prefix ‘pre’
quotes that all precancerous lesions become cancer,
whereas studies found this to be untrue.
• Hence it was recommended in WHO workshop of 2005
to abandon the distinctions between precancerous
lesions and conditions and to use the term “Potentially
Malignant Disorders” instead, incorporating both the
terminologies.
7. • The latest WHO monograph on head and
neck tumors (2005) used the term
“Epithelial precursor lesions” and defined it
as “ Altered epithelium with an increased
likelihood for progression to squamous cell
carcinoma”.
• It is also mentioned that word ‘altered’ the
definition means epithelial dysplasia.
8. History
• Oral candidiasis in infants was recognized
first by Hippocrates (400 B.C.)
• The terms premalignant ( pre- preliminary and
malignant-cancerous) lesions and conditions
were coined by Romanian physician Victor
Babeş in1875.
• In 19th century, Trousseus called Oral
Thrush as “ Disease of the diseased”
9. • Plummer-Vinson syndrome is one
manifestation of iron deficiency anaemia and
was first described by Plummer in 1914 and
by Vinson in 1922 under the term ‘hysterical
dysphagia’
• The term leukoplakia was coined by
shwimmer in 1877 & In 1994,it was
classified and by the WHO.
10. • Oral submucous fibrosis was first described
by Joshi and Schwartz among East Indian
Women in 1952.
• Tissue therapy in oral submucous fibrosis ,
as a new method of therapy was introduced
by Filatov in 1933 and later developed in
1953.
11. • In oral submucous fibrosis ,The attendant
trismus is a result of juxta-epithelial
hyalinisation and secondary muscle
involvement .
Muscular degeneration and fibrosis
was first studied by Binnie and Cawson
in 1972.
12. History - Definitions
• A premalignant lesion is “A morphologically altered tissue
in which oral cancer is more likely to occur than in its
apparently normal counterpart”
-WHO workshop 1978
• Premalignant condition is ‘a generalized state associated
with a significantly increased risk of cancer’.-
-WHO workshop 1978
13. • Premalignant condition is defined as by
WHO workshop 2005-
‘It is a group of disorders of varying etiologies, usually
tobacco characterized by mutagen associated, spontaneous
or hereditary alterations or mutations in the genetic material
of oral epithelial cells with or without clinical and
histomorphological alterations that may lead to oral
squamous cell carcinoma transformation.’
15. • “It is a group of disorders of varying etiologies, usually
tobacco characterized by mutagen associated,
spontaneous or hereditary alterations or mutations in
the genetic material of oral epithelial cells with or
without clinical and histomorphologicalalterations that
may lead to oral squamous cell carcinoma
transformation”
(Ref -Oral potentially malignant disorders: Precising the
definition)
- Oral Oncology journal (2012)
PMD (Potentially malignant disorders)
16. NEW CLASSIFICATION FOR ORAL
POTENTIALLY MALIGNANT DISORDERS
SARODE, SARODE, KARMARKAR, TUPKARI
(Ref - Oral Oncology xxx, 2011)
CLASSIFIED OPMD INTO 4 GROUPS:
Group I: Morphologically altered tissue in which external
factor is responsible for the etiology and malignant
transformation.
Group II: Morphologically altered tissue in which chronic
inflammation is responsible for malignant transformation
(chronic inflammation mediated carcinogenesis).
17. Group III: Inherited disorders that do not necessarily alter
the clinical appearance of local tissue but are associated with
a greater than normal risk of PMD or malignant
transformation.
Group IV: No clinically evident lesion but oral cavity is
susceptible to Oral squamous cell carcinoma.
18. Group I: Morphologically altered tissue in which external
factor is responsible for the etiology and malignant
transformation.
1. Habit related
a. Tobacco associated lesions
• Leukoplakia
• Tobacco pouch keratosis
• Stomatitis palatine nicotini
b. Betel nut associated
• Oral submucous fibrosis
c. Sanguinaria-associated keratosis
19. 2. Non-habit related
• Actinic cheilosis
• Chronic candidiasis
Certain strains of Candida have been shown to produce
nitrosamines a chemical carcinogen (external factor) and
hence, candidiasis is included under Group I.
20. Group II: Morphologically altered tissue in which chronic
inflammation is responsible for malignant transformation
(chronic inflammation mediated carcinogenesis).
Group II a. Chronic inflammation caused by internal
derangement.
• 1. Lichen planus
• 2. Discoid lupus erythematosus
21. II b: Chronic inflammation caused by external factors.
1. Chronic mucosal trauma
2. Lichenoid reactions
3. Poor oral hygiene
4. Chronic infections
• Chronic bacterial infections
• Chronic viral infections
• Chronic fungal infections
5. Other pathologies associated with prolonged untreated
chronic inflammation of the oral cavity.
22. • Group III: Inherited disorders that do not necessarily alter
the clinical appearance of local tissue but are associated
with a greater than normal risk of PMD or malignant
transformation.
1. Inherited cancer syndromes
• Xeroderma pigmentosum
• Ataxia telangiectasia
• Fanconi’s anemia
• Li Fraumeni syndrome
24. Group IV: No clinically evident lesion but oral cavity is
susceptible to Oral squamous cell carcinoma.
1. Immunosupression
• AIDS
• Immunosupression therapy (for malignancy or organ
transplant)
2. Alcohol consumption and abuse
3. Nutritional deficiency
• Sideropenic dysphagia
• Deficiency of micronutrients
25. Oral leukoplakia, as defined by the WHO, is
“ A predominantly white lesion of the oral mucosa
that cannot be characterised as any other definable
lesion.”
(Ref – WHO workshop 2012)
J Oral Pathol Med (2012) 36: 575–80
Leukoplakia
26. Etiology -
• The exact etiology is unknown.
• But some predisposing factors can be identified that are
• PREDISPOSING FACTORS ARE BEST REMEMBERED
AS 6 S
Smoking , Spirit , Sharp tooth , Spicy food , Syphilis, Sepsis
27. • A. SMOKING
• B. CHEWING
• Most important causative factor
• Roed-Petersen & co-workers found a strong correlation between
bidi smoking and presence of leukoplakia in the residents of
Bombay. 20% of the smokers in the age group of 60-89yrs had
leukoplakia whereas 5% of non-smokers of the same age group
were affected.
• Pindborg & colleagues pointed out that tobacco produces a
specific effect on the oral mucosa, leading to a characteristic
appearance of pumice stone . Similar lesions are seen in patients
who apply snuff to the labial sulcus
TOBACCO-
28. • Alcohol-Heavy consumption of alcohol is second most
important risk factor, it acts synergistically with tobacco.
• Candida infection-Candida albicans infection (chronic
hyperplastic candidiasis) may play a role in the etiology of
leukoplakia.
• Human papilloma viruses-HSV1, HPV, HHV6, HHV8
(HHV = Human Herpes Viruses)
(HSV = Herpes Simplex Viruses)
(HPV = Human Papilloma Virus)
29. • Syphilis :
Hobaeck, Cooke and Renstrup found that this has a
minor role. There is a higher incidence of leukoplakia
among patients of syphilitic glossitis than non-
syphilitic background.
• Vitamin Deficiency :
Vit A deficiency will cause metaplasia and
keratinization of epithelial structures(particularly
glands
30. • Male predilection
• Mostly occurs in 4th to 7th decade of life.
• Oral leukoplakias are found on the Upper and lower
alveolus(36%) buccal mucosa(22 %) , lips (11%), palate
(11%), floor of mouth (9%), gingiva(8%), Tongue(7%),
retromolar trigone(6%)
(Ref -Oral potentially malignant disorders: Precising the definition)
Otorhinolaryngology clinics –An International journal may-sept. 2009
CLINICAL FEATURES
32. • Leuko means white & Plakia means plaque.( Greek term)
• The term is strictly a clinical one and does not imply a
specific histopathologic tissue alteration.
• It makes the diagnosis dependent not so much on definable
appearances but on the exclusion of other entities that
appear as oral white lesions.
34. HOMOGENOUS-
• Uniform white patch lesion with smooth or
corrugated surface sometimes, slightly raised
mucosa. Usually plaque like, some are smooth,
may be wrinkled or criss-crossed by small crack
or fissure.
• Malignant transformation – 1 to 7%.
• Types –
1. Smooth
2. Furrowed
3. Ulcerative
35. NON-HOMOGENOUS LEUKOPLAKIA
TYPES -
1. Ulcerative or Erosive
2. Verrucous (proliferative verrucous leukoplakia) or
Nodular
3. Speckled (High malignant transformation)
(Ref- WHO workshop 1994)
36. • Ulcerative- Red ulcerative lesion (Atrophic epithelium )
with small white specks or nodules over it.
• Verrucous -Warty surface (white lesion with hyperplastic
surface) or Heaping up of the surface or like a nodule on an
erythematous background. white lesion with a granular
surface is associated with candida.
• Speckled- Mixed red and white patches on an irregular
surface.
37. • Hairy leukoplakia is a condition that is characterised by
irregular white patches on the side of the tongue and
occasionally elsewhere on the tongue or in the mouth.
Etiology -
It is a form of leukoplakia often arises in response to
chronic irritation. Hairy leukoplakia is associated with
Epstein-Barr virus (EBV) and occurs primarily in HIV-
positive individuals.
Hairy leukoplakia
38. Clinical features
• Male predilection
• Most common in 40 – 60 years of age
(Recent studies show higher incidences in young
adults)
It occurs on the lateral
margins of the tongue
often bilaterally. The
lesions are white,
sometimes corrugated
and may be proliferative
to produce a shaggy
carpet like appearance
39. • A clinical staging system for oral leukoplakia
(OL-system) on the lines of TNM staging was
recommended by WHO in 2005 taking the size (L)
and the histopathological features (P) of the lesion
into consideration.
Clinical Staging
40. • Lx: Size not specified.
• L1: Single or multiple lesions together <2 cm.
• L2: Single or multiple lesions together 2-4 cm.
• L3: Single or multiple lesions together >4 cm.
• Px: Epithelial dysplasia not specified.
• P0: No epithelial dysplasia.
• P1: Mild to moderate epithelial dysplasia.
• P2: Severe epithelial dysplasia.
• Stage I: L1 P0.
• Stage II: L2 P0.
• Stage III: L3 P0 or L1/ L2 P1.
• Stage IV: L3 P1 or Lx P2.
Clinical Staging
41. • Leukoplakia is purely a clinical terminology and
histopathologically it is reported as epithelial
dysplasia.
• WHO in 2005 proposed five grades of epithelial
dysplasia based on architectural disturbances and
cytological atypia.
Histopathology
42. HISTOLOGICAL GRADING OF LEUKOPLAKIA
• 1. Squamous Hyperplasia –
• 2. Mild Dysplasia – better prognosis.
• 3. Moderate Dysplasia.
• 4. Severe Dysplasia.
• 5. Carcinoma in-situ – poor prognosis.
• It has been recently proposed to modify the above 5-tier
system into a binary system of ‘high risk’ and ‘low risk’
lesions to improve clinical management of these lesions.
43. Diagnosis
• A provisional diagnosis of leukoplakia is made
when a predominantly white lesion at clinical
examination cannot be clearly diagnosed as any
other disease or disorder of the oral mucosa .
A biopsy is mandatory.
A definitive diagnosis is made when any
aetiological cause other than tobacco/areca nut use
has been excluded and histopathology has not
confirmed any other specific disorder.
45. • The first step in treatment is to arrive at a definitive
histopathologic diagnosis.
• Therefore, a biopsy is mandatory and will guide the
course of treatment. Tissue to be obtained for biopsy,
should be taken from the clinically most "severe" areas
of involvement .
• Multiple biopsies of large or multiple lesions may be
required.
TREATMENT AND PROGNOSIS
46. I . NON-SURGICAL TREATMENT
• Photodynamic Therapy
• Chemoprevention
• L-Ascorbic Acid (Vitamin C)
• α-Tocoferol (Vitamin E)
• Retinoic Acid (Vitamin A)
• Vitamin A derivative, isotretinoin, and 13-cis retinoic acid:
28,500IU per day.
47. • Beta-carotene 150,000 IU of beta-carotene
twice per week for six months.
• Bleomycin-Topical bleomycin in treatment of
oral leukoplakia was used in dosages of
0.5%/day for 12 to 15 days or 1%/day for 14
days.
49. • Chemoprevention may also be useful, but it remains
primarily experimental.
• Isotretinoin (13-cis-retinoic acid, a form of vitamin A)-
alone or in combination with betacarotene has been reported
to reduce or eliminate some leukoplakic lesions in short
term studies.
Chemoprevention
50. • However, to date there is insufficient evidence from well-
designed clinical trials to support the effectiveness of such
medical therapies in treating oral dysplasia or preventing the
progression of oral dysplasia to squamous cell carcinoma.
51. II. Surgical Management
• SURGICAL MANAGEMENT:
FOUR methods are available for the removal of leukoplakia
patches of the oral mucosa
1. Scalpel excision / Stripping
2. Electrocautery
3. Cryotherapy
4. CO2 Laser therapy
52. Scalpel Excision
• The traditional method .
• The area is outlined including few millimetres of normal
tissue. It is incised with scalpel and patch (leukoplakia) is
undermined by scalpel or by blunt dissection to a depth of 2
to 4 mm. This allows leukoplakia to be removed in one
piece. The mucosal defect if small is closed primarily or it
is covered by transported local mucosal flaps. Larger
defects are grafted with split thickness skin graft.
• Advantages –
whole of patch can be taken in one piece for
histopathological examination and in addition no special
equipments are required.
53. • Disadvantages -
• Persistent bleeding, which makes accurate excision
difficult. In the floor of mouth care has to be taken
for submandibular duct and lingual artery.
• There is contraction and scarring resulting in
restricted movement of oral soft tissues.
• The skin grafts when used remains white and masks
any recurrence of leukoplakia.
• Recurrence rate - 20 to 35 %
54. Electrocautery ( Fulguration )
Fulguration with electrocautery appliance is another
treatment of leukoplakia. This procedure requires
local or general anaesthesia. The healing process is
slow and painful.
Procedure -
Here multiple areas of the lesion are pierced with
electrocautery and left to heal.
55. Cryotherapy is a method of superfreezing
tissue in order to destroy it.
Procedure –
• Cryotherapy is done using a cotton swab that has been
dipped into liquid nitrogen or a probe that has liquid
nitrogen flowing through it. The technique involves
freezing the mucosa with the cryoprobe for 1.5 to 2
minutes, then waiting for 2 minutes, followed by further
freezing of 1.5 to 2 minutes. Thicker lesions may require 2
to 3minutes freezing.
Cryotherapy-
56. Advantages -
1. Simple, Painless, out-patient procedure, well tolerated by
patients including the elderly.
2. During the healing phase there is absence of infection and
pain and the wound is cleaner without foul odour.
3. General anaesthesia is not required.
4. There is little scar formation,
5. There is no intra or post operative bleeding and the
procedure may be repeated on several occasions.
57. Disadvantages
1. There is no surgical specimen for histopathological
examination.
2. The zone of tissue elimination is variable resulting
in inaccurate margin of destruction. Post-
operatively there is marked oedema.
3. There is unpleasant delayed necrosis of the treated
area which separates as a slough and it might
stimulate epithelial changes (particularly in cases
of advanced stages of pre-malignant state).
58. • Soko and colleagues found a recurrence rate of 20% in
patients who are treated by cryotherapy .
• Long-term follow-up after removal is extremely important
because recurrences are frequent additional types of
leuloplakias may develop. This is especially true for the
verruciform or granular types, 83% of which recur and
require additional removal or destruction.
59. CO2 Laser Therapy :
• This destroys soft tissue in a unique manner and is ideal
means of removing leukoplakia.
• CO2 laser beam wavelength - 10.6μ
• Well absorbed by water and hence by soft tissues.
• The absorbed energy causes vaporisation of the intra and
extra cellular fluid and destruction of cell membrane. The
cell debris are released and burned in the laser beam,
depositing a carbonised layer on the tissue surfaces.
60. • There are two techniques which are used to remove the
leukoplakia using CO2 laser
1. Excision.
2. Vaporisation
• To excise a patch of leukoplakia, the laser is used to cut
around the margins, which can be held in tissue forceps
while the laser undermines the leukoplakic patch.
• Vaporisation of leukoplakia is by moving the laser beam
back and forward across the surface of lesion. It has the
risk of leaving small bits of abnormal tissue which are
deep under thickly keratinized tissue.
61. Advantages
1. There is excellent visibility and precision when
dissecting through the tissue planes.
2. There is little contraction or scarring.
3. Patients usually feel less pain when compared
with scalpel excision.
62. Disadvantages
1. High cost of equipment.
2. Requires protection of patient’s as well as
surgeon’s eye,
3. There is delayed wound healing.
4. Frame and colleague reported a 20 %
recurrence rate following removal of
leukoplakia by CO2 laser therapy.
64. • This condition was first described by Joshi
(1952) and by Schwatz among East Indian
Women.
• This is an insidious chronic disease affecting
any part of oral cavity including pharynx. It
is considered to be POTETIALLY
MALIGNANT DISORDER .
65. (J.J Pindborg and Sirsat 1966)
“ It is an insidious chronic disease affecting any part of the
oral cavity and sometimes the pharynx. Although
occasionally preceded by or associated with vesicle formation
,it is always associated with juxta-epithelial inflammatory
reaction followed by a fibro-elastic changes of the lamina
propria with epithelial atrophy leading to stiffness of the oral
mucosa and causing trismus and inability to eat.”
DEFINITION
66. • OSMF is a crippling fibrotic disorder seen commonly in
India and Indian subcontinent. Sporadic cases are seen in
Malaysia, Nepal, Thailand and South Vietnam.
• Population between 20 to 40 years of age are most
commonly affected .
• Incidence of OSMF in India is 0.2-0.5% of population.
EPIDEMIOLOGY
67. Etiology of OSMF:
Exact etiology is unknown. The predisposing factors are,
1. Chronic Irritation
- Chilies, Lime, Areca nut, Tobacco.
2. Defective iron metabolism
3. Bacterial Infection
4. Collagen disorder
5. Immunological disorders
7. Genetic disorder.
68. Chronic irritation:-
• Pathogenesis of OSMF lies in the continuous action of mild
irritants.
Chillies:-
• "Capsaicin" an active extract from capsicum.
• The active principle irritants of chillies (Capsicum annum
and Capsicum frutescence) .
69. Areca nut –
It contains,
• ARECOLINE, ARECAIDINE
-Fibroblast proliferation
-Stimulate collagen synthesis
• TANNIN, CATHECHIN-
- Makes collagen fibrils resistant to
collagenase.
70. • The data regarding the sex predilection is conflicting.
Earlier it was thought to be common in females.
• But at present, study ratio shows 2.3: 1=M:F
• Age group - 2nd to 4th decade of life.
CLINICAL FINDINGS
71. Prodromal symptoms
Initial symptoms Later
Burning sensation on eating
spicy food
Blisters on the palate
Ulceration or recurrent
stomatitis
Excessive salivation
Defective gustatory sensation
Dryness of mouth.
Difficulty in opening mouth
Inability to whistle, blow
Difficulty in swallowing
Referred pain to the ear
Changes in tone of the voice
due to vocal cord involvement
Sometimes deafness due to
occlusion of eustachian tubes
72. COMMON SITES INVOLVED-
• Buccal mucosa, faucial pillars, soft palate, lips and hard
palate.
• The fibrous bands in the buccal mucosa run in a vertical
direction, sometimes so marked that the cheeks are almost
immovable.
• In the soft palate the fibrous bands radiate from the
pterygomandibular raphe or the faucial pillars and have a
scar like appearance.
73. • The uvula is markedly involved, shrinks and appears as a
small fibrous bud.
• The faucial pillars become thick, short, and extremely hard.
• The tonsils may be pressed between the fibrosed pillars.
• The lips are often affected and on palpation, a circular band
can be felt around the entire lip mucosa.
• When gingiva is affected, it is fibrotic, blanched and devoid
of its normal stippled appearance.
77. Staging of OSMF:
• Stage I : Stage of stomatitis & vesiculation
• Stage ll : Stage of fibrosis
• Stage III :Stage of sequelae and complication
(Ref -Pindborgh JJ-1989)
78. Stage I : Stomatitis & vesiculation
Stomatitis includes erythmatous mucosa,
vesicles, mucosal ulcers,melanotic mucosal
pigmentation.
79. Stage II: (Fibrosis):-
• There is inability to open mouth completely and stiffness in
mastication. As disease advances there is difficulty in
blowing out cheek & protruding tongue. Sometimes pain in
ear and speech is affected. On examination there in
increasing amount of fibrosis in the submucosa. This
causes blanching of mucosa.
• Lips & checks become stiff & lose their normal resistance.
Shortening & disappearance of uvula in advanced cases.
• Mucosa of floor of mouth show blanching & stiffness
80. Stage III (Sequelae & Complication)
• Patient presents with all the complaints as in stage II. Also
there may be evidence of leukoplakia.
• Changes in mucosa are whitish or brownish black.
• Pindborg et al (1967) found that OSMF was found in 40%
cases of oral cancer than in general population (1.2%).
81. Recent classification for OSMF
- Chandramani More et al 2011
• Clinical staging –
S1 -Stomatitis or blanching of oral mucosa
S2 –Presence of fibrous bands over buccal
mucosa, oropharynx with or without
stomatitis.
S3 - Presence of fibrous bands over buccal
mucosa, oropharynx and any part of oral
cavity with or without stomatitis.
82. • S4 a –
Anyone of above stage with potentially
malignant disorders
Eg- leukoplakia, erythroplakia.
• S4 b –
Anyone of above stage with oral carcinoma
83. Recent classification for OSMF
- Chandramani More et al 2011
Functional staging -
M1- Interincisal mouth opening upto or > 35 mm
M2- Interincisal mouth opening between 25-35 mm
M3 - Interincisal mouth opening between 15-25 mm
M4 - Interincisal mouth opening <15 mm
84. DIAGNOSIS IS BASED ON :
Clinically appreciable blanching and pallor.
Palpable bands and restriction-of mouth opening.
Severe burning sensation of mouth, aggravated by use of
even moderate spicy food.
Biopsy report.
85. Histopathological findings -
• Atrophic Oral epithelium.
• Loss of rete pegs .
• Epithelial atypia may be observed.
• Hyalinization of collagen bundles.
86. MANAGEMENT -
Various modalities of treatment have been tried.
1.Restriction of habits/ Behavioral therapy.
2.Non-surgical therapy.
3.Surgical therapy.
4.Oral Physiotherapy.
87. Restriction of habits/behavioral therapy-
The consumption of pan, betel nut, chillies, spices, &
commercially available, pan masalas, guthkas with or
without tobacco is increasing in India. So people should be
encouraged to stop these habits.
Affected patients should be explained about the disease and
possible malignant potential of OSMF.
Possible irritants should be removed.
Nutritional supplements.
88. NON-SURGICAL THERAPY:-
• Antioxidants
• Intralesional injections of hyaluronidase. Hydrocortisone
• Use of Placentrix 2ml solution at interval of 3 days.
• Topical application -
1. 4% Acetic acid (At PH 6.5) 3 times daily.
2. 5 Fluorouracil
89. Systemic administration of immunomodulators -
• Levamisole 150mg for 3 weeks ,orally
• Dapsone 75 mg O.D for 90 days, orally
90. SURGICAL TREATMENT -
Fibrotomy (scalpel, electrocautery, laser)
Coronoidectomy & Temporalis myotomy
• Extraction of third molars
Reconstruction
(Bilateral nasolabial flaps, Pedicled tongue flaps, Buccal fat pad, Split
thickness skin grafting, Collagen membrane & Temporalis fascia)
(Ref -Oral submucous fibrosis, a new concept in surgical management. Report of
100 cases.J. N. Khanna & N. N. Andrade: IJOMS)
92. ErythroplaSia
• Also known as ERYTHROPLASIA OF QUEYART
• This was first described by Queyart in 1911 as a
lesion occurring on glans-penis.
• It is clinically similar to conditions such as candidiasis,
tuberculosis, histoplasmosis and non-specific
conditions such as denture irritation.
WHO definition :-
• A fiery red patch that cannot be characterized
clinically or pathologically as any other definable
disease.
94. Incidence -
It is more common in males and occurs more frequently
in the 6th and 7th decade of life.
95. Clinical Presentation-
Red, often velvety, well-defined patches.
Most commonly present on
floor of mouth, retromolar
trigone area, lateral tongue.
• Usually asymptomatic.
• May be smooth to nodular.
96. • Homogenous form which appears as a bright red, soft
velvety lesion with straight or scalloped well demarcated
margins, often quite extensive in size, commonly found on
the buccal mucosa and sometimes on the soft palate,
more rarely on the tongue and floor of the mouth.
• Speckled leukoplakia / erythroplakia which is soft, red
lesions that are slightly elevated with an irregular outline
and a granular or fine nodular surface speckled with tiny
white plaques.
98. Treatment-
• The treatment is same as that for invasive carcinoma or
carcinoma-in-situ like surgery, radiation and cauterisation.
• Surgical excision if proven dysplastic/ malignant.
99. Candidiasis
Etiology
• Infection with a fungal organism of the Candida species,
usually Candida albicans.
• Associated with predisposing factors: most commonly,
immunosuppression, diabetes mellitus, antibiotic use, or
xerostomia (due to lack of protective effects of saliva).
100. Clinical Presentation
• Acute (oral thrush)
• Pseudomembranous.
• Painful white plaques representing fungal colonies on
inflamed mucosa.
• Erythematous (acute atrophic): painful red patches caused
by acute Candida overgrowth and subsequent stripping of
those colonies from mucosa.
101. Clinical Presentation-
Chronic
• Atrophic (erythematous): painful red patches; organism difficult to
identify by culture, smear, and biopsy.
• “Denture-sore mouth” : a form of atrophic candidiasis associated with
poorly fitting dentures; mucosa is red and painful on denture-bearing
surface.
• Median rhomboid glossitis: a form of hyperplastic candidiasis seen
on midline dorsum of tongue anterior to circumvallate papillae.
• Perleche: chronic Candida infection of labial commissures; often co-
infected with Staphylococcus aureus.
• Hyperplastic/chronic hyperplastic: a form of hyperkeratosis in which
Candida has been identified; usually buccal mucosa near
commissures; cause and effect not yet proven.
• Syndrome associated: chronic candidiasis may be seen in association
with endocrinopathies.
102.
103. Diagnosis-
Microscopic evaluation of lesion smears
• Potassium hydroxide preparation to demonstrate hyphae
• Periodic acid–Schiff (PAS) stain
• Culture on proper medium (Sabouraud’s, corn meal, or
potato agar)
• Biopsy with PAS, Gomori’s methenamine silver (GMS), or
other fungal stain of microscopic sections
104. • Differential Diagnosis
• Leukoplakia
• Erythroplakia
• Atrophic lichen planus
• Histoplasmosis
• White lesion due to denture irritation
105. Treatment-
• Topical or systemic antifungal agents.
• For immunocompromised patients: routine topical agents
after control of infection is achieved, usually with systemic
azole agents.
• Correction of predisposing factor, if possible.
• Some cases of chronic candidiasis may require prolonged
therapy (weeks to months).
Prognosis-
• Excellent in the immunocompetent host.
106. Topical therapy
• Nystatin oral suspension (100,000 units/mL); rinse 5 mL and swallow
4 times/day
• Clotrimazole (Lotrimin) solution 1%; rinse 5 mL and swallow 4
times/day
Systemic therapy
• Fluconazole (Diflucan) 100 mg #15; 2 tablets on the first day, 1 tablet
days 2–7, 1 tablet every other day for days 8–21
• Ketoconazole (Nizoral) 200 mg #21; 1 tablet every day with breakfast
× 21 d
107. Lichen Planus
Etiology-
• Unknown.
• Autoimmune. T cell–mediated disease targeting basal
keratinocytes.
• Lichenoid changes associated with galvanism, graft-versus-
host disease (GVHD), certain drugs, contact allergens.
108. Incidence -
• Up to 3 to 4% of Indian population has oral lichen planus
• 0.5 to 1% of population has cutaneous lichen planus; 50%
also have oral lesions.
• More common in White females (60%)
• Occurs in 4th to 8th decades of life.
Clinical Presentation-
• Variants: reticular (most common oral form); erosive
(painful); atrophic, papular,(plaque types); bullous (rare)
• Bilateral and often symmetric distribution
• Oral site frequency: buccal mucosa (most frequent), then
tongue, then gingiva, then lips (least frequent)
112. INTRA EPITHELIAL CARCINOMA
This occurs frequently on the skin(Bowen’s disease) but
also on mucous membrane.
Incidence -
• Shafer also found the occurrence as 23% in floor of
the mouth, 22% on the tongue, 20% on the lip.
• It is more common in elderly men.
113. CLINICAL STUDY:
• Shafer found that 45% of the lesions of
carcinoma –in-situ were leukoplakic, 46%
were erythroplakic, 9% were a
combination of leukoplakic and
erythroplakic patches, 13% were ulcerated
lesions, 5% were white ulcerated lesions,
1% were red ulcerated lesions and 11%
didn’t have specific appearance.
115. ACTINIC (SOLAR) KERATOSIS,
ELASTOSIS AND CHELITIS
• Actinic keratosis is also potentially malignant disorder
associated with long term exposure to radiation and may be
found on the vermilion border of the lips as well as other
exposed skin surfaces.
• Clinical features -
• On the skin surfaces and the vermilion border of the lip, the
lesion is crusted and keratotic.
• On the labial mucosa exposed to sun, a white area of
atrophic epithelium develops with underlying scarring of the
lamina propria referred to as elastosis. When this atrophic
tissue abrades or ulcerates, it is called actinic chelitis.
116. Treatment
• 5 flurouracil is found to be effective.
But dysplastic changes in epithelium remains.
So adequate follow-up is required unless
surgical removal is done.
118. Clinical Presentation-
• Usually in men in Western countries and India.
• Mucosal pouch with soft, white, fissured appearance.
• Leathery surface due to chronic tobacco use over many
years.
121. Treatment
• Discontinuation of habit.
• If dysplasia is present, stripping of mucosal site.
Prognosis
• Generally good with tobacco cessation.
• Malignant transformation to squamous cell carcinoma or
verrucous carcinoma occurs but less frequently.
122. DISCOID LUPUS ERYTHEMATOSIS
• WHO has defined the oral lesions of DLE as
“circumscribed, slightly elevated, white patches that
may be surrounded by a (red) telengiectatic halo. A
radiating pattern of very delicate white lines is usually
observed. The oral lesion may or may not be
accompanied by skin lesion.”
• Clinical differentiation from leukoplakia and lichen
planus is difficult. Immunofluorenscent techniques
usually show a good correlation between the clinical
appearance of the oral lesion and their histologic
counterpart.
•
124. SIDEROPENIC DYSPHAGIA (PLUMMER
VINSON SYNDROME)
• Iron deficiency anaemia is one manifestation of
Plummer-Vinson syndrome and was first
described by Plummer in 1914 and by Vinson in
1922 under the term ‘hysterical dysphagia’.
• Iron deficiency anaemia occurs especially in
women.
125. • The clinical features are pale skin and
mucous membrane, spoon shaped nails
(Koilonychia), atrophic glossitis, tongue is
smooth and glazy. It is accompanied by
dysphagia and oesophageal webs.
• Laboratory findings show hypochromic
microcytic anaemia of varying degree.
• The patients respond well to iron therapy
and high protein diet.
126. Recent advances
• Temporalis myofascial flap for reconstruction in OSMF.
• Dr. S. Sankara Narayanan, at the Stem Cell Therapy Unit of
KMC Hospital, Trichy, in Tami Nadu has reportedly
developed a non-surgical form of treatment using Autologous
Bone Marrow Stem Cells-Stem Cell Therapy- to treat OSMF
and to change the malignant potential. The doctor along with
his associates claimed they have successfully treated 3 patients
with OSMF by using this medical technology.
127. Nano particles for oral cancer diagnosis are
more accurate and less invasive to the body. Many
cancer cells have a protein, epidermal growth factor
receptor (EGFR), non cancer cells have much less of this
protein. By attaching gold nano particles to an antibody
for EGFR, researchers have been able to bind the
nanoparticles to the cancer cells which show different
light scattering and absorption spectra than benign cells.
Pathologist can thereafter use these results to identify
malignant cells in biopsy sample.
128. CONCLUSION
Patient presenting with Potentially malignant disorders
should undergo a careful examination to identify any
causative factors, which are best eliminated at the first stage
of the treatment. However, many patients may not have any
obvious causative factor. A biopsy of the lesion is necessary
to demonstrate the histological features of the lesion and
detect any existing invasive carcinoma. Frequent monitoring
of histopathological changes is essential to obtain an accurate
assessment of histological activity of the lesion and to try to
predict its future behavior. The subsequent management of
the patient depends on how “high risk” the lesion is.
129. references
Books -
[1] R.A.Cawson’s essentials of Oral Pathology and Oral
Medicine . 7th Edition
[2] Burkitts Oral Pathology 5th Edition
[3] Shafer, Hine & Levy: A textbook of oral pathology. 4th
edition.
130. Articles –
1. Nanotechnology : A new era in dentistry
JADA 2012
2. Oral potentially malignant disorders: Precising
the definition.
Otorhinolaryngology clinics –An International journal may-sept. 2009
131. 4. Classification of OSMF.
Swati Gupta, Jigar joshi , JIAOMR
5. NEW CLASSIFICATION FOR ORAL POTENTIALLY
MALIGNANT DISORDERS
S. SARODE, SARODE, KARMARKAR, TUPKARI
(Ref - Oral Oncology xxx, 2011)
6. Precancerous lesions of oral cavity.
-Uday pawar, Pankaj C.
Otorhinolaryngology –International Journal 2009.
A provisional diagnosis of leukoplakia is made when a predominantly white lesion at clinical examination cannot be clearly diagnosed as any other disease or disorder of the oral mucosa .
A biopsy is mandatory.
Such lesions as lichen planus , morsicatio (chronic cheek nibbling), tobacco pouch keratosis, nicotine stomatitis, leukoedema and white sponge nevus must be ruled out before a clinical diagnosis of leukoplakia can be made.
5 s – Smoking , spirit , sharp tooth , spicy food , syphilis, SEPSIS.
Other factors are , vitamin deficiency, endocrine disturbances, galvanism and actinic radiation
Higher incidence of leukoplakia
Uniform white patch with smooth surface & slightly raised mucosa. Its usually plaque like but may be wrinkled or criss-crossed by small crack or fissures.
leukoplakia occurring in floor of mouth and ventral surface of tongue is called as Sublingual keratosis .
Anti-retroviral drugs -- Acyclovir , valacicyclovir
Gention violet – dye used for hairy leukoplakia and candidiasis
White sponge nevus - Noted in early life, family history, large areas involved, genital mucosa may be affected - Biopsy not indicated
Acute pseudomembranous candidosis - The membrane can be scraped off leaving an erythematous/raw surface - Swab for culture
Leukoedema - Bilateral on buccal mucosa,it cant be made disappear on stretching.
Lichen planus - other form such as reticular is also associated
Photodynamic therapy (PDT)involves the use of a photoactive dye (photosensitizer) that is activated by exposure to light of a
specific wavelength in the presence of oxygen. The transfer of energy from the activated photosensitizer to available oxygen
results in the formation of toxic oxygen species, such as singlet oxygen and free radicals. These very reactive chemical species
can damage proteins, lipids, nucleic acids, and other cellular Components of lesion. Applications of PDT are growing rapidly
in treatment of oral premalignant and malignant conditions.
Scalpel excision or CO2 laser and elecrocautery used to remove leukoplakia will have specimen for histopathological examination whereas this is not possible using cryotherapy. Recurrences rate is about 20% regardless of the method.
The procedure is done in the doctor's office. It usually takes less than a minute.
When fibrosis involves pharynx-
40 mg of triamcinolone acetonide is injected submucosally into faucial pillars, retro-molar area and buccal mucosa. On average 150 to 200 mgs of corticosteroids are injected in divided doses at 10 days interval for a period of 2 to 3 months.
The human placental tissue extract has growth stimulation effects and also development of immune system. This contains water soluble factors which are growth stimulant for keratinocytes. It increases hummoral immune mechanism by increase in IgM levelsslecific for bacterial toxins
It contains nucleotides, vitamins , amino acids, fatty acids and trace elements.
Vitamins present are vitamin E, B1, B2, pantothenic acid, B6, nicotinic acid, biotin, P aminobenzoic acid, folic acid, B12, choline inositol.
4% acetic acid has capability of solubilizing cross-linked molecules in collagen and it causes collagenolysis
5 fluorouracil is immunomodulator
Temporalis myotomy and coronoidectomy are performed in case of degenerative changes in temporalis muscle.
White elevated hair like fungal growth on buccal mucosa
Reticular form is most common and consists of slightly elevated, fine, whitish lines (wickham’s striae) that produce either a lace like lesion, a pattern of fine radiating lines or annular lesions.
Malignant transformation in these lesions are considered to be around 10%.