Red lesions of the oral mucosa can be caused by a variety of factors including trauma, infections, inflammatory conditions, and systemic diseases. Erythematous candidiasis presents as erythematous patches or areas on the tongue and palate caused by Candida infections. Lichen planus causes erythematous lesions that may be difficult to distinguish from other conditions like erythema multiforme. Reactive lesions like pyogenic granulomas and peripheral giant cell granulomas develop in response to local irritation or trauma. Geographic tongue appears as migrating erythematous lesions surrounded by white borders on the dorsal tongue.
Fibro-osseous lesions of the jaws
Fibrous dysplasia
Cemento-osseous dysplasia
Focal cemento-osseous dysplasia
Periapical cemento-osseous dysplasia
Florid cemento-osseous dysplasia
Ossifying fibroma
Juvenile aggressive ossifying fibroma
Cherubism
Fibro-osseous lesions (FOL) are characterized by replacement of normal bone architecture by collagen fibers and fibroblasts containing calcified tissue.
They include a wide variety of lesions of developmental, dysplastic and neoplastic origins with clinical and radiographic presentation and behavior.
Because of the histological similarities between diverse diseases, proper diagnosis requires correlation of history, clinical and radiographic findings.Fibrous Dysplasia
2. Reactive (dysplastic lesions arising in the tooth-bearing area (presumably of periodontal origin).
a. Periapical cemento-osseous dysplasia
b. Focal cemento-osseous dysplasia
c. Florid cemento-osseous dysplasia
3. Fibro-osseous neoplasms (widely designated as cementifying fibroma, ossifying fibroma or cemento-ossifying fibroma.Bone dysplasias
a. Fibrous dyspla i. Monostoticii. Polyostotic
iii. Polyostotic with endocrinopathy (McCune-Albright)
iv Osteofibrous dysplasia
b. Osteitis deformansc. Pagetoid heritable bone dysplasias of childhood
d. Segmental odontomaxillary dysplasia
2. Cemento-osseous dysplasias
a. Focal cemento-osseous dysplasia b. Florid cemento-osseous dysplasia
3.Inflammatory/reactive processes
a. Focal sclerosing osteomyelitisb. Diffuse sclerosing osteomyelitis
c. Proliferative periostitis
4. Metabolic Disease: hyperparathyroidism
5. Neoplastic lesions (Ossifying fibromas)
a. Ossifying fibromab. Hyperparathyroidism jaw lesion syndrome
c. Juvenile ossifying fibroma i. Trabecular typeii. Psammomatoid type
d. Gigantiform cementomas
Fibro-osseous lesions of the jaws
Fibrous dysplasia
Cemento-osseous dysplasia
Focal cemento-osseous dysplasia
Periapical cemento-osseous dysplasia
Florid cemento-osseous dysplasia
Ossifying fibroma
Juvenile aggressive ossifying fibroma
Cherubism
Fibro-osseous lesions (FOL) are characterized by replacement of normal bone architecture by collagen fibers and fibroblasts containing calcified tissue.
They include a wide variety of lesions of developmental, dysplastic and neoplastic origins with clinical and radiographic presentation and behavior.
Because of the histological similarities between diverse diseases, proper diagnosis requires correlation of history, clinical and radiographic findings.Fibrous Dysplasia
2. Reactive (dysplastic lesions arising in the tooth-bearing area (presumably of periodontal origin).
a. Periapical cemento-osseous dysplasia
b. Focal cemento-osseous dysplasia
c. Florid cemento-osseous dysplasia
3. Fibro-osseous neoplasms (widely designated as cementifying fibroma, ossifying fibroma or cemento-ossifying fibroma.Bone dysplasias
a. Fibrous dyspla i. Monostoticii. Polyostotic
iii. Polyostotic with endocrinopathy (McCune-Albright)
iv Osteofibrous dysplasia
b. Osteitis deformansc. Pagetoid heritable bone dysplasias of childhood
d. Segmental odontomaxillary dysplasia
2. Cemento-osseous dysplasias
a. Focal cemento-osseous dysplasia b. Florid cemento-osseous dysplasia
3.Inflammatory/reactive processes
a. Focal sclerosing osteomyelitisb. Diffuse sclerosing osteomyelitis
c. Proliferative periostitis
4. Metabolic Disease: hyperparathyroidism
5. Neoplastic lesions (Ossifying fibromas)
a. Ossifying fibromab. Hyperparathyroidism jaw lesion syndrome
c. Juvenile ossifying fibroma i. Trabecular typeii. Psammomatoid type
d. Gigantiform cementomas
The presentation explain white lesions in oral cavity and the classification the demonstrate the etiology, histopathology, diagnosis and treatment for each one.
Dentists play an important role in the diagnosis and management of desquamative gingivitis. The importance of being able to recognise and properly diagnose this condition is accentuated by the fact that a serious and life threatening disease may initially manifest as desquamative gingivitis.
The presentation explain white lesions in oral cavity and the classification the demonstrate the etiology, histopathology, diagnosis and treatment for each one.
Dentists play an important role in the diagnosis and management of desquamative gingivitis. The importance of being able to recognise and properly diagnose this condition is accentuated by the fact that a serious and life threatening disease may initially manifest as desquamative gingivitis.
This PowerPoint presentation demonstrate a useful review of Oral candidiosis, including its different types, clinical presentations, differential diagnosis, and treatment options.
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
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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2. Red lesions are a large, heterogeneous group
of disorders of the oral mucosa.
Traumatic lesions, infections, developmental
anomalies, allergic reactions, immunologically
mediated diseases, premalignant lesions,
malignant neoplasm, and systemic diseases
are included in this group.
3. The red color of the lesions may be due to
thin epithelium,
inflammation,
dilatation of blood vessels or increased
numbers of blood vessels,
extravasation of blood into the oral soft tissues.
13. ERYTHEMATOUS
CANDIDIASIS
Erythematous candidiasis is a relatively
common form of candidiasis, with a high
incidence in HIV-infected patients and rarely in
patients receiving broad-spectrum antibiotics
or steroids.
It may be acute or chronic.
14. Etiology : Smoking , treatment with broad
spectrum antibiotics , steroids
Also known as antibiotic sore mouth, Atrophic
oral candidiasis.
15. Clinical features : Clinically, it is characterized
by erythematous patches or large areas,
usually located on the dorsum of the tongue
and palate.
Not just reflect atrophy but increased
vascularization
Diffuse borders distinguish it from erythroplakia
Palate and dorsum of tongue are the sites
commonly affected.
Burning sensation is a common symptom.
17. MANAGEMENT
Identify the predisposing factor and eliminate it
Proper denture hygiene
Antifungals , topical and systemic
Surgical excision of the lesion
20. DEEP MYCOSIS
Rare in the developed countries, except in HIV
disease and other immunocompromised
persons
Histoplasmosis
Cryptococcosis
Blastomycosis
Paracoccidiomycosis
25. LICHEN PLANUS
Etiology : The etiology of OLP is not known.
Autoreactive T lymphocytes
Stress
Association of OLP with hepatitis C virus
26. LICHEN PLANUS
Erythematous (atrophic) OLP is characterized
by a homogeneous red area.
Present in the buccal mucosa or in the palate,
striae are frequently seen in the periphery.
Some patients may display erythematous OLP
exclusively affecting attached gingiva. This
form of lesion may occur without any papules
or striae and presents as desquamative
gingivitis.
Therefore, erythematous OLP requires a
histopathologic examination in order to arrive
at a correct diagnosis.
27. Erythematous OLP of the gingiva exhibits a
similar clinical presentation as mucous
membrane pemphigoid.
In pemphigoid lesions, the epithelium is easily
detached from the connective tissue by a
probe or a gentle searing force (Nikolsky’s
phenomenon).
A biopsy for routine histology and direct
immunofluorescence are required for an
accurate differential diagnosis.
28. Ulcerating conditions such as erythema
multiforme and adverse reactions to
nonsteroidal antiinflammatory drugs (NSAIDs)
may be difficult to distinguish from ulcerative
OLP.
The former lesions, however, do not typically
appear with reticular or papular elements in
the periphery of the ulcerations.
29. HISTOPATHOLOGIC
FEATURES
A saw-toothed appearance to the rete pegs,
“liquefaction degeneration,” or necrosis of the
basal cell layer;
an eosinophilic band may be seen just
beneath the basement membrane and
represent fibrin covering the lamina propria.
A dense subepithelial band–shaped infiltrate of
lymphocytes and macrophages is also
characteristic of the disease.
31. MANAGEMENT
sub- and supragingival plaque and calculus
removal
steroid gels in prefabricated plastic trays may
be used for 30 minutes at each application to
increase the concentration of steroids in the
gingival tissue.
32.
33. REITER S DISEASE
Reiter s syndrome - Arthritis , urethritis,
mucocutaneous lesions and conjunctivitis
Unknown etiology
Clinical features
Prevalent among adult men, between 20-30
yrs of age
Urethritis may be the first sign of disease
Arthritis is often bilateral and polyarticular
Conjunctivitis is often mild
34. ORAL MANIFESTATIONS
Painless, red, slightly elevated areas with a
white circinate border on the buccal mucosa,
lips and gingiva mistaken for aphthous ulcers
Palatal lesions appear as small bright red
purpuric spots while lesions on the palate
resemble geographic tongue
35. HISTOLOGIC FEATURES
Parakeratosis, acanthosis, neutrophil
infiltration of the epithelium occur
Sometimes microabscess formation similar to
psoriasis occurs
Treatment : disease undergoes spontaneous
regression , antibiotics and corticosteroids are
used.
37. GRAFT VERSUS HOST
DISEASE
The major cause of GVHD is allogeneic
hematopoietic cell transplantation, also an
autologous transplantation may entail GVHD.
In GVHD, it is the transplanted
immunocompetent tissue that attempts to
reject the tissue of the host.
Recognition of alloantigens by donor T
lymphocytes
Interaction between the recipient’s APCs and
the donor’s T lymphocytes
38. Affects the entire GI system, including mouth
and skin and the liver.
Oral lichenoid reactions as part of GVHD may
be seen both in acute and chronic GVHD.
The clinical lichenoid reaction patterns are
indistinguishable from what is seen in patients
with OLP, that is, reticulum, erythema, and
ulcerations, but lichenoid reactions associated
with GVHD are typically associated with a
more widespread involvement of the oral
mucosa
39. The skin lesions often present with pruritic
maculopapular and mobilliform rash, primarily
affecting the palms and soles.
Violaceous scaly papules and plaques may
progress to a generalized erythroderma, bulla
formation, and, in severe cases, a toxic
epidermal necrolysis–like epidermal
desquamation.
40. Diagnosis
The presence of systemic GVHD facilitates the
diagnosis of oral mucosal changes of chronic
oral GVHD.
In some instances, oral mucosa be the primary
or even the only site of chronic GVHD
involvement.
It is not possible to distinguish between OLP
and oral GVHD based on clinical and
histopathologic features.
42. BARTONELLA INFECTION
Bacillary angiomatosis (BA) , also called
epithelioid angiomatosis, is a disease
characterized by unique vascular lesions
caused by infection with small, gram-negative
organisms of the genus Bartonella.
Virtually all patients with this disease are
infected with HIV. BA occurs most frequently in
the later stages of HIV infection.
43. Cutaneous BA is characterised by the
presence of lesions on or under the skin.
papules or nodules which are red, globular
and non-blanching, with a vascular
appearance
a purplish lichenoid plaque
a subcutaneous nodule which may have
ulceration, similar to a bacterial abscess.
44. While cutaneous BA is the most common form
of BA, BA can also affect several other parts of
the body, such as the brain, bone, bone
marrow, lymph nodes, gastrointestinal tract,
respiratory tract, spleen and liver.
Symptoms vary depending on which parts of
the body is affected.
45. The best method for diagnosis of cutaneous
BA remains biopsy with histopathologic study.
Tissue specimens reveal a characteristic
vascular proliferation on routine hematoxylin &
eosin staining, in addition to numerous bacilli
demonstrable by modified silver staining or
electron microscopy.
46. These organisms are not visualized following
staining for fungi or acid-fast mycobacteria;
staining with Brown-Brenn tissue Gram's stain
is also negative, which distinguishes
the Bartonella bacilli from most other small,
gram-negative rods.
49. PYOGENIC GRANULOMA
RESPONSE OF THE TISSUE TO
NONSPECIFIC INFECTION
It is a tumor like growth that is considered an
exaggerated conditioned response to minor
trauma
Also called pregnancy tumor
Etiology : calculus, food materials, and
overhanging dental restoration margins
50. The prevalence of pregnancy epulides
increases toward the end of pregnancy (when
levels of circulating estrogens are highest),
and they tend to shrink after delivery (when
there is a precipitous drop in circulating
estrogens).
This suggests that hormones play a role in the
etiology of the lesion, secondary to an
increase in angiogenic factor expression and a
reduction in the apoptosis of granulation
tissue.
51. Both pyogenic granulomas and pregnancy
epulides may mature and become less
vascular and more collagenous, gradually
converting to fibrous epulides.
52. They are composed of proliferating endothelial
tissue, much of which is canalized into a rich
vascular network with minimal collagenous
support. Neutrophils, as well as chronic
inflammatory cells, are consistently present
throughout the edematous stroma, with
microabscess formation.
Histologically, differentiation from a
hemangioma is important.
53. MANAGEMENT
The existence of these lesions indicates the
need for a periodontal consultation, and
treatment should include the elimination of
subgingival irritants and gingival pockets
throughout the mouth, as well as excision of
the gingival growth.
56. PERIPHERAL GIANT CELL
GRANULOMA
Peripheral giant cell granuloma or the so-
called “giant cell epulis” is the most common
oral giant cell lesion.
It normally presents as a soft tissue purplish-
red nodule consisting of multinucleated giant
cells in a background of mononuclear stromal
cells and extravasated red blood cells.
This lesion probably does not represent a true
neoplasm, but rather may be reactive in
nature, believed to be stimulated by local
irritation or trauma, but the cause is not
certainly known.
57. ETIOLOGY : local irritation due to plaque or
calculus, poor dental restorations, ill fitting
dentures, dental extractions
CLINICAL FEATURES : common in females
Asymptomatic, rapid growth rate , occurs on
gingiva or alveolar process frequently anterior
to molars.
It can be sessile or pedunculated
Dark red, vascular in appearance commonly
exhibits surface ulceration.
58. HISTOLOGIC FEATURES
Non encapsulated mass of tissue composed of a
delicate reticular and fibrillar connective tissue
stroma containing ovoid or spindle shaped young
connective tissue cella and multi nucleated giant
cells.
Capillaries are numerous around the periphery of
the lesion
Foci of hemorrhage with liberation of hemosiderin
pigment
Spicules of newly formed osteoid or bone are
often found scattered through out the vascular
and cellular fibrous lesion.
64. GEOGRAPHIC TONGUE
Geographic tongue, also known as erythema
migrans ,ectopic geographic tongue or
erythema circinata migrans, benign migratory
glossitis, is a common benign hereditary
disorder of unknown etiology that primarily
affects the dorsal surface of the tongue.
clinical features : Rarely, other areas of the
mucosa are also affected.
65. Clinically it is often asymptomatic , patients
may complain of smarting sensation,
tenderness or a burning sensation, particularly
upon eating sour food.
It manifests as circumferentially migrating and
leaves an erythematous area behind,
scattered, flat, irregular red lesions that are
often surrounded by a grey-yellowish
(keratotic) ring.
Sometimes, it occurs in individuals with
psoriasis.
66. Red areas extend, heal and are then replaced
by new lesions in other areas. Geographic
tongue sometimes affects patients with fissured
tongue (lingua plicata).
Diagnosis/Histopathological features :
In the peripheral region of erythema migrans,
characteristic histopathological features are:
hyperkeratosis, acanthosis and elongation of
the epithelial rete ridges.
67. In the red portion of the lesion, localised loss of
filiform papillae is seen with epithelial atrophy
and mild subepithelial T lymphocyte infiltration.
In addition, the epithelial surface is frequently
necrotic, and collections of neutrophils with
formation of microabscesses are observed
within the epithelium. Because these features
are reminiscent of psoriasis, this is called
a psoriasiform mucositis.
68. Differential diagnosis :
The histopathological appearance of mucosal
lesions in psoriasis pustulosa
generalisata and Reiter's syndrome cannot be
distinguished from erythema migrans.
It may also be mistaken for lichen planus.
70. LUPUS ERYTHEMATOSUS
Definition : Lupus erythematosus is a chronic
immunologically mediated disease.
Etiology : Autoimmune. the main feature is the
formation of antibodies to DNA, which may
initiate immune complex reactions, in
particular a vasculitis.
Clinical features : Two main forms of the
disease are recognized: discoid (DLE)
and systemic (SLE). Oral lesions develop in
15–25% of cases in DLE and in 30–45% of
cases in SLE, usually in association with
71. Three subtypes of lupus-specific skin lesions
have been described: acute, subacute, and
chronic.
Acute cutaneous lupus occurs in 30 to 50% of
patients and is classically represented by the
butterfly rash–mask-shaped erythematous
eruption involving the malar areas and bridge
of the nose but typically (as opposed to
dermatomyositis [DM]) sparing nasolabial
folds.
Bullous lupus and localized erythematous
72. Subacute lupus – cutaneous , non indurated
psoriasiform annulay polycyclic lesions that
resolve without scaring , although occasionally
with post inflammatory dyspigmentation
Chronic cutaneous lupus – classic discoid rash
localised or generalised, hypertrophic lupus in
verrucous form, mucosal lupus, lichen planus
overlap
73. The oral lesions are characterized by a well-
defined central atrophic red area surrounded
by a sharp elevated border of
irradiating whitish striae, brush border
appearance.
Telangiectasia, petechiae, edema, erosions,
ulcerations, and white hyperkeratotic plaques
may be seen.
Buccal mucosa, gingiva, and labial mucosa
are the most commonly affected intraoral sites.
Isolated erythematous areas are also
common, especially on the palate.
74. Differential diagnosis : Lichen planus,
geographic glossitis, speckled leukoplakia,
erythroplakia, cicatricial pemphigoid, syphilis.
Treatment : Steroids, Nonsteroidal anti-
inflammatory drugs (nsaids) are frequently used in
SLE for symptomatic relief of arthritis but are of
little benefit in more severe disease.
Cyclosporine, tacrolimus, sirolimus, methotrexate,
and intravenous immunoglobulins have also been
used in SLE. Antimalarials, such as
hydroxychloroquine, are effective in cutaneous
lupus with fewer adverse effects.
75.
76.
77. ERYTHROPLAKIA
Definition : Erythroplakia, or Queyrat
erythroplasia, is a premalignant lesion that
rarely occurs on the oral mucosa.
It is defined as a red patch or plaque that
cannot be classified clinically or pathologically
under any other condition.
Etiology : Unknown ( smoking and alcohol
abuse are important risk factors )
78. Clinical features : It appears as a usually
asymptomatic, fiery red, well demarcated
plaque, with a smooth and velvety surface.
The red lesions may be associated with white
spots or small plaques. The floor of the mouth,
retromolar area, soft palate, and tongue are the
most common sites of involvement.
79. Homogeneous erythroplakia
Erythroplakia interspersed with patches of
leukoplakia
Granular or speckled erythroplakia
Erythroplakia occurs more frequently between
the ages of 50 and 70 years. Over 91% of
erythroplakia s histologically demonstrate
severe dysplasia, carcinoma in situ, or early
invasive squamous-cell carcinoma at the time
of diagnosis.
82. THERMAL BURN
Definition and etiology : Thermal burns to
the oral mucosa are fairly common, usually
due to contact with very hot foods, liquids, or
hot metal objects.
Clinical features : Clinically, the condition
appears as a red, painful erythema that may
undergo desquamation, leaving erosions.
83. The lesions heal spontaneously in about a
week. The diagnosis is made exclusively on
clinical grounds.
Differential diagnosis : Chemical burn,
traumatic lesions, herpes simplex, aphthous
ulcers, drug reactions.
Treatment : No treatment is required.
84. DRUGS AND CHEMICAL BURN
Aspirin tablets/powder
Tooth ache drops containing creosote,
guaiacol, phenol derivatives
Dental medicaments such as chromic acid,
trichloroacetic acid, silver nitrate, beechwood
creosote, eugenol, paraformaldehyde, ticture
of iodine
85. DRUGS
Erythema multiforme – antibiotics like
sulfonamides, tetracyclines, amoxicillin,
ampicillin. Anticonvulsants – phenytoin,
barbiturates
Stevenson johnson syndrome –
acetaminophen and NSAID s
87. AVITAMINOSIS B12
Avitaminosis is any disease caused by
chronic or long-term vitamin deficiency or
caused by a defect in metabolic conversion,
such as tryptophan to niacin. They are
designated by the same letter as the vitamin
Avitaminosis B12 causes pernicious anemia
88. The clinical symptoms are weakness, fatigue,
shortness of breath and neurologic
abnormalities.
The presence of oral signs and symptoms,
include glossitis, angular cheilitis, recurrent
oral ulcer, oral candidiasis, diffuse
erythematous mucositis and pale oral mucosa.
Management is through vitamin supplements
93. PURPURA
Purpura is a condition of red or purple
discolored spots on the skin that do
not blanch on applying pressure.
The spots are caused by bleeding underneath
the skin usually secondary to vasculitis.
They measure 0.3–1 cm (3–10 mm),
whereas petechiae measure less than 3 mm,
and ecchymoses greater than 1 cm
94. Purpura are a common and nonspecific
medical sign.
Platelet disorders (thrombocytopenic purpura)
Primary thrombocytopenic purpura
Secondary thrombocytopenic purpura
Post-transfusion purpura
Vascular disorders (nonthrombocytopenic
purpura)
Microvascular injury, as seen in senile (old age)
purpura, when blood vessels are more easily
damaged
95. Hypertensive states
Deficient vascular support
Vasculitis, as in the case of Henoch-Schönlein
purpura
Coagulation disorders - Disseminated
intravascular coagulation (DIC)
Scurvy (vitamin C deficiency) - defect in
collagen synthesis which results in weakened
capillary walls and cells
98. IDIOPATHIC THROMBOCYTOPENIC
PURPURA
Definition Thrombocytopenic purpura is a
hematological disorder characterized by a
decrease in platelets in the peripheral blood.
Etiology Presumably a nonspecific viral
infection, myelotoxic agents.
99. Clinical features The oral manifestations
consist of red lesions in the form of petechiae,
ecchymoses, or even hematomas, usually
located on the palate and buccal mucosa.
Spontaneous gingival bleeding is a constant
early finding.
Purpuric skin rash, epistaxis, and bleeding
from the gastrointestinal and urinary tract are
common.
100. Laboratory tests Peripheral platelet count,
bone-marrow aspiration, bleeding and clotting
times.
Differential diagnosis Aplastic anemia,
leukemias, polycythemia vera,
agranulocytosis, drug reactions.
Treatment Steroids, platelet transfusions,
cessation of drug treatment if it is drug-related.
102. TELANGECTASIA
Persistent dilatation of small, superficial blood
vessels; rarely inherited
They are red seldom over 5mm in diameter
and blanch readily on digital pressure, which
easily differentiates them from red petechiae.
They may occur as red solitary lesions or
multiple lesions.
103.
104. The uncommon Osler-Weber-Rendu
syndrome (hereditary haemorrhagic
teleangiectasia; HHT) is inherited via an
autosomal dominant trait, however, family
history can be negative.
Clinically, oral and peri-oral telangiectasias are
observed, as well as telangiectasias in the
nose, the gastro-intestinal tract and on the
palms of the hands. They may bleed which
may cause chronic iron-deficiency anaemia.
106. SCLERODERMA
Scleroderma is a rare autoimmune disorder of
blood vessels and connective tissue, which is
divided into a progressive systemic and a
localised form (circumscribed scleroderma).
The disease most commonly affects adult
middle-aged females. In later stages,
development of a mask-like face with restricted
mouth opening (microstomia), telangiectasias,
smooth tongue surface and shortened lingual
frenum.
108. CREST SYNDROME
A relatively mild variant is characterised by
subcutaneous calcification (CREST syndrome:
calcinosis cutis, Raynaud's phenomenon,
esophageal dysfunction, sclerodactyly and
telangiectasia); frequent association with
Sjögren's syndrome.
111. Treatment and prognosis
Osler-Weber-Rendu syndrome: local
haemostasis (cryo-surgery or laser), treatment
of anaemia.
Scleroderma: management is difficult;
enhancement of micro-circulation ,
corticosteroids, in some cases
immunosuppressants. Prognosis is dependent
on type of disease; from favourable to poor
and lethal.
112. ANGIOMA
Developmental vascular malformation
(hamartoma) or benign vascular tumour. Two
types - cavernous and capillary types.
In the oral cavity, the most common
mesenchymal tumour of infancy.
Commonest localisation: tongue, lips, buccal
mucosa.
113. Capillary hemangiomas are further classified into
juvenile , senile , nevus flammeus
Juvenile hemangioma
Most common type of capillary hemangioma
Majority occur in head and neck region shortly
after birth
Period of rapid growth then begin to regress after
about a year
Fully developed hemangioma is elevated,
lobulated, sharply circumscribed, and bright red
They require no treatment.
115. Senile hemangioma
Start appearing in early adulthood, and the
number of lesion increases with age.
The lesions are bright red and vary in dia from
1mm to several mm s.
The larger lesions are soft and dome shaped.
117. Nevus flammeus
Also known as port wine stains, are present at
birth are unilateral and located on face and
neck
Sharply circumscribed and range from small
red macules to large red flat patches that are
blanched by pressure.
Haemangiomatous vascular malformation of
the face related to maxillary division of the
trigeminal nerve (port wine stain) and
involvement of the leptomeninges occur
in Sturge-Weber syndrome
122. ANGIOKERATOMAFABRY S DIASEASE
Angiokeratoma is a benign cutaneous lesion
of capillaries, resulting in small marks of red to
blue color and characterized by
hyperkeratosis.
Angiokeratoma corporis diffusum refers
to Fabry's disease is a rare genetic lysosomal
storage disease, inherited in an X-
linked manner. Fabry disease can cause a
wide range of systemic symptoms. It is a form
of sphingolipidosis, as it involves dysfunctional
metabolism of sphingolipids.
123. Clinical features – dermatological
manifeatations – Angiokeratomas occur
commonly on the thighs, lower abdomen, and
groin)
Anhidrosis (lack of sweating) is a common
symptom, and less
commonly hyperhidrosis (excessive sweating).
Ocular involvement may be present
showing cornea verticillata (also known as
vortex keratopathy), i.e. clouding of the
corneas. This clouding does not affect vision.
127. SQUAMOUS CARCINOMA
The early stage of squamous-cell carcinoma
may present as an asymptomatic, atypical red
patch.
The clinical features are identical to
erythroplakia, erythematous candidiasis, or
contact reactions to dental materials.
In these cases, a biopsy should be taken to
allow a conclusive diagnosis.
128.
129.
130.
131. KAPOSIS SARCOMA
Malignant neoplasm composed of spindle cells
and vascular elements
Occurs in homosexual men affected with AIDS
commonly
Classic , Endemic and epidemic types
Classic or sporadic type – commonly occurs in
older persons of jewish origin, involves the
skin of lower extremities
Oral mucosal involvement is rare in this
132. Endemic form – occurs in native black
population
Epidemic form affects those with HIV and
other immunological disorder
Lesions widely distributed over the skin
Mucosa and lymph nodes are involved and
response to treatment is poor
133. KS can involve any oral site but most
frequently involves the attached mucosa of the
palate, gingiva, and dorsum of the tongue.
Lesions begin as blue purple or red purple flat
discolorations that can progress to tissue
masses that may ulcerate.
The lesions do not blanch with pressure. Initial
lesions are asymptomatic but can cause
discomfort and interfere with speech, denture
use, and eating when lesions progress.
134.
135. The differential diagnosis includes
ecchymosis, vascular lesions, and salivary
gland tumors.
Definitive diagnosis requires biopsy. Because
KS is a multicentric neoplastic disease,
multiple sites of involvement can occur,
including skin, lymph nodes, gastrointestinal
tract, and other organ systems.
136. TREATMENT
Surgical excision, electrocautery and radiation
therapy.
Patients with disseminated disease may be
treated with immunomodulators and single
agent or combination chemotherapy.
137.
138.
139. WEGENER S
GRANULOMATOSIS
Granulomatosis with polyangiitis (GPA),
formerly referred to as Wegener's
granulomatosis (WG), is a systemic disorder
that involves both
granulomatosis and polyangiitis.
It is a form of vasculitis (inflammation of blood
vessels) that affects small- and medium-size
vessels in many organs
Oral cavity: strawberry gingivitis, underlying
bone destruction with loosening of teeth, non-
specific ulcerations throughout oral mucosa
140.
141. MIDLINE LETHAL
GRANULOMA
Lethal midline granuloma is a condition
affecting the nose and palate.
Macroscopically the lesions usually look like
necrotic granulomas and are characterized by
ulceration and destruction of the nose and
paranasal sinuses with erosion of soft tissues,
bone and cartilage of the region.
142. The patients show an aggressive and lethal
course with rapid destruction of the nose and
face (midline), therefore the term “lethal
midline granuloma”.
This disease occurs around the fourth decade
and occurs commonly in males.
143. The major symptoms are nasal stuffiness with
or without nasal discharge.
Oral or nasal ulcer with conjunctivitis may also
occur. Perforation of the nasal septum with
mutilation of the surrounding tissues
eventually occurs.
Morphologically it is characterized by
extensive ulceration of mucosal sites with a
lymphomatous infiltrate that is diffuse, but has
an angiocentric and angiodestructive growth
pattern.
146. DENTURE STOMATITIS
Definition : Denture stomatitis, or denture
sore mouth, is a frequent condition in patients
who wear dentures continuously for extended
times.
Etiology : Mechanical irritation from
dentures, Candida albicans, or a tissue
response to microorganisms living beneath the
dentures.
Also caused by bacteria such as
streptococcus, veillonella, lactobacillus,
prevotella and actinomyces.
147. Clinical features : The condition is
characterized by diffuse erythema, edema, and
sometimes petechiae and white spots that
represent accumulations of candidal hyphae,
almost always located in the denture bearing
area of the maxilla.
The condition is usually asymptomatic. The
diagnosis is based on clinical criteria.
Type I – localised to minor erythematous areas
caused by trauma from denture
148. Type II – affects major part of denture covered
mucosa
Type III – granular mucosa in the central part of
the palate
Differential diagnosis : Allergic contact
stomatitis due to acrylic.
Treatment : Improvement of denture fit, proper
oral hygiene, and topical antimycotics.
150. MEDIAN RHOMBOID GLOSSITIS
Definition : Median rhomboid glossitis is a
rare condition that occurs exclusively on the
dorsum of the tongue.
Etiology : Presumably developmental,
Candida albicans , bacteria may also be
involved.
Clinical features : It presents as a well-
demarcated erythematous rhomboid area,
151. along the midline of the dorsum of the tongue,
immediately anterior to the circumvallate
papillae.
The surface of the lesion may be smooth or
lobulated. Atrophy of filiform papillae.
Differential diagnosis : Candidiasis,
lymphangioma, geographic tongue, syphilis,
hemangioma.
Treatment : No treatment is required.
152. KISSING LESIONS
A concurrent erythematous lesion may be
observed in the palatal mucosa and it is called
kissing lesion.
Management is restricted to a reduction in
predisposing factors.
155. RADIATION MUCOSITIS
Definition and etiology : Oral radiation
mucositis is a side effect of radiation treatment
of head and neck tumors.
Clinical features : The oral lesions are
classified as early and late. Early reactions
may begin at the end of the first week of
radiotherapy, and consist of erythema and
edema of the oral mucosa.
156. Soon after, erosions or ulcers may develop,
covered by a whitish-yellow exudate.
Xerostomia, loss of taste, and burning and pain
during mastication, swallowing, and speech are
common. The diagnosis is made clinically.
157. Differential diagnosis : Mucositis due to
chemotherapy, graft-versushost disease,
erythema multiforme, herpetic stomatitis, lichen
planus.
Treatment : Supportive treatment. Cessation
of the radiation treatment, B-complex vitamins,
and sometimes low doses of steroids are
indicated.
159. POLYCYTHEMIA
Also called erythremia is chronic and
sustained elevation in the number of
erythrocytes and level of hemoglobin.
Primary
secondary
160. Primary – polycythemia vera is a neoplastic
condition of erythropoietic sysyem
Secondary – is a sustained elevation of
erythrocytes and hemoglobin usually resulting
from bone marrow stimulation caused by living
at high altitude or chronic pulmonary disease
such as emphysema
161. The entire oral mucosa of patients with
polycythemia has a deep red or purple color.
Soft palate and gingiva are prone to easy
bleeding and petechial hemorrhages may be
seen on the palate and labial mucosa
Infarcts may occur in the smaller blood vessel
leading to ulcers
164. PLASMA CELL GINGIVITIS
Definition : Plasma-cell gingivitis is a rare and
unique gingival disorder, characterized
histopathologically by a dense chronic
inflammatory infiltration of the lamina propria,
mainly of plasma cells.
Etiology : Unknown. Reactions to local
allergens, chronic infections, and plasma-cell
dyscrasias have been considered as possible
causes.
165. Clinical features : Clinically, both free and
attached gingiva are bright red and edematous,
with a loss of normal stippling. The gingivitis
may be localized or widespread, and is
frequently accompanied by a burning
sensation.
Rarely, similar lesions may be seen on the
tongue and lips.
Ulcers , epithelial sloughing and desquamation
may be present.
Patient may complain of pain, sensitivity and
bleeding of gingiva during brushing.
166. Laboratory tests : patch testing to identify the
allergen, Histopathological and histochemical
examination, immunofluorescence.
Histopathology : parakeratosis , epithelial
hyperplasia , dense infiltrate of plasma cells in
the lamina propria , dilated blood capillaries.
Differential diagnosis : Desquamative
gingivitis, erosive lichen planus,
vesiculobullous disorders.
167. Pubertal or pregnancy induced gingivitis,
plaque associated gingivitis.
Rapid onset - PCS.
Treatment : Remove the allergen if possible.
Pain control, Topical or systemic steroids.
Gingivectomies to recontour lesions that are
long standing and fibrotic.
172. ERYTHEMA MULTIFORME
EM is an acute, self-limited, inflammatory
mucocutaneous disease that manifests on the
skin and often oral mucosa, although other
mucosal surfaces, such as the genitalia, may
also be involved.
173. EM is classified as E M minor if there is less
than 10% of skin involvement and there is
minimal to no mucous membrane involvement,
whereas EM major has more extensive but still
characteristic skin involvement, with the oral
mucosa and other mucous membranes
affected.
Historically, fulminant forms of EM were
labeled Stevens- Johnson syndrome (SJS)
and toxic epidermal necrolysis [TEN (Lyell
disease)].
174. ETIOLOGY
EM is a hypersensitivity reaction, and the most
common inciting factors are infection,
particularly with HSV, or drug reactions to
NSAIDS or anticonvulsants.
Other viral, bacterial, fungal, and protozoal
infections and medications may also play a
role.
175. CLINICAL FEATURES
EM generally affects those between ages 20
and 40 years, with 20% occurring in children.
There is often a prodrome of fever, malaise,
headache, sore throat, rhinorrhea, and cough.
Skin lesions begin as red macules that
become papular, starting primarily in the hands
and moving centripetally toward the trunk in a
symmetric distribution. The most common
sites of involvement are the upper extremities,
face, and neck.
176. The skin lesions may take several forms—
hence the term multiforme - irregular bullae,
erosions, or ulcers surrounded by extensive
areas of inflammation, Severe crusting and
bleeding of the lips are common.
The classic skin lesion consists of a central
blister or necrosis with concentric rings of
variable color around it called typical “target”
or “iris” lesion that is pathognomonic of EM;
variants are called “atypical target” lesions .
177.
178. ORAL MANIFESTATIONS
mild erythema and erosion to painful
ulcerations.
When severe, ulcers may be large and
confluent, causing difficulty in eating, drinking,
and swallowing, and patients with severe EM
may drool blood-tinged saliva.
179.
180. Differential diagnosis : Primary HSV
gingivostomatitis, Autoimmune vesiculobullous
disease such as pemphigus and pemphigoid,
recurrent aphthous ulcers.
Management : systemic or topical analgesics,
corticosteroids, antiviral medication,
azathioprine and dapsone , antimalarials
prevents recurrence.
181. REFERENCES
Peripheral giant cell granuloma Padam
Narayan Tandon, S. K. Gupta,1 Durga Shanker
Gupta, Sunit Kumar Jurel,2 and Abhishek
Saraswat
Oral Manifestations of Vitamin B12 Deficiency:
A Case Report Hélder Antônio Rebelo Pontes,
DDS, MSc, PhD; Nicolau Conte Neto, DDS;
Karen Bechara Ferreira, DDS; Felipe Paiva
Fonseca; Gizelle Monteiro Vallinoto; Flávia
Sirotheau Corrêa Pontes, DDS, MSc, PhD;
Décio dos Santos Pinto Jr, DDS, MSc, PhD
182. Text book of Burket s oral medicine
Text book of Differential Diagnosis of oral and
maxillofacial lesions by Norman K Wood and
Paul W Goaz
Shafer s text book of oral pathology