Oral lichen planus (OLP) is a chronic inflammatory disease that causes bilateral papules, striations or plaques in the mouth. It predominantly affects adults over 40 years old and has a female to male ratio of 1.4:1. There are several types of OLP lesions including reticular, erosive, and plaque-like lesions. A T-cell mediated immune response triggers keratinocyte apoptosis in OLP lesions. Histological examination of biopsy samples is used to diagnose and differentiate OLP from other conditions. Treatment aims to reduce symptoms and involves topical corticosteroids, systemic steroids, or immunosuppressants like tacrolimus ointment.
“Oral lichen planus is a chronic immunologic inflammatory mucocutaneous disorder commonly found in oral cavity, where it appears as white, reticular, plaque or erosive lesions.”
“Oral lichen planus is a chronic immunologic inflammatory mucocutaneous disorder commonly found in oral cavity, where it appears as white, reticular, plaque or erosive lesions.”
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Lichen planus (LP) is a chronic mucocutaneous disorder
of the stratified squamous epithelium that affects oral
and genital mucous membranes, skin, nails, and scalp
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Lichen planus (LP) is a chronic mucocutaneous disorder
of the stratified squamous epithelium that affects oral
and genital mucous membranes, skin, nails, and scalp
Lichenoid Dermatoses, Characteristics of Lichenoid Dermatoses, What are the Major Lichenoid Dermatoses, Lichen planus (LP), Introduction of LP, Epidemiology of LP, Etiology of LP, Pathogenesis of LP, Clinical Features & Clinical variants of LP, Histopathology of LP, Immunohistochemistry of LP, Differential Diagnosis of LP, Treatment of LP
Malaria is the third leading cause of death due to infectious disease.
It affects 300- 500 million people annually worldwide and accounts for over 100 million deaths, mainly in African children under the age of 5 years. A child in Africa dies every 30 seconds of malaria.
Years of research and Millions of Dollars have been spend in the quest to eradicate this deadly infectious disease. The War is still on but is the mission impossible. This presentation was made during a graduate class to review the victories and the challenges so far in the treatment and vaccination against this disease.
More still need to be done but their seems to be light at the end of the tunnel.
Malaria is not inevitable, it can be eradicated, the mission is possible if only we devote ourselves to quality research and we never give-up. (Oseni Saheed Oluwasina (2013))
ORAL MANIFESTATIONS OF SYPHILIS-A reviewishita1994
Syphilis is an infectious disease of most extreme significance these days, which has made a rebound after the presence of AIDS.
It might introduce oral lesions in all stages.
A sharp information on its different oral signs is significant for appropriate determination and satisfactory treatment.
Infective syphilis is brought about by the anaerobic filamentous spirochete, Treponema pallidum.
Previously decade there has been a noteworthy ascent in the prevalence of infective syphilis in the created world.
Striking increments in the recurrence of syphilis have happened in Eastern Europe, and more modest ascents have been accounted for in Western Europe and the US.
Paget’s disease of bone with special reference to dentistry-an insightishita1994
Bone is a dynamic tissue that is constantly renewed. The cell populations that participate in this process; the osteoblasts and osteoclast are derived from different progenitor pools that are under distinct molecular control mechanisms. Together, these cells form temporary anatomical structures, called as basic multicellular units that execute bone remodeling. A number of stimuli affect bone turnover, including hormones, cytokines, and mechanical stimuli. All of these factors affect the amount and quality of the tissue produced. Paget’s disease is a bone disorder characterized by excessive and abnormal remodeling of the bone, resulting in distortion and weakness of affected bones. It is the second‑most common osteo dystrophic condition after osteoporosis.
Epidemiology and Diagnosis of Mucormycosisishita1994
Mucormycosis is an angioinvasive fungal infection due to fungi of the order Mucorales.
Depending on the clinical presentation it is classified as rhinocerebral, pulmonary, cutaneous, gastrointestinal, disseminated or other, which includes uncommon rare forms, such as endocarditis, osteomyelitis, peritonitis, renal, etc.
The disease was first described in 1876 when Fürbinger described in Germany a patient who died of cancer and in whom the right lung showed a hemorrhagic infarct with fungal hyphae and a few sporangia.
In 1885, Arnold Paltauf published the first case of disseminated mucormycosis, which he named “Mycosis mucorina”.
His drawings of the etiologic agent showed the presence of sporangiophores and rhizoid-like structures, and this led to the conclusion that the infection was most probably caused by Lichtheimia corymbifera.
Over time, more cases were diagnosed, and the incidence of the disease has increased.
Currently, Mucorales fungi are the next most common mold pathogens after Aspergillus, leading to invasive fungal disease in patients with malignancies or transplantation.
The incidence of mucormycosis has also increased significantly inpatients with diabetes, which is the commonest underlying risk factor globally.
Τhe epidemiology of mucormycosis is evolving as new immunomodulating agents are used in the treatment of cancer and autoimmune diseases, and as the modern diagnostic tools lead to the identification of previously uncommon genera/species such as the Apophysomyces or Saksenaea complex.
Oral cancer is the world’s 6th most common malignancy and has one of the lowest survival rates, often due to late diagnosis. The most important determinant factor in cancer survival is diagnostic delay and it directly affects the survival rate.
Most oral cancers are preceded by precancerous lesions and early cancers that can be identified by visual inspection of the oral cavity. Conventional oral examination is useful in the discovery of some oral lesions, but it does not identify all potentially premalignant lesions, as some are not readily apparent to visual inspection alone.
Adjunctive techniques have emerged that may facilitate early detection of oral premalignant and malignant lesions. Thorough clinical examinations being one of the best modalities in suspecting the pathology, the biggest disadvantage in the diagnosis lies in detecting the site of biopsy and also whether biopsy is required or not in early lesions.
Nowadays various diagnostic aids have been established in detecting such lesions but easy chair-side techniques can be used if possible. And one such technique is by using vital staining with dyes which is used for early recognition of lesion and also can improve the patient survival rate.
CLINICOPATHOLOGICAL FEATURES OF PERIPHERAL OSSIFYING FIBROMA IN A SERIES OF 4...ishita1994
Peripheral ossifying fibromas are benign mesenchymal lesions that usually arise in the anterior maxilla of young female patients. Histologically they consist of spindle cell proliferation with focal mineralization. We reviewed 48 specimens from 41 patients and recorded the clinical data, sex, and age of the patients, site, and size of the lesions, treatment, and postoperative outcome. Histologically the presence of mature, woven bone, cementum, and calcifications was evaluated and evaluated immunohistochemically. Lesions were more frequent in female patients in the third and fourth decade and were usually in the lower maxilla and smaller than 2 cm. All lesions were conservatively excised, and they relapsed in eight patients. Histopathologically, the lesions were poorly circumscribed, with moderately cellular proliferation, and with no discernible architectural pattern. All tumors showed some degree of mineralization, the presence of immature bone being the most common. Immunohistochemical examination showed staining of tumoral cells for smooth muscle actin and CD68. Lesions tended to occur more commonly in female patients, but one decade later than usually reported. We found a higher recurrence rate in lesions that contained cementum-like material but without bone formation, suggesting a lack of maturation in this group. Immunohistochemical results were consistent with myofibroblastic differentiation but they added no information about the behavior of the lesions.
Pathophysiology of myoepithelial cells in salivary glandsishita1994
In salivary glands and other exocrine glands, there are
star‑shaped cells lying between the basal lamina and the acinar
and ductal cells. These cells structurally resemble epithelial cells
and smooth muscles and, thus, are referred to as myoepithelial
cells (MECs). Because of their shape and interwoven processes,
they were commonly referred to as “star‑shaped cells” or
“basket cells.” Tamarin described these cells as being “like an
octopus sitting on a rock”.
Current concepts of pemphigus with a deep insight into its molecular aspectishita1994
Pemphigus vulgaris is an autoimmune bullous disease involving both the skin and mucosal areas, which
is characterized by intraepithelial flaccid blisters and erosions. The pathogenesis of this disease is not
yet completely established, but novel intuitions into its pathogenesis have recently been published. An
unanswered question in its pathophysiology is the mechanism of acantholysis or loss of keratinocyte
cell adhesion. Acantholysis seems to result from a communal action of autoantibodies against numerous
keratinocyte self‑antigens, of which desmogleins 1 and 3, desmocollins and nondesmosome components,
such as the mitochondrion, might take part in the disease initiation. Lately, apoptosis was described as
a possible underlying mechanism of acantholysis. Likewise, apoptolysis is assumed to be the association
between suprabasal acantholytic and cell death pathways. Hence, the present review focuses on the current
concepts in the pathogenesis of the pemphigus in a nutshell.
Cytoskeleton of a cell is made up of microfilaments, microtubules and intermediate filaments. Keratins are diverse proteins. These intermediate filaments maintain the structural integrity of the keratinocytes. The word keratin covers these intermediate filament-forming proteins within the keratinocytes. They are expressed in a specific pattern and according to the stage of cellular differentiation. They always occur in pairs. Mutations in the genes which regulate the expression of keratin proteins are associated with a number of disorders which show defects in both skin and mucosa. In addition, there are a number of disorders which are seen because of abnormal keratinization. These keratins and keratin-associated proteins have become important markers in diagnostic pathology. This review article discusses the classification, structure, functions, the stains used for the demonstration of keratin and associated pathology. The review describes the physiology of keratinization, pathology behind abnormal keratin formation and various keratin disorders.
Romanowsky staining or Romanowsky–Giemsa staining, is a prototypical staining technique, widely used in hematology and cytopathology.
They are used to differentiate cells for microscopic examination in air dried cytological smears or pathological specimens, especially blood and bone marrow films, and to detect parasites such as malaria within the blood.
Romanowsky stains is a neutral dye containing both acid and basic dyes in combination. It contains both azure B (electron acceptor) and eosin Y (electron donor).
The value of Romanowsky staining lies in its ability to produce a wide range of hues, allowing cellular components to be easily differentiated. This phenomenon is referred to as the Romanowsky effect, or more generally as metachromasia.
These stains allow better estimation of cell size, nuclear size, cell cytoplasm and identify ground substances by metachromasia.
The tissue section is colourless because the fixed protein has the same refractive index as that of glass. We use dyes that have specific affinity with the different tissue proteins and colour them differently.
Colour is seen by the eye as a result of the effect of certain electromagnetic waves on the rods and cones of the retina. These waves, which have a varying length, will determine the colour that is seen.
White light being composed of all the colours of the visible spectrum varies in wavelength from 4,000 Â to 8,000 Â.
If light of a specific wavelength is absorbed from white light the resultant light will then be coloured, the colour being dependent upon the particular wavelength that has been removed.
Ghost cells are translucent balloon shaped , elliptical epithelial cells are recognized as swollen, pale, eosinophilic cells.
They are seen either singly or in sheets with a clear conservation of basic cellular outline, generally with apparent clear areas or with some remnants indicative of the site previously occupied by the nucleus.
The transformation of epithelial cells into more resistant terminally differentiated apoptotic cells i.e., ghost cells are responsible for the banal behavior of neoplasms and they also help in relieving the stress of the forming neoplasm.
The most accepted nature of ghost cells is aberrant keratinization that is altered form of keratin as it doesn’t stain with normal cytokeratin antibodies.
Tonofilaments have been observed universally in the ghost cells of all the odontogenic or non-odontogenic tumors but these solely don’t satisfy their nature which is also found to be positive for enamel proteins in odontogenic tumors.
Although, studies prove an intricate functional relationship exists between Wnt and Notch signalling during development of neoplasms and in assigning cells to particular fates.
Their relationship along with other signalling pathways complex interaction during tumorigenesis also needs intensive evaluation and this would help revealing the missing link between odontogenic and non-odontogenic tumors exhibiting these similar looking mysterious ghost cells.
Mineralization (calcification) is the process of deposition of insoluble calcium salts in a tissue. It is one of the important steps in the formation of hard tissues of the body that is enamel, dentin, bone, and cementum. The synthetic cells, along with the help of the enzyme alkaline phosphatase, aid the mineralization process. The mineral content (inorganic portion) of all the hard tissues of the body is mainly in the form of Calcium hydroxyapatite crystals, Ca10(PO4)6(OH)2.
When calcium phosphate deposition is initiated, the crux is then to control spontaneous precipitation from tissue fluids supersaturated in calcium and phosphate ions and to limit it to well-defined sites. Formative cells achieve this by creating microenvironments that facilitate mineral ion handling and by secreting proteins that stabilize calcium and phosphate ions in body fluids and/or control their deposition onto a receptive extracellular matrix.
The synthetic cells achieve this property by secreting proteins that stabilize Calcium and Phosphate in the body fluids and control their deposition onto the extracellular matrix. These proteins are:
1. Salivary proteins
2. Enamel matrix protein
3. Dentin, cementum, and bone matrix proteins.
Histologically, the lesion shows a highly vascular proliferation that resembles granulation tissue.
Numerous small and larger endothelium-lined channels are formed that are engorged with red blood cells. These vessels sometimes are organized in lobular aggregates, and may be called as lobular capillary haemangioma.
The surface is usually ulcerated and replaced by a thick fibrinopurulent membrane.
A mixed inflammatory cell infiltrate of neutrophils, plasma cells, and lymphocytes is evident.
Neutrophils are most prevalent near the ulcerated surface; chronic inflammatory cells are found deeper in the specimen.
It is also called Oral Fibroma or Irritational Fibroma or Focal Fibrous Hyperplasia.
Fibroma is a benign neoplasm of fibrous connective tissue origin.
It is characterized by excessive proliferation of fibroblast cells with synthesis of large amount of collagen.
Although a large number of fibrous over-growths are found inside the oral cavity, most of these are reactive lesions occurring as a result of trauma or local irritation and therefore true fibromas are extremely rare.
Jain G et al (2017) stated that traumatic irritants include calculi, foreign bodies, overhanging margins, restorations, margins of caries, chronic biting, sharp spicules of bones, and overextended borders of appliances. Fibroma, a benign neoplasm of fibroblastic origin, is reactive in nature and represents a reactive hyperplasia of fibrous connective tissue in response to local irritation or trauma rather than being a true neoplasm.
8 th edition TNM classification and significance of depth of invasionishita1994
Diagnosis of oral cancer is completed for:
Initial diagnosis
Staging
Treatment planning
A complete history, and clinical examination is first completed, then a wedge of tissue is cut from the suspicious lesion for tissue diagnosis. In this procedure, the surgeon cuts all, or a piece of the tissue, to have it examined under a microscope by a pathologist.
Leukoplakia can be defined as a “white patch” or “plaque” in the oral cavity, which cannot be scrapped off and which cannot be characterized clinically or pathologically as any other disease.
This excludes lesions such as lichen planus, candidiasis, leukoedema, white spongy nevus, and obvious frictional keratosis.
The term leukoplakia should be used to recognise white plaques of questionable risk having excluded (other) known diseases or disorders that carry no risk for cancer-WHO 2005.
Mandibular central incisors are two in number
Mandibular central incisor and lateral are similar in anatomy and complement each other in function
They are smaller than the maxillary central incisors
Mandibular central incisor erupts between the age of 7 and 8 years
First tooth from the midline in each lower quadrant
Depth of invasion in oral squamous cell carcinomaishita1994
It is the most common malignant epithelial tissue neoplasm of the oral cavity.
It is derived from the stratified squamous epithelium.
Since oral squamous cell carcinomas constitute bulk of the oral malignancies (above 90 %) it is thus commonly referred to as Oral Cancer.
Tuberculosis is a disease characterized by granulomatous lesions caused by Mycobacterium Tuberculosis. A German scientist Robert Koch discovered the causative organism of TB in 1882.
Since time immemorial, it has been a global health problem. TB has shown a decline in its prevalence globally; however, it is still highly prevalent in Asian countries.
TB is usually overlooked in the differential diagnosis of oral lesions as it is supposed to be a rare entity.
Oral manifestations of TB occur either due to infected sputum or due to hematogenous spread.
TB is an age old disease and has been known to mankind for thousands of years.
Role of human papillomavirus and tumor suppressor genesishita1994
Oral cancer is synonymous to Squamous Cell Carcinoma (SCC) of oral mucosal origin that accounts for more than 90% of all malignant presentations at the aforementioned anatomical sites.
More than 300,000 new cases worldwide are being diagnosed with oral SCC (OSCC) annually.
Approximately, 30,000 (US) & 40,000(EUROPE).
Oral cancer is estimated by the WHO to be the 8th most common cancer worldwide.
In India & other Asian countries, oral & oropharyngeal carcinomas (OCs) comprise up to half of all malignancies, with this particularly high prevalence being attributed to the influence of carcinogens & region-specific epidemiological factors, especially tobacco & betel quid chewing.
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stockrebeccabio
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stock
Telegram: bmksupplier
signal: +85264872720
threema: TUD4A6YC
You can contact me on Telegram or Threema
Communicate promptly and reply
Free of customs clearance, Double Clearance 100% pass delivery to USA, Canada, Spain, Germany, Netherland, Poland, Italy, Sweden, UK, Czech Republic, Australia, Mexico, Russia, Ukraine, Kazakhstan.Door to door service
Hot Selling Organic intermediates
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
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.
2. INTRODUCTION
• Oral Lichen Planus
A chr onic inf lammat or y disease t hat causes
bilat eral papules, st riat ions or plaques
May cause eryt hema, erosions and blist er s
Found on buccal mucosa, t ongue and gingiva
Female: Male r at io: 1.4:1
Pr edominant ly seen in adult s over 40 year s.
0.5% t o 2% of gener al populat ion
Af f ect s all et hnicit ies
4. PATHOGENESIS OF
RETICULAR L.P.
Or al Lichen planus is a pur ely T cell mediat ed
inf lammat or y r esponse. Ther e are no B cells, plasma
cells and no deposit s of immunoglobulin or
complement .
The t r igger f or ker at inocyt e apopt osis in OLP is,
f or t he most part , unknown. However, t he
lymphocyt ic inf ilt rat e in OLP is composed almost
exclusively of T cells, and t he maj or it y of T cells
wit hin t he epit helium and adj acent t o damaged basal
ker at inocyt es are act ivat ed CD8+ lymphocyt es.
Ther ef ore, it is very pr obable t hat cyt ot oxic T cells
t r igger ker at inocyt e apopt osis in OLP.
5. PROPOSED
IMMUNOPATHOGENESIS
OF OLP
A lichen planus-specif ic ant igen is expr essed in
conj unct ion wit h MHC class 1 molecules on ker at inocyt es
at t he OLP lesion sit e.
Ant igen specif ic CD8+ T cells ar e act ivat ed in t he ar ea.
Act ivat ed ant igen-specif ic CD8+ cyt ot oxic T
lymphocyt es t r igger ker at inocyt e apopt osis, possibly by
secr et ed TNF-α.
The act ivat ed T lymphocyt es under go int r a-lesion clonal
expansion and r elease soluble mediat or s (cyt okines and
chemokines), which r ecr uit lymphocyt es f r om t he local
micr ovasculat ur e and cause migr at ion t owar d t he
epit helium.
6. This hypot hesis predict s t hat t he maj orit y of
lymphocyt es recruit ed t o t he OLPlesion sit e are not
specif ic f or t he lichen planus-specif ic ant igen. However,
t hey may cont ribut e t o t he pat hogenesis of OLPby
secret ing MMP-9, which leads t o epit helial basement
membrane disrupt ion.
Epit helial basement membrane disrupt ion allows f or t he
passage of lymphocyt es int o t he epit helium and denies
kerat inocyt es a cell survival signal, result ing in f urt her
kerat inocyt e apopt osis.
This hypot hesis predict s t hat t he earliest event s in OLP
lesion f ormat ion are conf ined t o t he epit helium and t hat
basement membrane and connect ive t issue changes occur
secondarily.
7. CLINICAL
PRESENTATION
Or al lesions-mor e persist ent and r esist ant t o
t r eat ment t han skin lesions
30-50% of pt s also have cut aneous lesions
Thr ee common t ypes
Ret icular
Er osive
Plaque
Var iant s of Plaque and Erosive t ypes
At r ophic
Bullous
8. CLINICAL
PRESENTATION
Ret icular lesions
Most common t ype
I nt erlacing whit e kerot ot ic lines wit h
eryt hemat ous border s (Wickham’s st riae)
Typically bilat erally on buccal mucosa,
mucobuccal f old and gingiva
Less common on t ongue, palat e and lips
Asympt omat ic
9. Erosive lesions
2nd
most common t ype
Mix of er yt hemat ous and ulcer at ed ar eas
surr ounded by radiat ing ker ot ot ic st r iae
Similar appearance t o candidiasis, pemphigus and
lupus
Lesions t end t o migrat e and of t en mult if ocal
Most ly buccal mucosa and vest ibule
Symptomatic:
Sore mout h sensit ive t o heat , cold, spices, and alcohol
Pain and bleeding on t ouch
Plaque lesions
Resemble f ocal leukoplakias
Var y f rom smoot h f lat ar eas t o r aised ir r egular
plaques
Of t en mult if ocal
Dorsum of t ongue and buccal mucosa
10. Variants of Erosive and Plaque lesions
Atrophic
Dif f use, eryt hemat ous pat ches
Causes signif icant discomf ort
Gingiva and buccal mucosa
Bullous
I nt raoral bullae on buccal mucosa and lat eral surf ace
of t ongue
Rupt ure soon af t er appearance result ing in classic
appearance of erosive lesions
11. DIAGNOSTIC TESTS
Clinical exam: f or r et icular LP wit h
char act erist ic appear ance of Wickham’s st r iae or
annular pat t er n on eryt hemat ous backgr ound
Histological and Direct Immunofluorescent
examinations: f or plaque and er osive LP because
t hey can r esemble ot her mucosal lesions including
malignancy
12. Histological exam
Requires biopsy
Varies based on t he t ype of lesion
Typically: epit helial hyperplasia, ort ho and para
kerat osis, acant hosis, at rophic areas wit h loss of ret e-
pegs, dense accumulat ion of T-lymphocyt es in t he basilar
cell layer
Direct Immunofluorescent examination
Requires biopsy
Dif f erent iat es bet ween ot her aut oimmune condit ions
Det ect s shaggy deposit ion of f ibrinogen along t he
basement membrane
13. HISTOLOGY:
RETICULAR LICHEN
PLANUS
Consist s of local areas of epit helial hyperplasia in which t he
surf ace cont ains a t hick layer of ort hokerat in or parakerat in.
The spinous cell layer may be t hickened (acant hosis) wit h
short ened and point ed ret e pegs(Wickham’s st riae).
Bet ween t hese areas t he epit helium is t hinned (at rophic),
wit h loss of ret e peg f ormat ion.
The adj acent cont ains a t hin, dense accumulat ion of T
lymphocyt es t hat move t hrough t he basement membrane and
are observed in t he basilar and parabasilar cell layers of t he
epit helium.
14. HISTOLOGY:
EROSIVE LICHEN
PLANUS
Exhibit an ext ensively t hinned epit helium wit h areas of
complet e loss of ret e peg f ormat ion and a dense inf ilt rat e of
T lymphocyt es.
This T lymphocyt e inf ilt rat e obscures t he basement
membrane and ext ends well int o t he middle and upper levels
of t he epit helium.
Liquef act ion of t he basement membrane and dest ruct ion of
t he basal cells is present in most areas.
Occasionally, sub epit helial separat ion will be present .
Of t en, t he epit helium is lost , exposing t he underlying
connect ive t issue.
The lymphocyt es are conf ined t o a narrow zone in t he upper
layers of t he connect ive t issue.
15. HISTOLOGY: PLAQUE
LICHEN PLANUS
Plaque LP resembles t he hist ology of ret icular LP because of
t he st riae pat t ern but it lacks t he int ermit t ent at rophic
areas of t he epit helium.
I t consist s of generalized hyperort hokerat osis or
hyperparakerat osis combined wit h acant hosis.
There may be loss of ret e pegs at t he epit helial and
connect ive t issue int erf ace or alt erat ion of t heir shape int o
a “saw-t oot h” pat t ern.
The basement membrane is not iceably t hickened.
The band of T lymphocyt es present in t he superf icial
connect ive t issue is more sparse t han I n ret icular LP, wit h
only occasional cells f ound in t he lower levels of t he
epit helium.
16. TREATMENT OF OLP
No t reat ment f or OLP is curat ive
Goal:
Reduce painf ul sympt oms
Resolut ion of oral mucosal lesions
Reduce risk of oral squamous cell carcinoma
I mprove oral hygiene
Eliminate exacerbating factors:
Repair def ect ive rest orat ions or prost hesis
Remove of f ending mat erial causing allergy
Diet:
Eliminat e smoking and alcohol consumpt ion
Eat f resh f ruit and veget ables (but avoid t omat oes and nut s)
Reduce St ress
17. Medicat ion
Topical cort icost eroids
0.05% clobet asol proprionat e gel
0.1% or 0.05% bet amet hasone valerat e gel
0.05% f luocinonide gel
0.05% clobet asol but yrat e oint ment
0.1% t riamcinolone acet onide oint ment
Can be applied direct ly or mixed wit h Orabase
18. Medicat ion
Syst emic St er oid Ther apy
Prednisone (f or 70kg adult )
• 10-20mg/ day f or moderat ely severe cases
• As high as 35 mg/ day f or severe cases
• Should be t aken in t he morning t o avoid insomnia
• Should be t aken wit h f ood t o avoid pept ic ulcerat ion
Azat hioprine (I muran) – I nhibit s synt hesis of DNA
• 1mg/ kg/ d f or 6-8 weeks
Met hylprednisolone (Medrol Dosepak)
• t o reduce pain and inf lammat ion
Prophylact ic use of 0.12% chlorhexidine gluconat e may
help reduce f ungal inf ect ion during cort icost eroid
t herapy
19. ALTERNATIVE
TREATMENT OF OLP
0.1% t opical t acr olimus oint ment 2x/ day
Tacr olimus: immunosuppressive macr olide
Suppr esses T-cell act ivat ion
I nt raoral ulcer at ion resolved af t er 3 mont hs of
daily applicat ion
Remission f or 1 year wit hout maint enance