White and Red oral mucosal lesions Lec 4&5

University of Basrah – اسم الكلية – القسم

First Semester White and Red oral

mucosal lesionsLec 4&5

Suroor Ali JabbarBDS. Msc Oral medicine

College Of Dentistry University Of Basrah

1

Oral mucosal lesions may be classified according to different characteristics

INFECTIOUS DISEASES• Oral Candidiasis• Hairy LeukoplakiaPREMALIGNANT LESIONS• Oral Leukoplakia and Erythroplakia• Oral Submucous FibrosisIMMUNOPATHOLOGIC DISEASES• Oral Lichen Planus• Drug-Induced Lichenoid Reactions• Lichenoid Reactions of Graft-versus-

Host Disease• Lupus Erythematosus

ALLERGIC REACTIONS• Lichenoid Contact Reactions• Reactions to Dentifrice and ChlorhexidineTOXIC REACTIONSReactions to Smokeless TobaccoSmoker’s PalateREACTIONS TO MECHANICAL• TRAUMA• MorsicatioOTHER RED AND WHITE LESIONSBenign Migratory Glossitis (Geographic Tongue)LeukoedemaWhite Sponge NevusHairy Tongue


white appearance of the oral mucosa may be caused by a variety of factors:• The oral epithelium may be stimulated to an increased production of keratin

(hyperkeratosis)

• abnormal but benign thickening of stratum spinosum (acanthosis)

• Intra- and extracellular accumulation of fluid in the epithelium may also result in

clinical whitening.

• Microbes, particularly fungi, can produce whitish appearance



A red lesion of the oral mucosa may develop as a result of :

• Atrophic epithelium characterized by a reduction in the number of epithelial cells

• Increased vascularization that is dilatation of vessels and/ or proliferation of vessels

Infectious DiseasesOral Candidiasis

Oral candidiasis is the most prevalent opportunistic infection affecting the oralmucosa. In the vast majority of cases, the lesions are caused by Candida albican.The pathogenesis is not fully understood, but a number of predisposing factors have been shown to convert C. albicans from the normal commensal flora (saprophytic stage) to a pathogenic organism (parasitic stage).C. albicans is usually a weak pathogen, affecting• The Very Young,• The Very Old,• The Very Sick.Most candidal infections only affect mucosal linings, but rare systemic manifestations may have a fatal course

• Oral candidiasis is divided into Primary and Secondary The primary infections are restricted to the oral and perioral sites, whereas secondary infections are accompanied by systemic mucocutaneous manifestations.

Immunopathologic Diseases Lichenoid Reactions


Etiology and PathogenesisC. albicans, C. tropicalis, and C. glabrata comprise together over % 80 of the species isolated from human candidal infection .

To invade the mucosal lining ,the microorganism must adhere to the epithelial surface; therefore, candidal strains with better adhesion potential are more virulent than strains with poorer adhesion ability.

The yeasts’ penetration of the epithelial cells is facilitated by their production of lipases and for the yeasts to remain within the epithelium, they must overcome constant desquamation of surface epithelial cells.



Primary Oral CandidiasisAcute

• Pseudomembranous• Erythematous

Chronic• Pseudomembranous• Erythematous• Plaque-like• Nodular• Candida-associated lesions• Denture stomatitis• Angular cheilitis• Median rhomboid glossitis

Secondary Oral Candidiasis• Familial chronic mucocutaneousCandidiasis• Diffuse chronic mucocutaneousCandidiasis• Candidiasis endocrinopathysyndrome• Familial mucocutaneous

candidiasis• Severe combined

immunodeficiency• DiGeorge syndrome• Chronic granulomatous disease• Acquired immune deficiencysyndrome (AIDS)



Predisposing Factors for Oral Candidiasis and Candida-Associated LesionsLocalDenture wearingSmokingAtopic constitutionInhalation steroidsTopical steroidsHyperkeratosisImbalance of the oral microfloraQuality and quantity of saliva

GeneralImmunosuppressive diseasesImpaired health statusImmunosuppressive drugsChemotherapyEndocrine disordersHematinic deficiencies



EpidemiologyThe prevalence of candidal strains, as part of the commensal oral flora, shows

�large geographic variations �Candidal strains are more frequently isolated from women. �A seasonal variation has been observed, with an increase during summer months. � Hospitalized patients have a higher prevalence of the yeasts. � In healthy individuals, blood group O and non-secretion of blood group antigens are separate and cumulative risk factors for oral carriage of C. albicans. � In complete denture-wearers, the prevalence of denture stomatitis has been reported variously from 11-67%.



Clinical Findings:

1- Pseudomembranous Candidiasis

Acute form of pseudomembranous candidiasis (thrush) is grouped with the primary oral candidiasis and is recognized as the classic candidal infectionThe infection predominantly affects patients taking antibiotics, immunosuppressant drugs, or having a disease that suppresses the immune system.



2- Erythematous Candidiasis

was previously referred to as atrophic oral candidiasis but can reflect atrophyerythematous surface may not just refelct atrophy but also increased vasicularization

The lesion has a diffuse border which helps distinguish it from sharper demarcation of erythroplakia .The infection is predominantly seen in the palate and the dorsum of the tongue of patients who are using inhalation steroids. Other predisposing factors that can cause erythematous candidiasis are smoking and treatment withbroad-spectrum antibiotics.



3- Chronic Plaque-Type and Nodular Candidiasis

Replaces the older term, candidal leukoplakia.• A white irremovable plaque• characterizes the typical clinical presentation, which

may be indistinguishable from oral leukoplakia• A positive correlation between oral candidiasis and

moderate to severe epithelial dysplasia• both the chronic plaque-type and the nodular type of

oral candidiasis have been associated with malignant transformation, but the possible role of yeasts in oral carcinogenesis is unclear.

It has been hypothesized that it may act through its capacity to catalyze nitrosamin production

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4- Denture Stomatitis

The most prevalent site for denture stomatitis is the denture-bearing palatal mucosa .It is unusual forthe mandibular mucosa to be involved. Denture stomatitis is classified into three different types.

_Type I: is limited to minor erythematous sites caused by trauma from thdenture._Type II : affects a major part of the denture-covered mucosa. _In addition to the features of type II, type III has a granular mucosa.

The denture serves as a vehicle that accumulates sloughed epithelial cells and protects the microorganisms from physical influences such as salivary flow. The microflorais complex and may, in addition to C. albicans containbacteria from several genera, such as Streptococcus-, Veillonella-,Lactobacillus.



5- Angular Cheilitis

Angular cheilitis presents as infected fissures of the commissures of the mouth, often surrounded by erythema• The lesions are frequently infected with both

Candida and Staphylococcus aureus.• loss of vertical dimension ,iron deficiencies, and

vitamin 12 deficiencies have been associated with this disorder.

• Dry skin may promote the development of fissures in the commissures, allowing invasion by the microorganisms.

• 30% of patients with denture stomatitis also have angular cheilitis, but this infection is only seen in 10% of denture-wearing

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6- Median Rhomboid GlossitisClinically characterized by an erythematous lesion in the center of the posterior

part of the dorsum of the tongue. -This area of erythema results from atrophy of the filiform papillae and the surface may be lobulated. -The etiology is not fully clarified, but the lesion frequently shows a mixed bacterial/fungal microflora.Biopsies yield candidal hyphae in more than 85% of thelesions.- Smokers and denture-wearers have an increased risk of developing median rhomboid glossitis as well as patients using inhalation steroids. Sometimes a concurrent erythematous lesion may be observed in the palatal mucosa (kissing lesions).- Median rhomboid glossitis is asymptomatic, and management is restricted to a

reduction of predisposing factors. The lesion does not entailany increased risk for malignant transformation.



7- Oral Candidiasis Associated with HIV

More than 90% of acquired immune deficiency syndrome (AIDS) patients have had oral candidiasis during the course of their HIV infection, and the infection is considered a portent of AIDS development .

The most common types of oral candidiasis in conjunction with HIV are pseudomembranous candidiasis, erythematous candidiasis, angular cheilitis, and chronic plaque-like candidiasis.

-As a result of the highly active antiretroviral therapy (HAART), the prevalence of oral candidiasis has decreased substantially.


Infectious Diseases

Oral Hairy Leukoplakia

Oral hairy leukoplakia (OHL) is the second most common HIV-associated oral mucosal lesion. HL has been used as a marker of disease activity since the lesion is associated with low CD4+ T-lymphocyte counts.The lesion is not pathognomonic for HIV disease since other states of immune deficiencies, such as caused by immunosuppressive drugs and cancer chemotherapy, have also been associated with OHL. Rarely, individuals with a normal immune system may present with OHL.




Chronic mucocutaneous candidiasis (CMC)

Embraces a heterogeneous group of disorders, which, in addition to oral candidiasis, also affect the skin, typically the nail bed and other mucosal linings, such as the genital mucosa. The face and scalp may be involved, and granulomatous masses can be seen at these sites.

- Approximately 90% of the patients with CMC also present with oral candidiasis.

-CMC can occur as part of endocrine disorders, including hyperparathyroidism and Addison’sdisease.




Severe combined immunodeficiency (SCID

Syndrome is characterized by a defect in the function of the cell-mediated arm of the immune system.Patients with this disorder frequently contract disseminated candidal infections.

Thymoma is a neoplasm of thymic epithelial cells that also entails systemic candidiasis. Thus, both the native and adaptive immune systems are critical to prevent development of systemic mucocutaneous candidiasis



Diagnosis and Laboratory Findings

• The detection of yeast organisms in the form of hyphae or pseudo-hyphae

• Salivary Culture : patient who display clinical sign of candidiasis usually have more than 400 CFU/Ml

• In chronic plaque-type and nodular candidiasis, cultivation techniques have to be supplemented by a histopathologic examination. This examination is primarily performed to identify invading and to identify epithelial dysplasia the presence of.organisms by PAS staining.



Management Treatment for fungal infections, which usually include antifungal regimens, will

not always be successful unless the clinician addresses predisposing factors that may cause recurrence. Local factors are often easy to identify but sometimes not possible to reduce or eradicate

• Antifungal drugs: belong to the groups of polyenes or azoles . Polyenes such as nystatin and amphotericin B are usually the first choices in treatment of primary

oral candidiasis and are both well tolerated. Polyenes are not absorbed from the gastrointestinal tract and are not associated with development of resistance.**If angular cheilitis comprises an erythema surrounding the fissure, amild steroid ointmen may be required to suppress the inflammation.

**Chlorhexidine may also be used but can discolor the dentureand also counteracts the effect of nystatin.

• Improvement of denture hygiene



Management There are several disadvantages with the use of azoles.

• They are known to interact with warfarin, leading to an increased bleeding propensity. This adverse effect may also be present with topical application

as the azoles are fully or partly resorbed from the gastrointestinal tract.

• Development of resistance is particularly compelling for fluconazole in individuals with HIV disease. In such cases, ketoconazole and itraconazole have

been recommended as alternatives.



Management There are several disadvantages with the use of azoles.

• They are known to interact with warfarin, leading to an increased bleeding propensity. This adverse effect may also be present with topical application

as the azoles are fully or partly resorbed from thegastrointestinal tract.

• Development of resistance is particularly compelling for fluconazole in individuals with HIV disease. In such cases, ketoconazole and itraconazole have

been recommended as alternatives.

Prognosis ======is good when predisposing factors associated with the infection are reduced or eliminated.

Persistent chronic plaque-type and nodular candidiasis have been suggested to be associated with an increased risk for malignant transformation compared with leukoplakia, not infected by candidal strains.


Infectious DiseasesOral Hairy Leukoplakia

is the second most common HIV-associated oral mucosal lesion. HL has been used as a marker of disease activity since the lesion is associatedwith low CD4+ T-lymphocyte counts.The lesion is not pathognomonic for HIV disease since other states of immune deficiencies, such as caused by immunosuppressive drugs and cancer chemotherapy

-is strongly associated with Epstein-Barr virus (EBV) and with low levels of CD4+ T lymphocytes. Antiviral medication, which prevents EBV replication, is curative-In AIDS, the prevalence may be as high as 80%.-in children the prevalence is lower compared with adults (2%).-is more frequently in men, but the reason for this predisposition.- A correlation between smoking and OHL has also been observed.



Clinical Findings-is frequently encountered on the lateral borders of the tongue but may also be observed on the dorsum and in the buccal mucosa.

-Thetypical clinical appearance is vertical white folds oriented as a palisade along the borders of the tongue. The lesions may also be seen as white and somewhat elevated plaque, which cannot be scraped off.

-is asymptomatic,although symptoms may be present when the lesion is superinfected with candidal strains

-it is important to always consider mucosal lesion whenever the border of the tongue is affected by white lesions, particularly in immunocompromised patients.



DiagnosisA diagnosis of OHL is usually based on clinical characteristics, but histopathologic

examination and detection of EBV can be performed to confirm the clinical diagnosis

ManagementOral hairy leukoplakia can be treated successfully with antiviral medication,but this is not often indicated as this disorder is not associated with adverse symptoms. In addition,the disorder has also been reported to show spontaneous regression. HL is not related to increased risk of malignant transformation.

Medication with HAART has reduced the number of HL to a few percent in HIV-infected patients.



DiagnosisA diagnosis of OHL is usually based on clinical characteristics, but histopathologic

examination and detection of EBV can be performed to confirm the clinical diagnosis

ManagementOral hairy leukoplakia can be treated successfully with antiviral medication,but this is not often indicated as this disorder is not associated with adverse symptoms. In addition,the disorder has also been reported to show spontaneous regression. HL is not related to increased risk of malignant transformation.

Medication with HAART has reduced the number of HL to a few percent in HIV-infected patients.


PREMALIGNANT DISORDERSOral Leukoplakia and Erythroplakia

The development of oral leukoplakia and erythroplakia as premalignant lesions involves different genetic events.

Activation of oncogenes and deletion and injuries to suppressor genes and genes responsible for DNA repair will all contribute to a defective functioning

of the genome that governs cell division.-Following a series of mutations, a malignant transformation may occur.

-carcinogens such as tobacco may induce hyperkeratinization, Which is reversablefollowing cessation, but at some stage, mutations will lead to an unrestrained proliferation

-global review points at a prevalence of 2.6%

-Most oral leukoplakias are seen in patients beyond the age of 50 and infrequently encountered below the age of 30.

-leukoplakias are more common in men but a slight majority for women has been found in some studies.



Oral erythroplakia : is not as common as oral leukoplakia, and the prevalence has been estimated to be in the range of 0.02%–0.1%.56 The gender distribution is reported to beequal.

Clinical FindingsOral leukoplakia is defined as a white plaque of questionable risk having excluded (other) known diseases or disorders that carry no increased risk for cancer.

This disorder can be further divided into a : homogeneous and a nonhomogeneous type

*The typical homogeneous leukoplakia is clinically characterized as a white, often well-demarcated plaque with an identical reaction pattern throughout the entire lesionThe surface texture can vary from a smooth and thin to a leathery appearance with surface fissures sometimes referred to as “cracked mud.” The demarcation is usually distinct,which is different from an OLP lesion, where the white components have a more diffuse transition to the normal oral mucosa*The nonhomogeneous type of oral leukoplakia may havewhite patches or plaques intermingled with red elements , called Speckled leukoplakia or erythrolukoplakia



• Oral leukoplakia may be found at all sites of the oral• Nonsmokers have a higher percentage of leukoplakias at the border of the tongue

compared with smokers• Floor of the mouth and the lateral borders of the tongue have been considered high-risk

sites for malignant transformation .

These sites have also been found to have a higher frequency of loss ofheterozygosity compared with low-risk sites.• However, the distinction between high- and low-risk sites has beenquestioned leaving:• the size of the lesion• and the homogenous/non-homogenous pattern being for the prognosis



A nonhomogeneous leukoplakia

A homogeneous leukoplakia

Erythroplakia at the alveolar ridge. The patient

later developed a squamous cell carcinoma



**Oral leukoplakias, where the white component is dominated by papillary projections, similar to oral papillomas, are referred to as verrucous or verruciform leukoplakias

**Oral leukoplakias with this clinical appearance but with a more aggressive proliferation pattern and high recurrence rate are designated as proliferative verrucous leukoplakia

PVL is usually• Seen in older women, and the lower gingiva is a predilection site.• The malignant potential is very high ands verrucous carcinoma or squamous cell

carcinoma may be present at the primary examination.• similar to what is seen in oral papillomas, the PVL has been suspected to have a viral

etiology.



• Erythroplakia: is defined as a red lesion of the oral mucosa that excludes other known pathologies . Erythroplakia is usually asymptomatic, although some experience a burning sensation with food intake

• A special form of erythroplakia has been reported to be related to chutta reverse smoking which predominantly practiced in India.

DiagnosisThe diagnostic procedure of oral leukoplakia and erythroplakia is identical. The

provisional diagnosis is based on the clinical observation of a white or red patch that is not explained by a definable cause, such as trauma. If trauma is suspected, the cause, such as a sharp tooth or restoration, should be eliminated. If healing does not occur in two weeks,a tissue biopsy is essential to rule out malignancy.





Dysplasia: may be found in homogeneous leukoplakias but is much more frequently encountered in nonhomogeneous leukoplakias and in erythroplakias.

• Epithelial dysplasia is defined in general terms as a precancerous lesion of stratified squamous epithelium characterized by cellular atypia and loss of normal maturation.

• Carcinoma in situ is defined as a lesion in which the full thickness of squamous epithelium shows the cellular features of carcinoma without stromal invasion.

prevalence of dysplasia in oral leukoplakias varies from 1%–30%, presumably due to various lifestyle factors involved and due to subjectivity in

the histopathologic evaluation.



******Squamous cell carcinomas are almost equall yprevalent in patients subjected and not subjected to surgery.This may be explained by genetic defects even in clinically normal mucosa surrounding the removed lesion and is supported by a concept referred to as field cancerization.

• Malignant transformation of oral leukoplakias has been reported in the range of 1%–20% over 1 to 30 years

• Homogeneous oral leukoplakias are associated with a decreased risk for malignant transformation than nonhomogeneous leukoplakias and erythroplakias, and lesions not exceeding 200 mm2 appear to have a better prognosis than larger lesions.

• No consensus has been reached regarding management and follow-up of oral leukoplakias and erythroplakias. A general recommendation is to reexamine the premalignant site irrespective of surgical excision every three months for the first year. If the lesion does not relapse or change in reaction pattern, the follow-up intervals may be extended to once every six months. New biopsies should be taken if new clinical features emerge. Following five years of no relapse, self-examination may be a reasonable approach.

Oral Submucous Fibrosis

Oral Submucous Fibrosis is a chronic disease affecting the oral mucosa,as well as

the pharynx and the upper two-thirds of the esophagus.

Areca nuts which is used by several hundred million individuals in different parts of

Asia behind the etiology of this disorder which is a dose dependant .

Areca nuts Arecoline has the capacity to modulate matrix metalloproteinases, lysyl

oxidases, and collagenases, all affecting the metabolism of collagen, which leads to

increased fibrosis .

• Genetic predisposition is of importance for the etiology behind oral submucous

fibrosis.


Oral complications are most commonly observed: on the lips, buccal mucosa, retromolar area, and soft palatal mucosa It is widespread in India, Pakistan, Bangladesh, and Sri Lanka and in immigrants coming from these regions • The global incidence s estimated at 2.5 million individuals. • The prevalence in Indian populations is 5% for women and 2% for men. • Individuals in less than 20 years old seem to be affected more commonly in

other age groups.

Clinical Findings • The first signs are erythematous lesions, sometimes in conjunction with

petechiae, pigmentations ,and vesicles. followed by a paler mucosa, • The most prominent clinical characteristics include fibrotic bands located

beneath an atrophic epithelium. • Increased fibrosis eventually interferes with speech, tongue mobility, and a

decreased ability to open the mouth. • The atrophic epithelium may cause inability to eat hot and spicy food.


Diagnosis The diagnosis of oral submucous fibrosis is based on the clinical characteristics

and patient report of chewing habit. An international consensus has been reached where at least one of the following characteristics should be present :•• Palpable fibrous bands •• Mucosal texture feels tough and leathery •• Blanching of mucosa together with histopathologic features consistent with oral submucous fibrosis (atrophic epithelium with loss of rete ridges and juxta-epithelial hyalinization of lamina propria)


Management Products derived from areca nuts are carcinogenic, r

egardless of concomitant use of tobacco products. Thus, treatment of oral submucous fibrosis should be focused on cessation of the chewing habits. If this is successfully implemented, early lesions have a good prognosis as they may regress. • Several treatment strategies have been tried, such

as: topical and systemic steroids, • supplement of vitamins and nutrients, • repeated dilatation with physical devices, • and surgery. None of these treatments have reached

general acceptance and the long-term results are uncertain.

Malignant transformation of oral submucous fibrosis has 7–13% and the incidence over a 10-year period at approximately 8%.


Represent a family of lesions with : different etiologies ,with a common clinical and histologic appearence. • Neither clinical nor histopathologic features enable discrimination between different

lichenoid reactions but may be used to differentiate lichenoid reactions from other pathologies of the oral mucosa.

Oral lichenoid reactions include the following disorders •• Oral lichen planus •• Lichenoid contact reactions • Lichenoid drug eruptions •• Lichenoid reactions of graft-versus-host disease (GVHD)

These lesions represen a delayed hypersensitivity reaction to constituents derived from dental materials or flavoring agents in other ingested substances for foods and other ingested substances



• The etiology is not known• It has become evident that the immune system has a primary role in the developm

ent of this disease. This is supported by the histopathologic characteristics of a subepithelial band–formed infiltrate dominated by T lymphocytes and macrophages and the degeneration of basal cells known as liquefaction degeneration

• It is complicated to identify a single etiologic factor behind OLP. Other factors, such as stress, may also be of importance to establish this inflammatory process. It is not unusual that patients report that they have been exposed to negative social events months before the onset of the disease. Altogether, this makes the etiology behind OLP a multifactorial process

Oral Lichen Planus


Oral Lichen Planus

During recent years, an association between OLP and hepatitis C virus (HCV) has been described in populations from Japan and some Mediterranean countries. This association has not been observed in northern European countries or the United States. Arabic countries.

• prevalence OLP have been reported and vary from 0.5–2.2% • Among referred patients, women is higher than that of men. • The mean age at the time of diagnosis is approximately 55 years

Clinical Findings OLP may contain both red and white elements which can be a part of the following clinical types:

Reticular Plaque-likeBullous

Erythematous

UlcerativePlaque-like

OLP is considered to be a premalignant disorder the risk is low and presumably does not exceed an incidence of 0.2% per year


• The etiology is not known• It has become evident that the immune system has a primary role in the developm

ent of this disease. This is supported by the histopathologic characteristics of a subepithelial band–formed infiltrate dominated by T lymphocytes and macrophages and the degeneration of basal cells known as liquefaction degeneration

• It is complicated to identify a single etiologic factor behind OLP. Other factors, such as stress, may also be of importance to establish this inflammatory process. It is not unusual that patients report that they have been exposed to negative social events months before the onset of the disease. Altogether, this makes the etiology behind OLP a multifactorial process

Oral Lichen Planus


Oral Lichen Planus

The explanation of the different clinical manifestations of OLP is related to the magnitude of the subepithelial inflammation, A mild degree of inflammation provoke the epithelium to produce hyperkeratosis , while more intense inflammation, will lead to partial or complete deterioration of the epithelium.

Clinical findings Typically, the reticular, papular, and plaque-like are asymptomatic, although the patient may experience a feeling of roughness

• The bullous form is very unusual but may appear as bullous structures surrounded by a reticular network.

• Erythematous (atrophic) OLP is characterized by a homogeneous red area. When this type of OLP is present in the buccal mucosa or in the palate, striae are frequently seen in the periphery of the lesion

• Ulcerative lesions are the most disabling form of OLP Clinically, the fibrin-coated ulcers are surrounded by an erythematous zone with white striae in the periphery.


Oral Lichen Planus


Oral Lichen Planus

Clinical Manifestation Cutaneous lesions may be seen in approximately 15% of patients with OLP.

The classic appearance of skin lesions consists of pruritic erythematous flat topped. The predilection sites are the trunk and flexor surfaces of arms and legs

• The most frequent extra-oral mucosal site involved is the genital mucosa; 20% of women presenting with OLP also have genital involvement , Symptoms including burning, pain, vaginal discharge.

• following intense scratching of the lesions, trauma may aggravate the disease, which is referred to as a .

• Koebner phenomenon This phenomenon may also be of relevance for OLP, which is continuously exposed to physical trauma during mastication and brushing


Oral Lichen Planus

• OLP can often be separated from LCRs to dental materials, which are most often detected on the buccal mucosa and the lateral borders of the tongue. OLP, on the other hand, usually displays a more general involvement

• Oral GVHD has the same clinical appearance as OLP, but the lesion is usually more generalized. The lichenoid reactions are frequently seen simultaneously with other

characteristics, such as xerostomia and the presence of localized skin involvement and liver dysfunction, even if an oral lichenoid reaction may emerge as the only clinical sign ofGVHD.

• Oral lichenoid drug eruptions have the same clinical and histopathologic characteristics as OLP.

• The patient’s disease history may give some indication as to which drug is involved, but OLP may not start when the drug was firs introduced. Withdrawal of the drug are the most reliable ways to diagnose lichenoid drug eruptions but may not be possible to carry out.


Oral Lichen Planus

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 force (Nikolsky’s phenomenon). A biopsy for routine histology and direct immunofluorescence are required for an accurate differential diagnosis.

Discoid lupus erythematosus (DLE) shows white radiating striae sometimes resembling those of OLP. The striae present in DLE are typically more prominent, with a more marked hyperkeratinization, and the striae may abruptly terminate against a sharp demarcation Histopathologic criteria for lupus erythematosus have been reported to discriminate against OLP

Note :Esophageal lichen planus has been described to occur simultaneously with OLP in some patients, the main complaint being dysphagia


Oral Lichen Planus

Diagnosis

Papules or reticular components have to be present in order . a correct clinical diagnosisto establish a diagnosis • These pathognomonic components may exist together with plaque-like, erythematous,

bullous, or ulcerative lesions • In patients with gingival erythematous lesions, it may be difficult to find striae or

papules. Biopsy

Management

Since the etiology behind OLP is unknown, basic conditions for development of preventive therapies are lacking • All current treatment strategies are aiming to reduce or eliminating symptoms. • Several topical drugs have been suggested, including steroids, retinoids, and

ultraviolet phototherapy.


Oral Lichen Planus

Management Among these, topical steroids are widely used and accepted as the primary treatment of choice very potent steroids as clobetasol propionate in favor of intermediate steroids such as acetonide triamcinolon

• Cyclosporine may be considered a second choice, although the efficacy has been questioned.

• Tacrolimus should only be used by experts when symptomatic OLP lesions are recalcitrant to topical steroids

Topical steroids• are preferably used as a mouth rinse or a gel as formulas are often easier for

the patient to administer than a paste.• A reasonable approach may be to apply the drug two to three times a day

during three weeks followed by tapering during the following nine weeks until a maintenance dose of two to three times a week is reached.

• �When potent topical steroids are used, a fungal infection may emerge, and a parallel treatment with antifungal drugs may be necessary.

Immunopathologic Diseases Lichenoid ReactionsDrug -Induced Lichenoid Reactions

As the clinical and histopathologic appearances resemble a delayed hypersensitivity reaction, • Drugs or their metabolites, with the capacity to act as haptens, trigger (type of

antigen) a lichenoid reaction. • Penicillin, gold, NSAID, and sulfonamides are examples of drugs that have been

related to the development of DILRs • Predominantly unilateral and present with an ulcerative reaction pattern. • A correct diagnosis is easier to establish when a patient develops the reaction after

starting a new drug • May not develop for several months after A new drug is started. It may also take

several weeks before the reaction disappear following withdrawal.

Management• DILRs are not usually seen in conjunction with severe life-threatening reactions such

as toxic epidermal necrolysis.• Discontinuance of the drug and symptomatic treatment with topical steroids are often

sufficient.• The patient should be properly educated about the responsible drug to prevent future

REACTION

Immunopathologic Diseases Lichenoid ReactionsLichenoid Reactions of GVHD• The major cause of GVHD is allogeneic hematopoietic cell. Oral lichenoid reactions

as part of GVHD may be seen both in acute and chronic GVHD transplantation.

• Clinically are indistinguishable from OLP, but lichenoid reactions associated with

GVHD are typically associated with a more widespread involvement

• It is not possible to distinguish between OLP and oral GVHD based on clinical and

histopathologic features.

Management• The same treatment strategy as for OLP may be used for chronic oral GVHD.

• Opportunistic infections should always be considered in immunosuppressed patients.

• The development of secondary malignancies has been recognized as a potentially

serious complication of GVHD.

• Patients with a history of oral GVHD should therefore be examined for oral

malignancies as part of the medical follow-up

Immunopathologic Diseases Lichenoid ReactionsLupus Erythematosus


• Both the natural and the adaptive parts of participating, with the latter involving

both B and T lymphocytes

• Environmental factors are of importance as sun exposure, drugs, chemical

substances, and hormones which all have been reported to aggravate the disease.

• A genetic predisposition is supported by an elevated risk for siblings to develop LE

• Medications :More than 80 different drugs have been associated with the onset of

SLE, including hydralazine, methyldopa, chlorpromazine, isoniazid, quinidine, and

procainamide

• SLE predominantly affects women of reproductive age, and the prevalence decreases

during the menopause, supporting an involvement of hormones in the pathogenesis of

LE as well as the fact that the disease can be precipitated by hormonal drugs.

• There are large variations in the distribution of the disease between different ethnic

groups.


• The oral lesions observed in SLE and discoid lupus erythematosus are similar in their characteristics, both clinically & histopathologically

The typical clinical lesion comprises white striae with a radiating orientation, and these may sharply terminate toward the center of the lesions, which has a more

erythematous appearance

• The most affected sites are the gingiva, buccal mucosa, tongue, and palate. Lesions in the palatal mucosa can be dominated by erythematous lesions

These lesions may form butterfly-like rashes over the cheeks and nose known as malar rash.

• Oral mucosa lesions compatible with LE may be the first sign of the disease• The classic categorization of LE into SLE and DLE has during recent years been

supplemented with acute cutaneous lupus erythematosus and subacute .lupus erythematosus.

American College of Rheumatology Criteria for Systemic Lupus Erythematosus


Laboratory Findings

1.Antinuclear antibodies (patients with other rheumatologic diseases, such as Sjogren’ssyndrome and rheumatoid arthritis)

2. Moderate to high titers of anti-DNA and anti-Smith antibodies are almost pathognomonic of SLE

3.Direct immunohistochemistry to reveal granular deposition of IgM, IgG, IgA, and C3 (lupus band test)

Diagnosis Oral mucosal lesions seen in conjunction with different types of LE are clinically and histopathologically indistinguishable. Liquefaction degeneration may also be present, which may result in diagnostic problems in relation to OLP

Management • The oral lesions may respond to systematic treatment used to for the disease• topical steroids : such as clobetasol propionate gel 0.05%, betamethasone

dipropionate 0.05%, or fluticasone propionate spray 50 μg aqueous solution are usually required

Oral lesion ========== as a Mirror University of Basrah –College of dentistry


LCRs are considered due to a delayed hypersensitivity reaction to constituents derived from dental materials. The majority of patients are patch test positive to mercury (Hg),which lends support to LCR being an allergic reaction.Although Hg is usually considered the primary etiologic factor, other amalgam constituents may also initiate LCR.

Allergic ReactionsLichenoid Contact Reactions

• LCRs are considered to be a type of delayed hypersensitivity reaction to constituents derived predominantly from amalgam fillings materials,

• LCRs display the same reaction patterns as seen in OLP, but The most apparent clinical difference between OLP and LCR is the extension of the lesions which confined to sites that are regularly in contact with dental materials.

• The majority of this type of LCR resolve following treatment with chlorhexidin


Allergic ReactionsLichenoid Contact Reactions

DiagnosisThe diagnosis is primarily based on the topical relationship to dental materia

• The patch test • Histopathology

Management

Replacement of dental materials in direct contact with LCR will result in cure or considerable improvement in at least 90% of the cases.There is no need for replacement of restorative materials that are not in direct contact with the LCR. Healing does not seem to depend on what type of dental material is used for replacement

. Reactions to Dentifrice and Chlorhexidine

Delayed hypersensitivity reactions to toothpastes and mouthwashes have been reported, The compounds responsible for the allergic reactions may include cinnamon or preservatives ,flavor additives and These constituents may also be used in chewing gum and produce similar forms of gingivostomatitis.


Toxic Reactions Reactions to Smokeless Tobacco

Smokeless tobacco represents a nonhomogeneous group of compounds used with different intraoral application methods. •Three different geographic areas are of special interest: South Asia, the United States, and Scandinavia

In United States, and Scandinavia

Smokeless tobacco can be divided into three different groups: chewing tobacco,moist snuff, and dry snuff.

In India, tobacco is often used in combination with betel leaf, sliced areca nut, which increases the toxicity of the compound. There is a definitive association between this form of smokeless tobacco and oral cancer


Toxic Reactions Reactions to Smokeless Tobacco

• The mildest form, of the lesion wrinkles at the site of application whereas high consumers may display a white and leathery lesion with ulcerations. Hyperkeratinization, acanthosis, and epithelial vacuolizations together with different degrees of subepithelial inflammation.

• Gingival retractions are the most common adverse reaction with a smokeless tobacco habit. These retractions are irreversible, whereas the mucosal lesion usually regresses within a couple of months.

The carcinogenic potential of smokeless tobacco has been a subject of considerable debate, however, no doubt that smokeless tobacco products contain nitrosamines ,polycyclic hydrocarbons, aldehydes ,heavy metals which all have a potential to cause harm.

Immunopathologic Diseases Lichenoid ReactionsSmoker’s Palate

The most common effects of smoking are presented clinically as • dark brown pigmentations (smoker’s melanosis) and as • white leathered lesions (nicotine stomatitis) or smoker’s palate,

As a part of this lesion a Red Dots may present representing orifices of minor salivary glands, which can be enlarged and display metaplasia

• The prevelance of smoker palate range from 0.1 _2.5 %

• is a common clinical feature in high consumers of pipe tobacco and cigarettes and among individuals who practice inverse smoking.

Immunopathologic Diseases Lichenoid ReactionsReactions to Mechanical Trauma

Morsicatio• parafunctional behavior is done

unconsciously and is therefore difficult to bring to an end

• Morsicatio is most frequently seen in the buccal and lip mucosa

• Typically,morsicatio does not entail ulcerations but encompasses A shreded Area.

• In cases of more extensive destruction of oral tissues by habitual chewing, a psychiatric disorder should be suspected.

Immunopathologic Diseases Lichenoid ReactionsReactions to Mechanical Trauma

Frictional Hyperkeratosis• Oral frictional hyperkeratosis is typically

clinically characterized by a white lesion without any red elements.

• The lesion is observed in areas of the oral mucosa subjected to increased friction

• prevalence has been reported to be in the range of 2%–7%.

• Frictional hyperkeratosis is often seen in edentulous areas of the alveolar ridge.

• Asymptomatic but can cause anxiety to the patient (supposed as a malignant or premalignant lesion)

Immunopathologic Diseases Lichenoid ReactionsOther Red and White Lesions

Benign Migratory Glossitis (Geographic Tongue, Erythema migrans)

is an annular lesion affecting the dorsum and margin of the tongue.The typical clinical presentation comprises a white, yellow, or gray slightly peripheral zone•ONE of the most prevalent oral mucosal lesions,• Single or multiple •Heredity has been reported, suggesting the involvement of genetic factors in the etiology.•The most frequently reported prevalence is in the range of 1%–2.5%.

Assotiated with: 1-Reiter Dz (Artheritis,uveitis ,conjunctivitis)2- Generlized pustular psoriasia


Leukoedema

• The etiology of leukoedema is not clear • Leukoedema is a white and veil-like alteration of the

oral mucosa that is merely considered a normal variant. The condition is often bilaterally in the buccal mucosa and sometimes at the borders of the tongue.

Leukoedema is less clinically evident after stretching the mucosa but reappears after this manipulation is discontinued

• The condition is asymptomatic and has no malignant potential.

• The clinical features of leukoedema are quite different from oral keratosis, such as leukoplakia, as the demarcation is diffuse and gentle stretching results in a temporary disappearance

Treatment There is no demand for Treatment


• It is initiated following mutations in those genes that are coding for epithelial keratin of the types K4 and K13

• It has been listed as a autosomal dominant disorder( rare disorder) by the National Institutes of Health, a prevalence below 1 in 200,000

• The clinical appearance usually commences during adolescence with equal gender distribution.

• The typical clinical appearance is a white lesion with an elevated and irregular surfaces comprising fissures or plaques formation covered by parakeratinized or non-keratinized epithelium

• The disorder may also involve extraoral sites as esophagus , and anogenital mucosa.

DiagnosisA differential diagnostic is problematic with other oral dyskeratoses, such as oral plaque type candidiasis and leukoplakia

White Sponge Nevus


• The etiology of hairy tongue is unknown in most cases. A number of predisposing factors have been related to this disorder,

• neglected oral hygiene,• a shift in the microflora,• antibiotics and• immunosuppressive drugs,• oral candidiasis,• excessive alcohol consumption,• oral inactivity,• and therapeutic radiation.• also associated with smoking habitsClinicallyHairy tongue is characterized by an impaired desquamation of the filiform papilla, which leads to the hairy-like.The elongated papillae have to reach lengths in excess of 3 mm to be classified as “hairy,” although lengths of more than just 15 mm have been reported in hairy tongue.

Managemant=======tretinoin (retinin acid- vitamin A)

Hairy Tongue

White and Red oral mucosal lesions Lec 4&5

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