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RESOURCE FACULTY PRESENTED BY

DR.ASHISH SHRESTHA ASSOCIATED PROFESSOR AND HOD

DR.TARAKANT BHAGATASSISTANT PROFESSOR (DEPARTMENT OF PUBLIC HEALTH DENTISTRY) BPKIHS,NEPAL

PAPULAR CHAUDHARY ROLL NO:491 4everpapular@gmail.com

SANTOSH PANDIT ROLL NO:502 bless288maniac@gmail.com BATCH 2011

ORAL MANIFESTATIONS OF SYSTEMIC DISEASE

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Oral Manifestations of Systemic Diseases

Many systemic diseases are reflected in the oral mucosa, maxilla, and mandible.

Mucosal changes may include ulceration or mucosal bleeding.

Immunodeficiency can lead to opportunistic diseases such as infection and neoplasia.

Bone disease can affect the maxilla and mandible.

Systemic disease can cause dental and periodontal changes

Drugs prescribed for a systemic disease can affect oral tissue.

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Oral Manifestations of Systemic Diseases (cont.)

Local factors may be involved in the manifestation of systemic disease in oral mucosa.

The mucosa may be more easily injured due to a systemic disease, and mild irritation and chronic inflammation may cause lesions that otherwise would not occur.

These may include Endocrine disorders, disorders of red and white blood cells,

disorders of platelets and other bleeding and clotting disorders, and immunodeficiency disorders

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Oral manifestations of systemic diseases

Auto immune diseasesAIDS

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Systemic lupus erythematous

Lupus characterized by acute and chronic inflammation of various tissues of the body.

When the skin is involved, the condition is called lupus dermatitis or cutaneous lupus erythematosus.

A form of lupus dermatitis that can be isolated to the skin, without internal disease, is called discoid lupus.

When internal organs are involved, the condition is referred to as systemic lupus erythematosus (SLE)

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CRITERIA FOR diagnosis of SLEMALAR RASH: fixed erythema over the

malar eminences(butterfly rash)DISCOID RASH: erythematous raised

patches with adherent keratotic scaling & follicular plugging.

PHOTOSENSITIVITY: Skin rashORAL ULCERS: oral or nasopharyngeal

ulceration,usually painlessARTHRITIS: Non erosive arthritisSEROSITIS: pleuritis & pericarditisRENAL DISORDER: persistent

proteinuriaNEUROLOGIC DISORDER: seizures,

psychosis

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7 HEMATOLOGICAL DISORDER: hemolytic anemia, leucopenia,

lymphopenia, thrombocytopenia.

IMMUNOLOGIC: anti- ds DNA, anti Sm & antiphospholipid antibodies

ANTINUCLEAR ANTIBODY: abnormal

(for the diagnosis of SLE four or the above criteria should either be present simultaneously or serially)

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8Oral aspects

Characteristic oral lesions, non specific ulceration, salivary gland disease, TMJ disorders.

Angular cheilosis, mucositis, glossitis, glossodynia, dysgeusia, dysphagia, dry mouth.

Lip lesion: central atrophic & occasionally ulcerated area with small white dots surrounded by keratinized border composed of small radiating white striae.

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INTRA ORAL LESION:

composed of a central depressed red atrophic area surrounded

by 2-4 mm elevated keratotic zone that dissolve into a white line.

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Discoid lupus erythematus

DLE is a chronic, scaring, atrophy producing, photosensitive dermatosis.

DLE may occur in patients with SLE.

<5% DLE progress to SLE .

• PATHOPHYSIOLOGY Suggested that heat shock protein is induced in

keratinocyte followed by UV light exposure or stress, and this protein act as target for T-cell mediated epidermal cell cytotoxicity.

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Clinical features

Age: 3rd -4th decade.

Sex female>male.

Common sites:• Face, oral mucous membranes, chest, back and extremities.

• Cutaneous lesion are slightly elevated red of purple macules that are often covered by grey or yellow adherent scales.

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Contd…

• Forceful removal of scale result in “carpet track” extension .

• Typical “butterfly” distribution on malar region and across the bridge of the nose.

• Epidermoid carcinoma and less commonly basal cell carcinoma is reported in healed ulcer.

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Oral manifestation

Oral mucous membrane involvement rate is 20-50%.

Oral lesion in discoid form begin as erythematous area, some times slightly elevated but more often depressed.

No induration.

Occasionally superficial ,painful ulceration may occur with crusting or bleeding.

No scale formation .

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Margin are not well demarcated but frequently show narrow zone of keratinization.

Central healing may result in depressed scarring In case of tongue atrophy of papilla and severe fissuring may be seen.Erythematous, artophic plques , surrounded by kertotic border, may

involve the entire lip.

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an autoimmune disorder in which immunocytes damage the salivary and lacrimal glands, and other exocrine glands.

-primary Sjogren syndrome(SS-1)-dry mouth and dry eyes are seen in the absence of connective tissue disease. Also termed as SICCA Syndrome. Less common

-Secondary Sjogren syndrome(SS-2)-Dry mouth dry eyes along with the connective tissue disease and is more common.

Common connective tissue disorder are Rheumatoid arthritis, SLE, Polymyositis,

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incidence

Can affect any age, but onset is more common 40-60 yrsF>M

etiologySpecific antigen in SS is unknownPossible etiological factors may be

Genetic association to HLA class II antigens connective tissue disease Viruses such as EBV, Hep C, HIV Graft versus Host disease Liver disease

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Clinical presentationsA)oral signs and symptoms Dry mouth

and erythematous mucosa Cracker sign Burning sensation Salivary gland swelling and sialedinitis Caries Candidiasis Abnormal taste and malodour

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B) Ocular Signs and Symptoms Keratoconjuctivitis sicca Foreign body sensation Inability to tear Light intolerance

C)Others Fatigue Fever Kidney, muscle, nerve, liver, joint,

thyroid involvement Connective tissue disease

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SYSTEMIC SCLEROSIS

Autoimmune collagen vascular disease characterized by fibrosis, vascular alterations

Systemic sclerosis describes the multisystem nature.Clinical types: 1)circumscribed plaques or bands 2)linear morphea 3)fronto parietal lesion with or without hemiatrophy of face

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IncidenceGreatest incidence in 30-50 years of age.F:M = 3-6:1

EtiologyGenetic predisposition Microchimerism.CytomegalovirusOrganic solvent and other chemicalsChronic renal failure.Drugs such as Bleomycin

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Oral manifestations

Difficulty in opening mouth and loss of tongue movement due to perioral and lingual fibrosis

Lips become thin, rigid & fixed producing microstomiaMaxillary anterior teeth are exposed due to retraction

of lipsCrenations of buccal mucosa and tongue has been

reported

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Tongue, soft palate & larynx are usually involved causing mild edema followed by atrophy & induration of mucosal & muscular tissues.

Tongue becomes stiff & border like causing difficulty in eating & speaking.

Gingival tissues are pale & firm.Dysphagia, limited mouth opening, TrismusSalivary changes similar to Sjogren syndrome

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Classic radiographic finding is generalized symmetric widening of periodontal ligament space(2-4 times) which is seen in almost all the patient.

Bone resorption at the angle of mandibleAnd may destroy condylar and coronoid process of mandible

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Dental aspect

Dysphagia and pulmonary, cardiac or renal disease as potential C.I for G.A

Constriction of oral orifice leading to limited mouth opening(fish mouth)

Tongue become stiff and less mobile due to submucosal tissue involvement(chicken tongue)

Involvement of peri-articular tissue of TMJ together with microstomia limits assess to the mouth.

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The mandibular angle may be resorbed of rarely there is resorption of TMJ.

Penicillamine therapy may cause loss of taste, oral ulceration, lichenoid reaction and other complications

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26 pemphigus

Derieved from Greek word; pemphix: bubble\blister)

Refers to group of auto immune disease characterized by development of vesiculobullous lesion in the skin and mucous membrane.

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27Clinical features

Vesiculo – bullous lesions

Oral mucosa involvement (50-70%)

Nikolsky’s sign (+)

Bulla spread sign (+)

Sites – scalp, face, trunk, groin

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Oral manifestation

About 90% of the patients show oral lesion whereas 60% of the patients present as the first sign in oral mucosa.

May occur anywhere in the oral mucosa however common sites are palate, buccal, mucosa, gingiva

In gingiva may give rise to desquamative gingivitis

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Highly painful, bleed easilyFilled with clear watery fluid which may become hemorrhagic

or purulent with ragged borders.Size varies from few millimeters to several centimeters.Intact bulla is rarely seen, most of the time its eroded lesion

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Mucosal lesions heal without scarring. However, oral mucosa often shows the formation of keratotic lesion following healing

In addition, there will be foul smell, excessive salivation and difficulty in taking food

The course of the disease is very rapid, one either terminating in death or recovery within few days or weeks.

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31 Pemphigus vegetans

Benign variant of PV because the patient demonstrate the ability to heal the denuded areas.

Two types: Neumann type:similar to PV Hallopeau type: pustules rather than bullae

Gingival lesions may be lace-like ulcers with purulent surfaces on a red base or have a granular or cobblestone appearance

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Pemphigoid

Two major types of pemphigoidI. Bullous pemphigoid.II. Mucous membrane pemphigoid.

Though in contrast to pemphigus, lesion are larger and leave denuded area while they brust, do heal and rarely fatal.

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Bullous pemphigoid (BP)

Age - 60 – 80 years

Sex - M : F = 2 : 1Pathogenesis:

Interaction of auto-antibody with BP antigen on the

lamina lucida of the basement membrane

Complement activation and attraction of neutrophils and

eosinophils

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34Clinical features

Bullous lesions

Sites - Axillae, acral region, trunk

Oral mucosa - usually not often

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Mucous membrane pemphigoid(cicatricial pemphigoid)

Skin involvement is less common, oral mucosa being the most common site i.e 90% and 2nd being the conjuctiva

Age 60-80 yearsMale=female

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– Urticaria or eczema may persist for several weeks to several months before vesico-bullous lesion appear.

– These vesicles and bullae are thick-walled and tensed and may remain for some days. Rupture doesn’t always occur.

– Oral, eye and skin lesions are present.

– Bulla spread sign and Nikolsky’s sign are negative.

– Lesions heal with milia formation.

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Oral manifestations

Seen in 30-50% of patients

However oral lesions are smaller, less painful and form more slowly then pemphigus vulgaris

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Desquamative gingivitis most common oral manifestations and may be the only site

Gingival lesions consists of generalized edema, inflammation, and desquamation with localized areas of discrete vesicle formation

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Lichen planus

It is a rather common chronic mucocutaneous disease, which probably arises due to an abnormal immunological reaction.

Disease presented with characterstic volaceous polygonal puritic papules.

Malignant tranformation potential = 0.4-2%.

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Etiology

Exact etiological cause is unknown. Predisposing factors:I. Emotional stress.II. Trauma and infection.III. Grinspan’s syndrome.IV. Hereditary.

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Clinical feature

I. Age >40 years.II. Female to male ratio 1.4:1.III. Skin lesions. Small angular flat-topped only few mm in diameter. On course of

disease they may be discrete or gradually coalesce into larger plaque cover by fine glistening scale.

Initially disease lesion appears red, but they soon take reddish , purple and violaceous hue. Later on dirty brown colour develops.

Wickham’s straie.

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Oral manifestations- Commonly occurs in mucosal surface of buccal mucosa , vestibules,

tongue,lips, floor of the mouth, palate.

Appears weeks or months before the skin lesions.

Lesions are bilaterally symmetrical.

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Usually asymptomatic but patient may complaint of pain, burning sensation and intolerance to spicy food

Begins as small white papules that coalesce to form interlacing network of white lines (Wickham’s striae)

Erythematous atrophic and erosive (erosive OLP) white lesions are common

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Reticular OLP has classical features and do not require biopsy to diagnose

Hypertrophic white plaques may occur sometimes and intact bullae (bullous OLP) are rarely seen

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Common site is buccal mucosa(78-87%),followed by tongue and gingiva

Koebner’s phenomenon present

Oral lesions tend to be bilateral and symmetrical

Erosive lesion on gingiva resembles desquamative gingivitis

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Lichen Planus

Reticular, lace-like pattern

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Atrophic

Lichen Planus

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Lichen Planus

Erythematous LP with reticular pattern

From:   Eisen: Oral Diseases, 11(6).November 2005.338-349

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Lichen Planus

Erosive

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Lichen Planus

Desquamative gingivitis

From:   Eisen: Oral Diseases, 11(6).Novermber 2005.338-349

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Recurrent aphthous stomatitis

Definition: Recurring episodes of small, round or oval ulcers with circumscribe margin, erythematous halo and a yellow or grey floor, present from childhood or adolescence and each episode last for 1 to 4 weeks before healing

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Clinical Features

Common disease afflicts 20% of the population

High prevalence: higher socio-economic classes

Three main clinical types of RAS:1. Minor aphthous ulcers (Mikulicz ulcers): 80% 2. Major aphthous utcer (Sutton's ulcers): 10%

3. Herpetiform type ulceration: 10%

Main features of recurrent aphthousstomatitis

Feature Minor aphthae Major aphthae

Herpetiform

Age of onset

Symptoms Ulcer sizeShape of ulcerNumber of u1cers Sites affected

Duration of each UlcerOther comments

Childhood or adolescence

Minimal2-4 mm Round or ovoidUp to about sixNon-keratinised mobile mucosae, Vestibule, Labial, Buccal mucosa and floor of mouth,rarely dorsum of. tongue, Gingiva or palateUp to 10 daysHeal with little or no scar

Childhood or adolescenceMore painfulMay be 10mm or largerRound or ovoidup to about sixAny site

Up to 1 monthMay heal withscarring

Young adult

Extremely painfulInitially tiny, ulcers coalesceRagged10-100Any site but often on ventrum of tongue

Up to I monthAffect females predominantly

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BEHCET’S DISEASE

Rare multisystem, chronic disease characterized by oral and genital mucocutaneous ulcerations, skin rashes, arthritis, thrombophlebitis, uveitis, colitis, and neurologic symptoms.

Also known adamatiades syndrome.

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Reiter’s syndrome

Disease of unknown etiology. Common on age group of 25-35 years.Consider as an important complication of non gonococcal urethritis.Oral lesion occurs in less than 5% to 50% of patient with disease.Consist of tetrad of :1. Urethritis 2. Arthritis. 3. Conjunctivities.4. Mucocutaneous lesion.

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58 Oral manifestationsLesions are painless, red, slightly elevated areas with a white

circinate border on the buccal mucosa, lips and gingiva.

Palatal lesions appears as small ,bright red purpuric spots which darken and coalese. Tongue represents “geographic tongue”.

Note: Clinically similar lesion are seen on the glans penis, producing a circinate balanitis

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59Wegner granulomatosis

Disease of unknown etiology.Involve vascular renal and respiratory systems.Disease characterize by necrotizing and granulomatous vasculitis.Clinical types:1. Generalize or classic wegener’s granulomatosis.2. Localized or limited wegener’s granulomatosis.

3. Superficial wegener’s granulomatosis.

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60Oral manifestations

Starts with tumor like vegetations in mouth and nose, then inflammatory process starts in nose and inter dental papilla spreading upto periodontium.

Ulceration can occur, usually perforating in nature.

Strawberry gingiva characterized by ulceration, friable granular lesions.

Mobile teeth .

Palatal destruction resulting in oro nasal communication.

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61Oral manifestations of HIV

CLASSIFICATIONGroup 1 : LESIONS STRONGLY ASSOCIATED WITH HIV INFECTIONS Candidiasis : Eythematous Pseudomembranous Hairy leukoplakia Kaposi’s sarcoma Non- Hodgkin’s lymphoma

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Periodontal diseases : Linear gingiva erythema Necrotizing ulcerative gingivitis Necrotizing ulcerative periodontitis

Group 2 LESIONS LESS COMMONLY ASSSOCIATED WITH HIV Bacterial infections: M.avium - intracellulare M. tuberculosis Melanotic hyperpigmentation Necrotizing ulcerative stomatitis

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LESIONS SEEN IN HIV INFECTION Bacterial infections :Actinomyces israeli Escherichia coli Kliebsella pneumoniae Cat scratch disease

Drug reactions: Ulcerative Erythema multiforme Lichenoid reaction Toxic epidermolysis

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• Fungal infections other than candidiasis Cryptococcus neoformans Geotrichum candidiasis Histoplasma capsulatum Zygomycosis Aspergillus flavus

• Neurologic disturbances : Facial palsy Trigeminal neuralgia• Recurrent apthous stomatitis

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Oral manifestation can be broadly clasified as

Fungal lesions Viral lesions Bacterial lesions Neoplastic lesions HIV associated other lesions

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Fungal lesions

CandidiasisHistoplasmosisCryptococcus neoformans

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Viral lesions

Herpes simplexHerpes zosterHuman papilloma virusCytomegalovirusEpstein-Barr Virus(oral hairy leukoplakia)

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Bacterial lesion

Periodontal diseases : Linear gingival erythema Necrotizing periodontal disease(NUG,NUP)

TuberculosisSyphilis

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Neoplastic lesions

Kaposi’s sarcoma Oral squamous cell carcinoma Non –Hodgkin’s lymphoma

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Other lesions

Recurrent apthous ulcerHIV associated salivary gland disease

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CANDIDIASIS

The most common opportunistic infectionCD4 cells counts< 400 cells/mm^3 4 clinical presentation: Pseudomombranous or oral thrush Erythematous Hyperplastic Angular cheilitis

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Pseudomembranous candidiasis

Most common type. Usually asymptomatic. Usually extensive involving more than one site Manifests as white or yellowish single or confluent plaque that is

scrappable, exposing erythematous area. May also extend to oropharynx and esophagus.

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Erythematous/ atrophic

Site: dorsum of the tongue,palate and buccal mucosa. Appears as a reddish macular lesion, or depappilation on the dorsum

of the tongue. May present alone or in combination with pseudomembranous

candidiasis. Tongue lesion are also referred as central papillary atrophy. Long standing lesion:mucosal ulceration Some may complain of occasional burning sensation .

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Hyperplastic

Uncommon and found in severly immunocompromised. Manifests as white or discolored plaques which cannot be scrapped

out Burning sensation, Dysphagia Feeling of having large piece of cotton in mouth

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Angular cheilitis

Can be due to mixed infection of candida albicans and staphylococcus aureus.

Manifests as erythema &/or fissuring and/ or scaling of angle of mouth.

May be present with intraoral candidiasis.

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pseudomembranous Erythematous

Hyperplastic

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Thank you

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Oral Manifestations of systemic diseases II

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Learning objectives

Be able to enumerate the major oral

manifestations of blood disorders,renal

disorders,GI disorder, diabetes, respiratory

diseases

Be able to list the dental considerations and

management of these systemic disorders

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Blood Disorders

Disorders of Red Blood Cells and Hemoglobin

Disorders of White Blood Cells

Bleeding Disorders

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Disorders of Red Blood Cells and Hemoglobin

Iron Deficiency AnemiaPernicious AnemiaFolic Acid and Vitamin B12 Deficiency AnemiaThalassemiaSickle Cell AnemiaAplastic AnemiaPolycythemia

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Anemia

A reduction in the oxygen-carrying capacity of blood

Most often related to a decrease in the number of circulating red blood cells

Nutritional anemiasA deficiency in a substance required for the normal development of

red blood cells, commonly vitamins

Suppression of bone marrow stem cells

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Anemia (cont.)

Clinical features Pallor of skin and oral mucosa

Angular cheilitis

Erythema and atrophy of oral mucosa

Loss of filiform and fungiform papillae on the dorsum of the tongue

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Iron Deficiency Anemia

An insufficient amount of iron is supplied to bone marrow for red blood cell development.

May occur as a result of deficient iron intake, blood loss from heavy menstrual bleeding or chronic gastrointestinal bleeding, poor iron absorption, or an increased requirement for iron in situations such as pregnancy or infancy

Plummer-Vinson syndrome may result from long standing iron deficiency anemia. Includes dysphagia, atrophy of the upper alimentary tract, and a predisposition to

developing oral cancer

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Clinical Features and Oral Manifestations of Iron Deficiency Anemia

Often asymptomatic, may have nonspecific symptoms such as weakness and fatigue

In severe cases may see angular cheilitis, pallor of oral tissue, and an erythematous, smooth, painful tongue

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Pernicious Anemia

Probably an autoimmune disorder in most situations

May be caused by removal of the stomach, gastric cancer, or gastritis

Caused by a deficiency in intrinsic factor

Intrinsic factor is secreted by parietal cells in the stomach; it is necessary for absorption of vitamin B12

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Clinical Features and Oral Manifestations of Pernicious Anemia

Weakness, pallor, and fatigue on exertion

May see nausea, dizziness, diarrhea, abdominal pain, loss of appetite, and weight loss

Angular cheilitis, mucosal pallor, painful atrophic and erythematous mucosa, mucosal ulceration, loss of papillae on the dorsum of the tongue, and burning and painful tongue

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Folic Acid and Vitamin B12 Deficiency Anemia

From dietary deficiencies

Can occur in association with malnutrition

May be found with alcoholism or pregnancy

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Oral Manifestations of Folic Acid and Vitamin B12 Deficiency Anemia

Oral manifestations are indistinguishable from those of pernicious anemia.

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Thalassemia (Mediterranean or Cooley Anemia)

A group of inherited disorders of hemoglobin synthesis

An autosomal dominant inheritance pattern

The heterozygous form may be mildly symptomatic or asymptomatic.

The homozygous form is associated with severe hemolytic anemia.

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Clinical Features and Oral Manifestations of Thalassemia

Yellow skin pallor, fever, malaise, and weakness

The face includes prominent cheekbones, depression of the bridge of the nose, a prominent maxilla, and protrusion or flaring of maxillary anterior teeth.

Radiographs may show a “salt and pepper” pattern.

Some trabeculae are prominent, and others are blurred.

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Sickle Cell Anemia

An inherited blood disorder

When someone is heterozygous, it is called sickle cell trait.

When someone is homozygous, they are much more severely affected.

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Occurs before age 30 and is more common in women than in men

The red blood cells develop a sickle shape when there is decreased oxygen.

This can be triggered by exercise, exertion, administration of a general anesthetic, pregnancy, or even sleep.

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Clinical Features and Oral Manifestations of Sickle Cell Anemia

The person has weakness, shortness of breath, fatigue, joint pain, and nausea.

Radiographic There is a loss of trabeculation, and large, irregular marrow spaces

appear.

A “hair-on-end” pattern may be seen in the skull.

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Aplastic Anemia

A severe depression of bone marrow activity causes a decrease in all circulating blood cells. – pancytopenia

Primary aplastic anemia – the cause is unknown Secondary aplastic anemia – a result of a drug or chemical agent

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Oral Manifestations of Aplastic Anemia

Infection, spontaneous bleeding, petechiae, and purpuric spots

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Polycythemia

Polycythemia Vera

Secondary Polycythemia

Relative Polycythemia

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Oral Manifestations of Polycythemia

The oral mucosa may appear deep red to purple; the gingiva may be edematous and bleed easily.

Submucosal petechiae, ecchymosis, hematoma formation may be present.

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Disorders of White Blood Cells

Agranulocytosis

Cyclic Neutropenia

Leukemia

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Clinical Features and Oral Manifestations of Agranulocytosis

Sudden onset of fever, chills, jaundice, weakness, sore throat

Oral infection

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Leukemia

Malignant neoplasms of hematopoietic stem cells

Characterized by an excessive number of abnormal white blood cells in circulating blood

Unknown cause; some are investigating oncogenic viruses

There are many different types categorized as to whether they are acute or chronic.

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Acute Leukemias

Characterized by very immature cells and a rapidly fatal course if not treated

Acute lymphoblastic leukemia – involves immature lymphocytes

Primarily affects children and young adults

Good prognosis Acute myeloblastic leukemia – involves immature granulocytes

Primarily affects adolescents and young adults.

Prognosis is not as good.

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Clinical Features of Acute Leukemias

Weakness, fever, enlargement of lymph nodes, bleeding

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Oral Manifestations of Acute Leukemias

Gingival enlargement

Oral infection

Bleeding gums, petechiae and ecchymosis

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Chronic Leukemias

Slow onset

Primarily affect adults

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Clinical Features and Oral Manifestations of Chronic Leukemias

Easy fatigability, weakness, weight loss, anorexia

Pallor of lips and gingiva, gingival enlargement, petechiae and ecchymosis, gingival bleeding

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Bleeding Disorders

Purpura

Hemophilia

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Purpura

A reddish-blue or purplish discoloration of skin or mucosa from spontaneous extravasation of blood

May be due to a defect or deficiency in blood platelets

Blood may ooze from gingival margins.

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Thrombocytopenic Purpura

A bleeding disorder that results from a severe reduction in circulating platelets

Idiopathic thrombocytopenic purpura

If the cause is unknown

Immune thrombocytopenia

An autoimmune type of process

Secondary thrombocytopenic purpura

Often associated with drugs

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Clinical and Oral Manifestations of Thrombocytopenic Purpura

Spontaneous purpuric or hemorrhagic lesions on the skin

Patients bruise easily, may have blood in urine, have frequent nose bleeds.

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Nonthrombocytopenic Purpura

Bleeding disorders that can result from either a defect in capillary walls or disorders of platelet function

Vitamin C deficiency and infections or chemicals and allergy may be the cause of alterations in vascular walls.

Drugs, allergy, and autoimmune disease may cause disorders of platelet function.

Von Willebrand disease is an autosomal dominant disorder of platelet function.

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Oral Manifestations of Nonthrombocytopenic Purpura

Spontaneous gingival bleeding

petechiae

Ecchymoses

hemorrhagic blisters

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Hemophilia

A disorder of blood coagulation

Results in severely prolonged clotting time

Due to a deficiency in plasma proteins involved in coagulation

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Types of Hemophilia

The two most common types are type A and type B.

Transmitted as X-linked diseases through an unaffected carrier daughter to a son

Type ACaused by a deficiency of plasma thromboplastinogen or factor VIII

Type BChristmas diseaseLess common, the clotting defect is plasma thromboplastin or factor

IX

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Oral Manifestations of Hemophilia

Spontaneous gingival bleeding,

petechiae,

ecchymosis

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PATIENTS WITH RENAL DISORDERS

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INTRA ORAL FINDINGS

Soft tissue changes

Oral ulcers – Blood urea

nitrogen increases >

150mg/dl, it gets secreted

through saliva – ureamic

crystals – burn mucosa

becomes red

Uraemic stomatitis - Burning

sensation

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UREMIC STOMATITIS

Urea secreted in saliva

Urease enzyme produced by oral microflora

Liberates free ammonia

Damages oral mucosa

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INTRA ORAL FINDINGS

Soft tissue changes

Ulcers secondary to

anaemia, viral infections

(immunosupressed)

Gingival hyperplasia -

cyclosporine & nifedepine

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INTRA ORAL FINDINGS

Soft tissue changesSalivary glands - enlarged, xerostomiaGingival bleeding, petechiae, ecchymosis

due to platelet changesCandidal infection – immunosupressionHalitosis – uraemic odor, ammonical smellDysesthesia of lower lip

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Hard tissue changes

Staining in teeth – due to iron supplements

Reduced caries due to urea in saliva

Delayed tooth eruption

Enamel hypoplasia

Tooth Mobility

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RADIOGRAPHIC FEATURESMainly in cases with

hyperparathyroidismTooth appear more radiopaque in

background of osteoporotic boneLoss of trabeculations of boneGround glass appearanceTotal/ partial loss of lamina duraLoss of cortical outlines of inferior

alveolar sinus, cortex of mandiblePulpal calcifications

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RADIOGRAPHIC FEATURES

Mainly in cases with hyperparathyroidism

Multilocular radiolucency – osteitis fibrosa cystica/ browns tumor

Arterial & oral calcifications

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ORAL MANIFESTATIONS IN DIABETICS

More severe periodontal disease

Patients with multiple abscesses should be referred for blood sugar estimation

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ORAL MANIFESTATIONS IN DIABETICS

Sialosis – swelling of salivary

glands due to autonomic

neuropathy

Xerostomia may result from

hyperglycemia and

subsequent polyuria that

depletes the extracellular

fluids

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126Oral candidiasis &

angular chelitis

Oral mucosal lichenoid reactions - hypoglycaemics

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127Burning tongue - associated with

candidiasis or peripheral neuropathies

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Diseases of Respiratory tract

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UPPER - AIRWAY INFECTIONS

ALLERGIC RHINITIS AND

CONJUNCTIVITIS

SINUSITIS

PHARYNGITIS &TONSILLITIS

LOWER - AIRWAY INFECTIONS

ASTHMA

CYSTIC FIBROSIS

ACUTE BRONCHITIS

TUBERCULOSIS

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ORAL HEALTH CONSIDERATIONS for allergic rhinitis

ORAL DRYNESS

ORAL CANDIDIASIS (CORTICOSTEROIDS)

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ORAL HEALTH CONSIDERATIONS for sinusitis

Tooth Pain - Differentiate Between An Odontogenic Infection And Sinus Pain.

Sinus Infections Usually Present With Pain Involving More Than One Tooth.

Chronic Sinus Infections Are Often Accompanied By Mouth Breathing -

Gingivitis.

Prolonged Use Of Antibiotics - The Potential Development Of Bacterial

Resistance .

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ORAL MANIFESTATIONS of Asthma

Candidiasis

Decreased Salivary Flow

Increased Calculus

Increased Gingivitis

Increased Periodontal Disease

Increased Incidence Of Caries

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CONSIDERATION FOR DENTAL CARE

Fluoride Supplements - Particular Those

Taking Β2-agonists.

The Patient Should Be Instructed To Rinse His

Or Her Mouth With Water After Using Inhalers.

Oral Hygiene Should Be Reinforced To Reduce

Of Gingivitis And Periodontitis.

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ORAL MANIFESTATION of TB

RARE

MAINLY SEEN IN MIDDLE AGED & OLDER PEOPLE

SEX-MALES

MOST COMMONLY-TONGUE

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ORAL MANIFESTATION of TB

ORAL LESION –Ulcer,nodule,vesicle,granuloma,fissure

Ulceration ,Ragged Border,minimal Induration,granular Base

Sentinal Tubercle; nodules Seen Around Ulceration.

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Pregnancy- Oral Manifestations

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Dental Considerations(First Trimester)

Dental treatment is best avoided

Assess the current oral health of the patient

Educate the patient regarding the oral changes

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Nausea and vomiting – caused by increased levels of gonadotropins in the first trimester

Enamel erosion- gastric acids present in the vomit erode the inner surface of anterior teeth

Pregnancy induced gingivitis

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SECOND TRIMESTER

Organogenesis is complete and the risk to the foetus is at its lowest

safest period for any necessary elective dental treatment

140

Dental Considerations

Pregnancy Tumor- also

referred to asGranuloma

Gravidarum

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Diseases of GIT

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142GASTROESOPHAGEAL REFLUX DISEASE

Most common disease of upper GI tract

gastric contents passively move up from the stomach into the esophagus

Symptoms/signsHeart burn (pain/burning sensation extending from

epigastrium to the neck) – commonly felt after a mealesophagitis, esophageal ulceration & strictureChest pain (mimics anginal pain)Dysphagia

143

Oral Manifestations & Dental Considerations

erythema and mucosal atrophy

dysgeusia, sensitivity & erosion

(palatal aspects of upper

anteriors and premolars)

erosion leads to dentin

sensitivity & irreversible pulpal

involvement (gastric content

pH – as low as 1)04/15/2023

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Inflammatory Bowel Disease

Ulcerative colitisCrohn’s disease (regional enteritis, ileitis)

Ulcerative colitis

Inflammatory process usually extends from rectumproximally in a continuous fashion involvingvariable lengths of large intestine but confined tomucosa & superficial submucosa.

Bloody diarrhea – cardinal symptom

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CROHN’S DISEASE

Affects entire thickness of intestinal wall, in segments forms strictures and scarring

Small intestine - 40%Large intestine - 30%Both intestines- 30%

Pain & diarrheaFistulas which connect different sites in GIT, urinary

bladder,vagina, prostate and skin

Arthritis, uveitis & erythema nodosum of skin are common

in both diseases

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Oral Manifestations (Crohn’s disease)

Oral granulomatous lesions as a nodular mass in the mucobuccal fold

Lesions resembling aphthous ulcersCobblestone appearance on buccal mucosaLinear hyperplastic folds with ulcers in the vestibule

147

Crohn’s disease

Swollen & indurated lips

Granular red lesions on gingiva and alveolar mucosa and palatal ulcers (rarely)

Pustular lesions

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EATING DISORDERS

ANOREXIA NERVOSA AND BULIMIAAnorexiaindividuals who intentionally starve themselvesintense fear of becoming fat Anorexia usually develops between 14 - 18 years

Bulimia nervosa Individuals consume large amounts of food and

preventweight gain by vomiting, laxatives, diuretics,dieting, and/or exercising aggressively.

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Oral Considerations

erosion of the enamel on the lingual surfaces of the maxillary teeth

Parotid enlargement may develop as a sequela of starvation.

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REFERENCES

BURKETS-ORAL MEDICINETEXT BOOK OF ORAL MEDICINE by Anil Govindrao GhomSHAFER-TEXT BOOK OF ORAL PATHOLOGYNEVILLE-TEXT BOOK OF ORAL PATHOLOGYCARANZZA’S-CLINICAL PERIODONTOLOGYWIKEPEDIA

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Thank you