Oral ulcerations

Oral ulceration(O.U)

An ulcer is defined as an area of discontinuity of an epithelial surface, whereas erosion is a shallow defect with loss of epithelial layers down to and sometimes including the basallayer.
Examination of ulcer
Before carrying out any local examination of an ulcer, ascertain whether there is any known exciting factor such as trauma, etc., and also establish the duration of the ulcer.So far as the local physical examination of the ulcer is concerned, start the examination by palpating the dependent lymph-nodes associated with the ulcer.
1.The Situation of the Ulcer.
* The rodent ulcer at the side of the nose and beneath the eye.
* The carcinoma of the tongue at the side of the tongue.
*The gummatous ulcer often occurs at the junction of the hard and soft palates.
2.Is the Ulcer Single or Multiple.
3.Note the size of the ulcer.
4.Shape of the ulcer.- round, oval, crescentic, serpiginous, irregular, punched-out.
5.The floor of the ulcer.
a. Granulation. (red, pale, or flabby and may or may not bleed).
b. The floor may be smooth.
c. It may be covered with slough, membrane, etc.
d. The floor may be adherent to soft parts or bone.
e. The floor may be fungating as seen in the some clinical varieties of malignant disease.

6. The Edge of the Ulcer may be:-

a. Undermined ( tubercular ulcers).
b. Punched out (gummatous ulcers).
c. Rolled ( rodent ulcers).
d. Rolled, raised, and everted ( malignant ulcers
7. The condition of the parts surrounding the ulcers must be examined
8. Is the Ulcer painful ?
9. The General Condition of the Patient must always be considered.-
It can be classified into
* Primary O. U
Start as an ulcer from begining
* Secondary O. U
Secondarily to primary lesion or preceded by vesicles or bullae.
Primary O. U
1- Traumatic O. U
2- Infective O.U
*Acute infection ( acute necrotizing ulcerative gingivitis ,noma)
*Chronic infection ( Tuberculosis , Syphilis , Histoplasmosis)
3- Miscellaneous causes O.U
A. Recurrent aphthous stomatitis.
B. Behcet's syndrome.
C. Erythema multiforme.
D. Steven Johenson Syndrome.
E. Inflammatory bowel disease.[ crohn`s disease , ulcerative colitis ]
F. Cyclic neutropenia.
G. Uremic stomatitis.
H. Neoplastic ulcer.
I. Erosive lichen planus.
J. Lupus erythematosus.
K. Ulcer associated with blood disorders .. such as Anemia and Leukemia.
Primary oral ulceration:
It may be
1-Traumatic O.U
may result from
A. Physical agents
such asHeat....e.g. hot instrument, hot food
cold ….. cold drink , ice crème
B. Chemical agents
such asCMCP...phenol..Nahypochloride orconcentrated H2O2.
C. Mechanical agents
such as Sharp clasp. .dentureflanges. .sharptooth. .toothbrush bristles...cotton role burn(professional abuse )
D. Electrical agentselectric burn
Traumatic ulcerations are tender with grayish basesand red margin. It is usually covered by fibrin and debris.Healing takes place within( 3-4) days if theetiological factors and source of irritation is removed.
Note:- Biopsy of anyO. Uthat doesn't heal spontaneouslywithin 2 weeks after removing the cause is mandatory or indicated .


2-Infective O. U
Acuteinfective O.U
Acute necrotizing ulcerative gingivitisorVincent' infection or Trench mouth(ANUG)
ANUG is a unique bacterial infection thatcharacteristically affects the marginal and papillary gingiva. It is found mostoften in adolescent and young adults. The more important and constant of the microbes involvedinclude Treponemaspecies, Prevotellaintermedia, Fusobacterianucleatum, Peptostreptococcus micros, Porphyromonasgingivalis, Selenomonasspecies, and Campylobacter
The infection frequently occurs in the presence ofpsychological stress , smoking, local trauma , poor nutritional status, poor oral hygiene in addition to theImmunocompromised status such as AIDS and infectious mononucleosis. Since some of these fusospirochetal organisms are common in the periodontal tissues, many believe that it is the permissive environment of an immunocompromised host that allows these microbes to proliferate. The tissue destruction is most probably a result of the production of endotoxins and/or immunologic activation and subsequent destruction of the gingiva and adjacent tissues. In addition, patients show reduced neutrophil chemotaxis and phagocytosis, resulting in poor control of infection. The onset of acute form of thedisease is sudden with pain, tenderness, profuse salivation, metallic taste,bad odor and spontaneous bleeding from the gingival tissue.Thetypical lesions consist of necrotic punched-out ulceration developing mostcommonly on the interdental papillae and marginal gingiva. Also ulcerativelesion may developed on the cheek, the lip and the tongue .
Treatment
1-Improving oral hygiene with good instruction .
2-Scaling and polishing.
3-Oxidizing mouth wash such asH2O2solution 3%.
4-Antibiotic such as ampicillin250mg 4times daily for 1 week and metronidazole(Flagyl ) 200mg 3 times dailyfor 2 weeks.
5-Removal of stagnation area
6-Surgical correction in case of deformity.

CancrumorisorNoma;

It is rapidly progressiveopportunistic infection caused by components of the normal oral flora whichbecome pathogenic during periods of compromised immune status. The mostcommonly implicated M.O. are :-Fusobacteriumnucleatum, Borreliavincentii, Staphylococcus aureusPrevotellaintermedia ,and non hemolytic streptococcus species.Predisposing factors;Malnutrition, Dehydration, Poor oral hygiene , Recent illness.... Measles....TB. Malignancy ...... Leukemiaand AIDs.
Clinical features:
Noma typically arises in children aged 2....10years. The process often begins on the gingiva as ANUG which may extend eitherfacially or lingual to involve the adjacent soft tissue and form area calledANUMucositis. Zones of necrosis may also develop in soft tissue. Zones ofbluish-black discoloration of the overlying skin surface may develop. The gangrenous process starts as a painful, small, reddish-purple spot or indurated papule which ulcerates. The ulcer spreads to involve the labiogingival fold,It isalso associated with fetid odor ,pain,fever,malaise and lymphoadinopathy .Scarring may occur and sometime it is a fatal disease.

Treatment of noma:

Correction of inadequatenutrition
hydration and electrolyte balance
Penicillin and metronidazole
Plastic surgery
Chronicinfective O.U
Tuberculosis:
T.B is a chronic infectiousdisease caused by Mycobacterium tuberculosisTuberculosis is typically transmitted by way of infected airborne droplets of mucus or saliva that are forcefully expelled from the lungs, most commonly through coughing but also by sneezing and talking. Transmission by ingestion (e.g., of contaminated milk) occurs but is rare because of the use of pasteurized milk. A secondary mode of transmission—by ingestion—may occur when a patient coughs up infected sputum, thereby inoculating oral tissues. Oral lesions of TB may be initiated through this mechanism.The interval from infection to development of active TB is widely variable, ranging from a few weeks todecades; only 5% to 10% of cases result at thetime of the initial infection.Oral manifestation is usually theresult of secondary infection from a primary pulmonary source. Ulceration of thetongue is the most common oral lesion of T.B. The lesion is infectious and deepwith undermined border. Oral lesions of T.B. are uncommonbut can occur as nodular, granular, ulcerated or rarely firm leukoplakic areas. It is unclear whether oral lesionsdevelop from hematogenous spread or from exposure to infected sputum. Primary oral T.B. withoutpulmonary involvement is rare. Secondary oral lesions mostlypresent on the tongue, palate, and lip.
T.B. of the skin ........... is called Lupusvulgaris.
T.B. of the bone………..is called Tuberculousosteomyelitis.
T.B. ofcervical lymph node ...........is called. Scrofula
Groups at High Risk for Tuberculosis:
• Close contacts of persons who have TB
• Persons infected with HIV
• Injecting drug users
• Persons with medical risk factors (e.g., diabetes mellitus; renal failure; cancer of theblood, head, neck, or lung; gastrectomy those receiving immunosuppressive therapy equivalent to prednisone ≥15 mg/day or taking tumor necrosis factor inhibitors)
• Health care workers who serve high-risk persons
• Foreign-born persons (and migrant workers) from countries that have a high TB incidence orprevalence
• Medically underserved persons
Diagnosis ofT.B
History
Clinical examination and features
Chest x-ray
Swab&Culture
stain with Ziel.Nelson. stain
Biopsy (caseation necrosis )
Tuberculin test
PCR


Treatment of T.B
Mycobacteaum Tuberculosis can mutate and developresistance to single agent medications. To combat this ability multi agenttherapy is the treatment of choice. First line therapy
(Isoniazid hydrochloride [ INH ]300mg daily, Rifampicin600mg dailyfor 9months
Or
INH + Rifampicin +Pyrazinamide500mg..for 2months
Followed by INH + Rifampicin ...for 4months.

In resistance to any agent ..... Ethambutol ..orStreptomycin are alternative therapy .

Syphilis
It is a chronic infectioussystemic diseases with a number of stages caused by the spirochete TreponemaPallidum. The majority of syphilitic infection are acquired by sexual contact inadult life. These infections are called acquired syphilis to distinguish themfrom congenital Syphilis. Acquired syphilis is classified according to the typeof the lesion and temporal course of the disease into:-
Primary........Secondary..........Tertiary.
Primary syphilis
The lesion is the chancre, a slightly raised , ulcerated, firm plaque which is usually round and indurated with rolled raisededges. It begins as a papule before proceeding to ulcerated and may vary in sizefrom 5 mm to several cm in diameter. It is usually painless unlesssuperinfected. The chancre occurs at the site of entry of T.P. which is mostcommonly on the genitalia. The mouth is the 2nd most common site of involvementespecially lip and tongue .Chancre spontaneously disappearswithout therapy. At the same time the regional L.N. become firm enlarged and non-tender.Serological reactions are negative at first. They are highly infective, and treatment is most effective at this stage.

Diagnosis

Smear:- The organism can be demonstratedin material from primary lesion by Dark-field examination under the microscope.
Note :-Chancre is highly infectious
Secondary syphilis
The secondary lesions appearwithin 3-6 weeks after the primary lesions. A flu -like symptoms is common andpatients may develop generalized lymphdenopathy and generalized eruption onthe skin and mucosal surface. The typical syphiliticlesions in oral mucosa is Mucous patch.Mucous patches are small, smoothErythema macula – popular eruption or superficially grayish-white erosions found on M.M. of theoral cavity , vulva or penis. On the palate and tonsil they havealso been described as snail truck ulcers . Constitutional symptoms and signs (malaise, low-grade fever,headache, lacrimation, sore throat, weight loss, myalgias and multiplearthralgias, generalized lymphadenopathy) as well as cutaneous manifestations(macular syphilids, papularsyphilids, condylomatalata, nailinvolvement, hair loss& atypical rash). Secondary lesions are contagious andserological tests are positive. These tests are:- Wasserman& (VDRL ( VenerealDisease Research Laboratory


Tertiarysyphilis:
Which begins as a small, pale, raised area of themucosa that ulcerates and rapidly progresses to a large zoneof necrosis with denudation of bone and in the case of thepalate may eventually perforate into the nasal cavity. Themost common site for gumma formation is the hard palate,although the soft palate, lips, tongue, and face may beinvolved. The palatal lesions are usually midline. Gummas are painlessand have no infectivity. Atrophic or interstitial glossitis is another oral manifestation of tertiary syphilis. Clinically, there is atrophy of the filiform and fungiform papillae, which results in a smooth, sometimes wrinkled lingual surface. This appearance is probablydue to obliterative endarteritis of the lingual vasculature, leading to circulatory deficiency. Loss of the protective papillae subjects the dorsum of the tongue to many noxious stimuli, and leukoplakia frequently develops. All other manifestations of tertiary syphilis are essentially vascular in nature and result from an obliterative endarteritis. Cardiovascular syphilis is most commonly seen as an aneurysm of the ascending aorta. Neurosyphilis can result in a meningitis-like syndrome, Argyll Robertson pupils (which react to accommodation but not to light), altered tendon reflexes, general paresis, tabesdorsalis (degeneration of dorsal columns of the spinal cord and sensory nerve trunks), difficulty in coordinating muscle movements .

Congenital Syphilis

Syphilis or its sequelae occur in the newborn if the mother is infected while carrying the child. The disease is transmitted to the fetus in utero, usually after the 16th week, because before this time, the placenta prevents transmission of bacteria. Three characteristic lesionsreferred to as Hutchinsoniantriad have been associated with CongenitalSyphilis. These consist of
1-. Interstitial keratitisof the cornea .
2- 8th cranial nerve involvement
3-Deformed central incisor whichare screwdriver-shaped .
Other manifestations include:- Abnormality of first molaranatomy.Mulberrymolars.Saddlenose.Atrophicglossies.High palatal arch

Treatment of syphilis

The recommended regimen fortreatment of early syphilis of less than one year duration is
*Benzathine penicillin G 2.4million units I.M
*Penicillin allergic patients;Tetracycline hydrochloride 500mg /4times dailyfor15days.
*OrErythromycin 500mg /4 times daily for 15 days.
Histoplasmosis:
It is caused by the fungus Histoplasmacapsulatum, a dimorphic fungus that grows in the yeast form in infected tissue. Infection results from inhaling dust contaminated with droppings, particularly from infected birds or bats . Itis the most common systemic fungal infection. primary infection is mild, manifesting as a self-limiting pulmonarydisease that heals to leave fibrosis and calcification similar to tuberculosis. In a small percentage of cases, progressive diseaseresults in cavitations of the lung and dissemination of the organism to the liver, spleen, adrenal glands, and meninges. Patients with the disseminated form of the disease may develop anemia and leukopenia secondary to bone marrowinvolvement.Immunosuppressed or myelosuppressed patients are morelikely to develop the severe disseminated form of the disease.

Oral manifestations

Oral lesions are mostly chronic with nodular, indurated, or granular masses and ulceration; hard and soft tissue destruction may rarely occur. Up to 40 to 50% of cases with systemic histoplasmosis present with oral lesions. The major oral sites affected are the mucosa, tongue, palate, gingivae, andperiapical region of the teeth.The cervical lymph nodes are enlarged and firm. The clinical appearance of the lesions, as well as the accompanying lymphadenopathy, often resembles that of squamous cell carcinoma, other chronic fungal infections, or even Hodgkin’s disease.
Diagnosis
Definitive diagnosis of histoplasmosis is made by a culture of infected tissues or exudates on sabouraud’s dextrose agar or other appropriate media.Biopsy of infected tissue shows small oval yeasts within macrophages and reticuloendothelial cells as well as chronic granulomas, epithelioid cells, giant cells, and occasionally caseation necrosis.Skin tests and serology are not definitive because of significant numbers of false-negative and false-positive reaction.
Treatment
Mild to moderate cases of histoplasmosis can be treated withketoconazolor itraconazolefor 6 to 12 months. Immunosuppressedpatients or patients with severe disease require intravenousamphotericin B for up to 10 weeks.


3- Miscellaneous causes O.U
Recurrent Aphthous Stomatitis (RAS)
RAS is a common disease in humans. The reported prevalence in the general population varies from 15% to 20% . Itis probably the most common ulceration affecting the oral mucosa. RAS is defined as a recurrent oralnecrotizing ulceration which is characterized by theperiodicappearance of painful small, round or oval ulcer on the mucosa of the cheek, lips, tongue, soft palate, floor of the mouth and the pharynx with a bright-redcircular inflammatory zone around the ulcer with a psedomembrane ranging fromgray to yellow in color .The causes of RAS remainsidiopathic or as a result of a variety of predisposing factors.
Local factors[Trauma has been often identifiedas precipitating factor includingLocal anesthetic injection ,Sharp food , Tooth brush, Trauma from dental treatment

2-Systemic factors: RAS has been observed in severalsystemic disorders.

*Behcet's syndrome
*Cyclic neutropenia
*MAGIC syndrome( mouth and genitalulcer with inflammed cartilage).
*FAPA syndrome( periodicfever,aphthousulcer,pharyngitis and cervicaladenitis(.
*Nutritional deficiencies of iron, folic acid, B-complex vitamins Def,B-complex Def and zinc.
*Gastrointestinaldisorders asCeliac disease ,Ulcerative colitis&Crohn's disease
*HIV associated aphthous stomatitis
*Relative IgA Def
*Drugs as NSAIDs,Nicorandil&Methotrexate.

3-Microbial factors

It is also thought thatstreptococcus sangius and L-Form microorganism which were found to bepredominant in cases of RAS ,but it can't produce RAS in experimental animals.
4-Psychological factors, Stress and anxiety could play asignificant role in the initiation of RAS.
5-Hormonal factors, Ithas been suggested to be an important etiological factor
6-Genetic predisposition ,An inheritedpredisposition to the RAS has also been described further evidence for theinherited nature of this disorder. It is supported by several investigators who have associated certain histo compatibility antigen(HLA)types with RAS such as HLA B12, HLA B51 and HLA CW7.
7- Immunologic factors ,
Early work suggested either an autoimmune disorder or hypersensitivity to oral organisms such as Streptococcus sanguis. Investigations using more sophisticated immune assays have not supported the early work and suggest a role of lymphocyte toxicity, antibody-dependent cell mediated cytotoxicity, and defects in lymphocyte cell subpopulation.
8- Allergic factors
Hay and Reade reported the benefit of anelimination diet in some patients with suspected or provenallergy to foods such as milk, cheese, wheat, and flour. Coeliac disease ( Gluten sensitive entropathy) is a permanent intolerance to gliadin( Fraction of gluten) the protein component of wheat. It is inflammatory condition of the GIT that affect the small intestine in generally susceptible individuals. Oral manifestations of Coeliac disease are oral ulcer, glossitis, angular chelitis and enamel hypoplasia.
A detergent present in toothpaste, sodium lauryl sulfate(SLS), was suspected as an etiologic factor in RAS development.


9- Smoking factor
It is well documented that cessation of smokingincreases the frequency and severity of RAS.
RAS is a disorder characterized by recurring ulcers confined to the oral mucosa in patients with no other signs of disease . Many specialists and investigators in oral medicine no longer consider RAS to be a single disease but, rather, several pathologic states with similar clinical manifestations.Immunologic disorders, hematologic deficiencies, and allergic or psychological abnormalities have all been implicated in cases of RAS. RAS affects approximately 20% of the general population, but when specific ethnic or socioeconomic groups are studied, the incidence ranges from 5 to 50%.
RAS is classified according to clinical characteristics1-minor ulcers ;which comprise over 80% of RAS cases, are less than 1 cm indiameter and heal without scars.2- major ulcers (Sutton’s disease, periadenitis mucosa necroticarecurrens);are over 1 cm in diameter and take longer to heal and often scar. 3- herpetiform ulcersare considered a distinct clinical entity that manifests asrecurrent crops of small ulcers throughout the oral mucosa.

Clinical manifestations:

The first episodes of RAS most frequently begin during the second decade of life and may be precipitated by minor trauma, menstruation, upper respiratory infections, or contact with certain foods. The lesions are confined to the oral mucosa andbegin with prodromal burning an time from 2 to 48 hoursbefore an ulcer appears. During this initial period, a localized area of erythema developswithin hours. Multiple lesions are often present, but the number,size, and frequency of them vary considerably . The buccal and labial mucosa are most commonly involved.Lesions are less common on the heavily keratinized palate orgingiva. In minor RAS, the lesions reach a size of 0.3 to 1.0 cmand begin healing within a week. Healing without scarring isusually complete in 10 to 14 days.Most patients with RAS have between two and six lesions ateach episode and experience several episodes a year.
Patients with major ulcers develop deep lesions that are larger than 1 cm in diameter and may reach 5 cm . Large portions of the oral mucosa may be covered with large deep ulcers that can become confluent. The lesions are extremely painful and interfere with speech and eating. ”The lesions may last for months and sometimes be misdiagnosed as squamous cell carcinoma, chronic granulomatous disease, or pemphigoid. The lesions heal slowly and leave scars that may result in decreased mobility of the uvula and tongue and destruction of portions of the oral mucosa.
The least common variant of RAS is the herpetiform type, which tends to occur in adults in the third decad of life. The patient presents with small tiny irregular ulcers scattered over large portions of the oral mucosa.
Diagnosis of RAS
RAS is essentially diagnosed by exclusion of other diseases. A detailed history and examination. Laboratory investigation should be used when ulcers worsen or begin past the age of 25 years. Biopsies are only indicated when it is necessary to exclude other diseases, particularly granulomatous diseases such as Crohn’s disease or sarcoidosis.Patients with severe minor aphthae or major aphthous ulcers should have known associated factors investigated, abnormal levels of serum iron, foliate, vitamin B12, and ferritin Patients with abnormalities in these values should be referred to an internist to rule out malabsorption syndromes and to initiate proper replacement therapy. The clinician may also choose to have food allergy or gluten sensitivity investigated in severe cases resistant to other forms of treatment. HIVinfected patients, particularly those with CD4 counts below 100/mm3, may develop major aphthous .
Treatment of RAS
Medication prescribed should relate to the severity of the disease. *In mild cases with two or three small lesions, use of a protective emollient such as Orabase is all that is necessary.
*Pain relief of minor lesions can be obtained with use of a topical anesthetic agent or topical diclofenac.
*In more severe cases, the use of a high-potency topical steroid preparation, such as fluocinonide, betamethasone or clobetasol, placed directly on the lesion shortens healing time and reduces the size of the ulcers.The gel can be carefully applied directly to the lesion after meals and at bedtime two to three times a day, or mixed with an adhesive such as Orabase prior to application. Larger lesions can be treated by placing a gauze sponge containing the topical steroid on the ulcer and leaving it in place for 15 to 30 minutes to allow for longer contact of the medication.
*Other topical preparations that have been shown to decrease the healing time of RAS lesions include amlexanox paste(Aphthasol) 5% & topical tetracycline, which can be used either as a mouth rinse or applied on gauze sponges. Intralesional steroids can be used to treat large major RAS lesions .Levamisolcan be used to treat RAS lesions.
Drugs that have been reported to reduce the number of ulcers in selected cases of major aphthae include [colchicines,pentoxifylline, dapsone, short bursts of systemic steroids, and thalidomide] . Each of these drugs has the potential for side effects, and the clinician must weigh the potential benefits versus the risks.
Thalidomide has been shown to reduce both the incidence and severity of major RAS in both HIV-positive and HIV-negative patients, but this drug must be used with extreme caution in women during childbearing years owing to the potential for severe life-threatening and deforming birth defects.

Behcet's syndrome(B.S)

It is a chronic relapsing disease characterized by multiple signs&symptoms such as:-
1-Recurrent orogenital ulcerations.
2-Eye involvement.
3-Skin manifestations.
4-Other systemaffections
BS has an immune genetic basis because of strong associationwith certain HLA type. Four types of BS have been described depending on the majorsite of involvement.
1-Mucocutaneous.
2-Ocular .
3-. Arthritic .
4-Neurologic
Oralmucosal involvement is common to all four types also each type may progress tothe other types.Itaffects young people&is more common among males.
Etiology and Pathogenesis:
The cause of BD is unknown, but immune dysregulationncluding circulating immune complexes, autoimmunitycytokines, and heat shock proteins, is a major factor in thepathogenesis of BD. The HLA -B51 genotype is most frequentlylinked to BD, especially in patients with severe forms of the disease in Asia, but the exact nature of genetics in theetiology of BD is unclear. I t is theorized that BD results whena bacteria or virus triggers an immune reaction in a geneticallypredisposed individual.


Oral Lesion:
Recurrentpainful ulcer
Singleor multiple
Smallor large
Roundor oval
Yalowfloor&red margin
Affecting any part
Occur in 90%

Genital lesion:

Recurrent painfululcer
Affect scrotum inmale&vulva in female
Occur in 83%

Skin lesion:

Erythema nodosum.; It is appears as red tender lumps ornodule on the legs , ankle, face, neck&arms.
Acneform Skin rash.
Postural lesion

Eye lesion:

Consist of
Anterioruveitis….. characterized by (Pain, Blurring vision, Light sensitivity, Tearing&Redness)
Posterioruveitis……..Damaging retina


Diagnosis of Behcet's syndrome
Major criteria
1-Recurrent oral ulcer. 2-Recurrent genital ulcer. 3-. Eye involvement.
4-. Skin lesions. 5- (.+ve) pathergy test.
Positivepathergy is defined as an inflammatory reaction forming within 24 hours of aneedle puncture, scratch, or saline injection

Minor criteria

1-GIT lesions.2-CV lesions. 3-Vascular lesions. 4-Arthritic lesions.
5-CNS involvement. 6-(+ve) family history.
7-Laporatory changes such as:-
Leukocytosis.
Eosinophilia.
Increase ESR.
Treatment of B.S
Oral lesion :.Topical orintralesionalcortico- steriod.
Ocular +Oral+Skin: (Azothioprine ( Imuran 50mg tds) Prednisone)
Sever disease:Cyclosporine +Colchicine +Corticosteroid.
Mucocutaneuos +GIT:Colchicine +Thalidomide
Eye lesion: Pentoxifylline

Erythemamultiforme(E.M)

It is an acuteinflammatory disease of the skin&mucous membrane that cause a variety ofskin lesion.EM may occur once orrecurred&it should be considered in the DD of multiple acute oral ulcers.
EM has severalclinical presentation.(A mild self-limitingform&A sever life threatening form that maypresent as either Stevens-Johnson syndrome or Toxicepidermal necrolysis[TEN] )
Etiology of EM:
1-An Immune-mediated disease that may be initiated either by deposition ofimmune complexes in the superficial microvasculature of skin&mucosa orcell- mediated immunity.
2-Infections: Herpes simplex, Mycoplasma pneumonia, Histoplasmosis
3-Drugs : Sulfonamides, Carbamazepine, Phenytoin, Phenobarbital
Penicillin ,NSAIDs such as ....Oxycam, Allopurinol, Trimethoprim Sulfonamides combination.&Digitalis
4-Others :Malignancy , Radiation therapy , Vaccination , Crohn's disease
Sarcoidosis , Progesterone , Infectiousmononucleosis&Idiopathic.
Clinical forms:
1-EM minor.2-. Chronic EM minor. 3-. EM major
EM minor
Isa disease that involves the skin&oral mucosa.Theprodromal period may characterized bysevere headache, fever&malaise. Theprodromal period followed after 3-7 days by focal or diffuse area of Erythema ....followed by classic skin lesion (Target, Bull's eye, iris ) . Theskin lesions consist of central bull or pale area surrounded by edema&band of Erythema. Themouth is affected by painful wide spread shallow erosion or ulcerations which on the lips become crusted with blood .


Chronic EM minor
Itis the mildest form of EM. Skinlesions are smaller in size&of shorter duration.
EM major
Itis an acute form of the disease with sever involvement of both skin&MM.Acuteform EM Major is called Stevens Johnson syndrome (SJS( . EMMajor is characterized byoral, skin,genital&ocular lesions.Toxicepidermal necrolysis (TEN) It'san even more severe form of EM Major with a high motility rate.

Diagnosis of EM:

1-Clinical features
2-Immunological investigations.
3-PCR.....polymerasechain reaction
Treatment of EM:
Mild form: Treated withsupportive measures ,Topical steroid&local anesthetic mouth wash&Soft or liquiddiet.
Moderate to severe form: Treated with shortcourse of systemic corticosteroid.
Sever form: Treated with.Dapsone, Azathioprine, Levamisole,ThalidomideAnti-herpes drugs...such as (Acyclovir or Val acyclovir).

Managementof TEN

TEN patient is managed in burncenter. Administration of pooled mmunoglobulinis effective in TEN.
INFLAMMATORY BOWEL DISEAS
Inflammatory bowel disease (IBD) is a general classification of inflammatory processes that affect the large and small intestines.Ulcerative colitis Crohn’s disease together make up inflammatory bowel disease. Since many other intestinal diseases with known etiologies also have an inflammatory basis, it has been suggested that Crohn’s disease and ulcerative colitis should more appropriately be designated as idiopathic inflammatory bowel disease. Ulcerative colitis involves the mucosa and submucosa of the colon. Crohn’s disease or regional enteritis is an inflammatory condition involving all layers of the gut.Both diseases are of interest to the dentist because of their associated oral findings and the impact of their medical management (particularly the use of corticosteroids) on dental management.
Diagnosis and TreatmentDiagnosis of ulcerative colitis is made on the basis of *careful history, *physical examination, *gastrointestinal radiography *endoscopy, which involves direct visualization of the intestinal mucosa.
Most important is the sigmoidoscopic examination, which usually reveals the characteristic picture of multiple tiny mucosal ulcers covered by blood and pus.
The therapy for ulcerative colitis:
is aimed at reducing the inflammation and correcting the effects of the disease. 1- Sulfazalazine: is used to initiate and maintain a remission in ulcerative colitis. Its active moiety, 5-aminocsalicylate, has a direct anti-inflammatory effect on intestinal tissues without altering the colon flora.


2- Corticosteroids and corticotrophin:
(adrenocorticotropic hormone [ACTH]) are used in patients who have not responded satisfactorily to sulfazalazine. They are administered in high doses (eg, 40 to 60 mg of oral prednisone daily initially, then maintenance doses of 10 to 20 mg of prednisone daily).
3- Immunosuppressive agents:
such as azathioprine, cyclosporine, and mercaptopurine are being used, with varying results. Because of the risk of hematologic suppression and superinfection in patients taking these medications, they are reserved for patients who have not responded to traditional medical therapy. 4-Surgery:
Approximately 15 to 20% of patients will receive surgery for intractable disease. Proctocolectomy combined with ileostomy is a curative procedure for ulcerative colitis.With the new disposable ileostomy equipment available today, most patients can look forward to an active lifestyle and normal life expectancy.
Oral lesions:
1-Recurrent aphthous ulcers. Biopsy specimens of these multiple small nonhealingaphthous ulcers reveal granulomatous inflammation .
2-localized mucocele formation.
3-Oral lesions may precede the radiologic changes of the disease by up to 1 year.
4-Angular cheilitis and glossitis, all oral manifestations of anemia
5-Indurated polypoid tag like lesions in the vestibule and retromolar pad area.
6-Inflammatory hyperplasia of the oral mucosa with a cobblestone pattern.
7-Diffuse swelling of the lips and face.

8-persistent deep linear ulcerations with hyperplastic margins.

Frequently, patients will complain of pain associated with ulcerative lesions in the oral cavity. Palliative rinses, ointment, and topical steroids may be helpful. There appears to be an increased risk of dental caries that is probably related to dietary changes in patients with IBD. The causes of the dental caries and increased incidence of bacterial and fungal infections are multifactorial but appear to be related to either the patient’s altered immune status or diet.
CYCLIC NEUTROPENIA
Cyclic neutropenia is a rare disorder that occurs secondary toa periodic failure of the stem cells in the bone marrow. Thisfailure results from an abnormality in the regulation of bonemarrow precursor cells or an inhibitor of neutrophils releasedfrom monocytes. It is characterized by transient severe neutropenia that occurs approximately every 21 days. The neutrophil count lasts 3 to 7 days and is occasionally associated with elevations in monocytes. One-third of cases are inherited as an autosomal dominant trait, and two-thirds arise spontaneously during the first few years of life. The disease is frequently present during infancy or childhood, although there is an adult-onset form of the disease, and both sexes appear to be equally affected.The patient is healthy between neutropenic episodes, but at regular intervals the absolute neutrophil count falls quickly below 500/mm3; in some patients, the neutrophil count falls to 0.Normal hematopoiesis is not constant in the bone marrow of patients with cyclic neutropenia, causing fluctuations in marrow platelet and erythrocyte precursors and granulocytes.
Clinical Manifestations:The major signs and symptoms of cyclic neutropenia are related to infection occurring during neutropenic episodes.The most common signs are
1- fever,
2-stomatitis3- pharyngitis,
4- and skin abscesses.
The severity of the infections is related to the severity of the neutropenia. Some patients with severe periodic neutropenia experience few infections owing to a compensatory increase in monocytes, which act as phagocytes to prevent the spread of bacterial infection. Less frequently, patients experience lung and urinary tract infections and rectal and vaginal ulcers. Life expectancy is good for patients who receive careful monitoring.
Oral and Dental Considerations:
Oral lesions are common in cyclic neutropenia and may be the major clinical manifestation of the disease.The two most common oral manifestations are oral mucosal ulcers and periodontal disease.* The oral ulcers: recur with each new bout of neutropenia and resemble the large deep scarring ulcers seen in major aphthous stomatitis.*The periodontal manifestations: range from marginal gingivitis to rapidly advancing periodontal bone loss caused by bacterial infection of the dental supporting structures.
In patients with major aphthous ulcers or generalized rapidly advancing periodontal disease that cannot be explained by local factors alone, cyclic neutropenia should be ruled out as a possible cause. Suspicion of cyclic neutropenia should be particularly high when either of these oral diseases is seen in children.
Treatment.The universally accepted treatment for mostcases of cyclic neutropenia is careful monitoring of the patient for infection during neutropenic periods and vigorous early management of infection. In some patients, use of
*corticosteroids,*adrenocorticotropinor testosterone modulates the sharp reduction in marrow function.Unfortunately, these drugs are not successful for all patients. *The use of granulocyte colony-stimulating factor (G-CSF) has been employed to boost neutrophil levels.
Clinicians must remember that a single WBC count is nota sufficient test to rule out the diagnosis of cyclic neutropeniabecause the examination may be performed as the peripheralneutrophils are being replenished. A series of three total anddifferential WBC counts per week for 4 to 6 weeks is necessary to rule out this disease. Patients with known cyclic neutropenia require frequent dental treatment to minimize advancing periodontal disease. Routine treatment should be confined to the periods when the absolute neutrophil count is above 2,000/mm3. A white cell count taken the day of a dental procedure is a wise precaution because the neutrophil count can change rapidly. Oral hygiene must be carefully maintained, and patients should be recalled for oral hygiene every 2 to 3 months. The use of colony-stimulating factor has reduced oralulcers and periodontal disease in these patients .


Uremic stomatitis
Oral Manifestations
With impaired renal function, a decreased GFR, and the accumulation and retention of various products of renal failure, the oral cavity may show a variety of changes as the body progressesto a uremic state .
The general dentist should be able to recognize these oral symptoms as part of the patient’s systemic disease and not as an isolated occurrence. In studies of renal patients, up to 90% were found to have oral symptoms of uremia. Some of the presenting signs were an
*ammonia-like taste and smell,
*stomatitis,
*gingivitis,
*decreased salivary flow, xerostomia
*and parotitis.
As renal failure develops, one of the early symptoms may bea bad taste and odor in the mouth, particularly in the morning.This uremic fetor, an ammoniacal odor, is typical of any uremicpatient and is caused by the high concentration of urea in the saliva and its subsequent breakdown to ammonia. Salivary urea levels correlate well with the BUN levels, but no fixed linear relationship exists.An acute rise in the BUN level may resultin uremic stomatitis, which may appear as an erythemopultaceousform characterized by red mucosa covered with a thick exudate and a pseudomembrane or as an ulcerative form characterized by frank ulcerations with redness and a pultaceouscoat. In all reported cases, intraoral changes have been relatedto BUN levels < 150 mg/dL and disappear spontaneously when medical treatment results in a lowered BUN level. Although itsexact cause is uncertain, uremic stomatitis can be regarded asa chemical burn or as a general loss of tissue resistance andinability to withstand normal and traumatic influences.White plaques called “uremic frost” and occasionally found on theskin can rarely be found intraorally. This uremic frost resultsfrom residual urea crystals left on the epithelial surfaces after perspiration evaporates or as a result of decreased salivary flow.
A more common oral finding is significant xerostomia, probably caused by a combination of direct involvement of the salivary glands, chemical inflammation, dehydration, and mouth breathing (Kussmaul’s respiration).Salivary adenitis can occasionally be seen.Another finding associated with increased salivary urea nitrogen, particularly in children, is a low caries activity. This is observed despite a high sugar intake and poor oral hygiene, suggesting an increased neutralizing capacity of the urea arising from ureal hydrolysis. With the increased availability and improved techniques of dialysis and transplantation, many of the oral manifestations of uremia and renal failure are less commonly observed.

Neoplasticulcers

Squamouscell carcinoma
SCC of the oral cavity presents as an induratedulcer with raised rolled edges&a yellow to gray sloughing base.The commonest site is the lower lip. Thetongue,lower alveolus&floor of the mouth are the most oftenaffected.
Most patients with oral cancer are over 40 yrs ofage&more common in male.

Diagnosis:

1-Clinical features
2-Photodiagnosis
3-Tumor markers
4-Histopathological findings
Treatment of 0ral cancer:
1-Surgical
2-Laser
3-Chemotherpy
4-Radiation
5-Combination