This document describes various types of oral ulcers including their definitions, causes, clinical features and characteristics. It discusses traumatic ulcers caused by mechanical, chemical or thermal injury. It also covers infective ulcers and immunologic conditions that can cause ulcers like recurrent aphthous stomatitis, Behcet's syndrome, Reiter's syndrome and erythema multiforme. Specific ulcer types are defined and the clinical and pathological features of each type are detailed.

1. DR.ALIWAQAR HASAN
MDS Resident

2.  INJURYTOTHE ORAL MUCOSA MAY RESULT IN
A LOCALIZED DEFECT OFTHE SURFACE IN
WHICHTHE COVERING EPITHELIUM IS
DESTROYED LEAVING AN INFLAMMEDAREA
OF EXPOSEDCONNECTIVETISSUE.
 SUCH DEFECTSARE CALLED ULCERSOR
EROSIONS (TERMCOMMONLY USED FOR
SUPERFICIAL ULCER)
 THIS MAY EITHER FOLLOW MOLECULAR
DEATH OF SURFACE EPITHELIUMOR ITS
TRAUMATIC REMOVAL.
 ULCERATION ISTHE MOST COMMON LESION
OF ORAL MUCOSA AND ISTHE
MANIFESTATION FOR MANY LOCALAND
GENETIC DISORDERS.

3.  EROSION: SUPERFICIAL BREACH OF
THE EPITHELIUM WITH LITTLE DAMAGE
TO UNDERLYING LAMINA PROPRIA.
 EXCORIATION: BREECH OF
EPITHELIUM THAT IS DEEPER THAN AN
EROSION BUT SHALLOWER THAN AN
ULCER.
 ULCER: BREAK IN MUCOUS MEMBRANE
WITH LOSSOF SURFACETISSUE,
DISINTEGRATIONAND NECROSISOF
EPITHELIALTISSUE. Penetration into the
epithelial-connective tissue border, with its base
at a deep level in the submucosa, or even within
muscle or periosteum.

4.  THE SURFACE OF AN ULCER IS COVERED BY MASS OF FIBRIN WITH
INTERMINGLED, DEAD AND DYING POLYMORPHS WHICHWOULD
DRY ONTHE SKINTO FORM A CRUST OR SCAB.
 A SUPERFICIAL ULCER WITH NO EVIDENCE OF SIGNIFICANT
FIBRINOUS EXUDATION ONTHE SURFACE OF POLYMORPH
EXUDATION SUGGESTSTHE POSSIBILITY OF BULLOUS DISORDER.
 A HEAVY INFLAMMATORY INFILTRATE EXTENDS DEEP INTOTHE
UNDERLYING CONNECTIVETISSUE N BLOODVESSELS MAY SHOW
SLIGHT INFLAMMATORY VASCULITIS.
 GRANULATION TISSUE IS FORMED WITH DILATED BLOODVESSELS
AND HEAVY INFITRATE OF PLASMA CELLS, LYMPHOCYTES AND
POLYMORPHS.

5.  ULCER CONSISTSOF:
1. EDGE:-THIS ISAN IMPORTANT FINDING OF AN ULCERWHICH BY ITSELF NOT ONLY
GIVESCLUETO DIAGNOSISULCER BUT ALSOTOTHE CONDITION OF ULCER.
2. FLOOR:- THIS ISTHE EXPOSED PART OF AN ULCER.THE COVERINGOF FLOOR IS
IMPORTANT.
3. BASE (ON WHICHTHE ULCER RESTS):- FLOOR ISTHE EXPOSED SURFACE OF AN
ULCERWHEREASTHE BASE IS ONWHICHTHE ULCER RESTS. FLOOR IS SEEN BUTTHE
BASE IS FELT.
4. MARGIN:- IT’STHE POINTWHERETHE ULCER JOINSTHE NORMAL EPITHELIALTISUE.
RED GRANULATIONTISSUE HEALTHY AND HEALING
PALE AND SMOOTH GRANULATION
TISSUE
SLOW HEALING ULCER
BLACK MASS MALIGNANT MYELOMA

6.  CLINICAL
 PATHOLOGICAL

7. TYPES SURROUNDING
SKIN
ULCER FEATURES OTHER FEATUERS
SPREADING INFLAMED NO GRANULATIONTISSUE
IS SEEN
HEALING NOT
INFLAMMED
GRANULATIONTISSUE IS
PRESENT IN FLOOR
SLIGHT SEROUS
DISCHARGE IS
SEEN
CALLOUS INDURATONS PALE GRANULATION
TISSUE IS SEENAT FLOOR
AND INDURATIONSARE
SEENAT BASEAND EDGE
NOTENDENCY
TOWARDS
HEALING

8.  ULCERATIONS ARE CLASSIFIED ONTHE BASIS
OF ETIOLOGY.
CAUSES OF ORAL ULCERATIONS
 TRAUMA
 INFECTIVE DISEASES
 IMMUNOLOGIC DISEASES

9.  TRAUMATIC INJURY CAN OCCUR BYTHE FOLLOWING
MEANS
 MECHANICAL
 CHEMICAL
 THERMAL
 FACTITIOUS
 RADIATION
 EOSINOPHILIC ULCER (TRAUMATIC GRANULOMA)

10.  MECHANICAL TRAUMA OCCURSTHROUGH BITING, SHARP CUSPS,
OUTSTANDING TEETH OR ILL-FITTING INTRAORAL APPLIANCES
 SUCH ULCERS DON’T PRESENT A PROBLEM CLINICALLY, BUT 3
CRITERIA MUST BE FOLLOWED.
I. A CAUSE OFTRAUMA MUST BE IDENTIFIED.
II. THE CAUSE MUST FITTHE SIZE, SITE AND SHAPE OF ULCER.
III. ON REMOVAL OFTHE CAUSE,THE ULCER MUST SHOW SIGNS OF HEALING
WITHIN 10DAYS.
 CHRONICTRAUMATIC ULCERS MAY PRESENT FOR SEVERAL WEEKS
AND MAY BE DEEP CRATER LIKE LESIONS WITH ROLLED EDGESWHICH
ARE INDURATED ON PALPATION BECAUSE OF SURROUNDING
FIBROSIS.

11.  AVARIETYOF CHEMICALS MAY CAUSE ORAL ULCERATION
 HYDROGEN PEROXIDE
 PHENOL
 ASPIRIN
 SILVER NITRATE
 IT INCLUDES IRRITANTSOR CAUSATIVEAGENTS USED IN DENTAL PRACTICE
 THE PREPARATIONSUSED BY PATIENTS IN SELFTREATMENT OF ORAL COMPLAINTS
SUCH AS ANTISEPTIC MOUTHWASHESAND ASPIRIN (MISUSEDAS OBTUNDANT FOR
TOOTH RELIEF)
 THE ACTION OF ASPIRIN ISTIME AND DOSE DEPENDENT.THE SEVERITY RANGES
FROM ODEMATO NECROSISOFTHE EPITHELIUM
 ODEMATOUS EPITHELIUM RESEMBLES LEUKOEDEMAWHEREASTHE NECROTIC
EPITHELIUM RESEMBLES SOGGYWHITE PLAQUESWHICH LATER FORMS ULCER.

12.  ULCERATION DUETOTHERMALTRAUMA OCCURS
DUETOVERY HOT FOOD OR DRINKS, CAN OCCUR IN
ANY PART OF ORAL MUCOSA BUT MOST COMMONLY
SEEN IN PALATE.
 FACTITIOUS ULCERS MAY BETHE MANIFESTATION OF
STRESS, ANXIETY OR EMOTIONAL DISTURBANCES.
COMMON CAUSE ARE BITING OR CHEWING OF LIPS,
CHEEKS ORTONGUE AND DAMAGE (TO GINGIVA
FROM SHARP NAIL BITES)

13. FACTITIOUS ULCER- CHRONIC ULCERATIONOF
THE MANDIBULARALVEOLAR RIDGE
SECONDARYTO SELF-INDUCEDTRAUMA
TRAUMATIC ULCER DUETO
THERMAL BURN

14.  RADIATION INDUCED STOMATITIS
 SALIVARY GLANDS= XEROSTOMIA=
FRICTIONAL DAMAGE
 ATROPHY OF MUCOSA
 RADIATION OF BONES= DAMAGETO
VASCULAR BED
 OSTEORADIONECROSIS
 THE IMMEDIATE EFFECTS ARE ERYTHEMIA,
RADIATION MUCOSITIS AND ULCERATION
 OEDEMA DUETO OBSTRUCTION OF
REGIONAL LYMPHATICS MAY OCCUR

15.  ITS ALSO REFERRED TO AS TRAUMATIC GRANULOMA
OR EOSINOPHILIC GRANULOMA OF SOFT TISSUES
 IT IS PARTICULARLY ASSOCIATED WITH TRAUMA N
INJURYTO MUSCLE ALTHOUGH THE PATHOGENESIS
IS UNCLEAR
 IT OCCURS MOST COMMONLY ONTHETONGUE AND
PRESENTS CLINICALLY AS CHRONIC, WELL
DEMARCATED ULCER WHICH MAY MIMIC A SQ. CELL
CARCINOMA.

16.  HISTOLOGICAL EXAMINATION
SHOWS AN ULCER COVERED BY
THICK LAYER OF FIBROUS
EXUDATE WITH A DENSE,
CHRONIC INFLAMMATORY
CELL INFILTRATE IN ITS BASE
INVOLVING UNDERLYING
DAMAGED MUSCLE
 THE DEEPER PARTS CONTAIN
INFILTRATE RICH IN
HISTIOCYTES AND
EOSINOPHILS
 TRUE GRANULOMAS ARE NOT
PRESENT.

19.  IDIOPATHIC ULCERS
 BEHCET’S SYNDROME
 REITER’S SYNDROME
 ERTHEMA MULTIFORME
 DRUG REACTIONS
 CONTACT ALLERGIES
 WEGNER’S GRANULOMATOSIS
 MIDLINE GRANULOMA
 CHRONIC GRANULOMATOUS DISEASE
 CYCLIC NEUTROPENIA

20.  THERE ARE A GROUP OF IDIOPATHIC ULCERSWHOSE ARE
CHARACTERISED BY FREQUENT REOCCURANCES
 SUCH ULCERS ARE TERMED AS RECURRENTAPHTHOUS
STOMATITIS (RAS)
 BASED ON PRIMARILY THEIR CLINICAL FEATURES
3TYPES OF ULCERSARE RECOGNISED:
I. MINOR APHTHOUS ULCERS
II. MAJOR APHTHOUS ULCES
III. HERPETIFORM ULCERS

21. • HEREDITARY PREDISPOSITION
• TRAUMA
• EMOTIONAL STRESS AND PSYCOLOGICAL FACTORS
• BACTERIAL ANDVIRAL INFECTIONS
• ALLERGIC DISORDERS
• HAEMATOLOGICAL AND DEFICIENCY DISORDERS
• GASTROINTESTINAL DISORDERS

22. MINOR MAJOR HERPETIFORM
AGE OF ONSET
(YEARS)
10-19 10-19 20-29
NUMBER OF
ULCERS
1-5 1-10 10-100
PRINCIPAL
SITES
LIPS, CHEEKS,
TONGUE
PALATE, PHARYNX FLOOR OF MOUTH,
PALATE, PHARYNX,
GINGIVA
SIZEOF
ULCERS(MM)
<10 >10 1-2 BUT OFTEN
COALEASE
DURATION IN
DAYS
7-14 >30 10-30

23.  THIS ACCOUNTS FOR 80% OR MORE CASES OF
RAS
 ITS CHARACTERISED BY ROUND OR OVAL
ULCERS WHICH AFFECT NON-KERATINISED
AREAS OF ORAL MUCOSA ANDTHEY HAVE
GREY/YELLOW BASE WITH ERYTHEMATOUS
MARGIN
 THEY HEAL WITHOUT SCARRING AND TEND
TO RECUR AT 1-4 MONTH INTERVALS,
WHICH ISVARIABLE

25.  THEY OCCUR ANYWHERE IN MOUTH INCLUDINGTHE
KERATINISED ORAL MUCOSA BUT THE LIPS, SOFT
PALATE,TONSILLAR AREAS AND OROPHARYNX ARE
COMMON SITES
 THEY HEAL WITH SCARRING ANDTENDTO RECUR AT
LESS MONTHLY INTERVALS AND MAY BE ASSOCIATED
WITH SEVERE DISCOMFORT ANDWITH DIFFICULTY IN
EATING AND SPEAKING
 THE EXTENSION IS DEEPER AND MAY PRESENTAS
CRATER LIKE ULCERS WITH ROLLED MARGINSWHICH
ARE INDURATED ON PALPATION BECAUSE OF
UNDERLYING FIBROSIS.

27.  ITS CHARACTERISED BY MULTIPLE, SMALL, PIN-
HEADED ULCERSTHAT CAN OCCUR IN ANY PART OF
ORAL MUCOSA
 WHEN HUNDREDS OF ULCERS ARE CLUSTERED
TOGETHER,THEY CONFLUENCE ,WHICH RESULTS IN
LARGER AREAS OF ULCERATION WITH IRREGULAR
OUTLINE
 THEY HEAL WITHIN 2-3WEEKS WITH SCARRING
 THE ULCERSTENDTO RECURAT LESSTHAN MONTHLY
INTERVEL AND MAY BE ASSOCIATEDWITH SEVERE
DISCOMFORT

29.  IT’S A RARE DISORDER
CHARACTERISED BY
RECURRENTAPHTHOUS
STOMATITIS
 IT MAY BE SEEN AS GENITAL
ULCERS, EYE LESIONS, SKIN
LESIONSOR RAPID ACUTE
INFLAMMATION OF SKIN IN
RESPONSE TO MINOR
TRAUMA
 IMMUNE MEDIATED
MUCOSAL DAMAGE AND
VASCULITIS ASSOCIATED
WITH HYPERACTIVITY OF
NEUTROPHILS ARE INVOLVED
IN PATHOGENESISOF
LESIONS.

30.  THERE IS A CONSIDERABLE LOSS OF
TISSUE DEPRESSINGULCER WELL
BELOW THE SURFACE AND
INFLAMMETION EXTENDS DEEPLY
INTO SUBCUTANEOUS FAT
 THE SURFACE IS COVERED BY
FIBRINOUS EXUDATE INFILTRATED BY
POLYMORPHS FORMING SCAB
 A LAYER OF GRANULATIONTISSUE
WITH DILATED CAPILLARIES AND
EDEMA IS SEEN
 SOME BLOOD VESSELS SHOW
EXTENSIVE FIBROUS PROLIFERATION
OF SUBENDOTHELIAL CONECTIVE
TISSUE.

31.  CLINICAL FEATURES INCLUDE ARTHRITIS, URETHRITIS,
CONJUNCTIVITIS OR UVEITIS, ORAL ULCERS.
 THE CAUSE IS UNKNOWN BUT IT S IMMUNE RESPONSE
TO BACTERIAL ANTIGEN WHICH USUALLY FOLLOWS
STD OR SHIGELLA DYSENTARY.
 IT MAY RECUR .THE DURATION ISWEEKSTO MONTHS
 ORAL LESIONS HAVE BEEN DESCRIBED AS RELATIVELY
PAINLESS APHTHOUS ULCERS OCCURING ALMOST
ANYWHERE INTHE MOUTH.

32.  DIAGNOSIS IS DEPENDENT ON
RECOGNITION OFTHEVARIOUS SIGNSAND
SYMPTOMSASSOCIATEDWITHTHE
SYNDROME
 ERYTHROCYTE SEDIMENTATION RATE
IS ELEVATED IN THE ACUTE PHASE OF
THE DISEASE BUT PERSISTS AFTER
ARTHRITIS RESOLVES.

33.  EM IS A SELF LIMITING HYPERSENSITIVITY
REACTIONCHARACTERISED BY TARGET
SKIN LESIONS AND ORAL ULCERATIVE
LESIONS
 ITS DIVIDED INTO A MINOR FORM
USUALLY ASSOCIATEDWITH HSV TRIGGER
AND A SEVERE FORM TRIGGERED BY
CERTAIN SYSTEMIC DRUGS
 OTHER FACTORS LIKE MALIGNANCY,
AUTOIMMUNE DISEASES, RADIOTHERAPY
TRIGGER EM
 DRUGS PRECIPITATING EM ARE
BARBITURATES, SULFONAMIDES AND
ANTISEIZURE MEDICATIONS.

34.  EM IS USUALLY ACUTE, SELF LIMITED PROCESS
THAT AFFECTS SKIN OR MUCOUS MEMBRANE
AFFECTING MOSTLY YOUNG ADULTS
 THE TERM ERYTHEMA MULTIFORME WAS
COINED TO INDICATE THE MULTIPLE NVARIED
CLINICAL APPEARANCESTHAT ARE ASSOCIATED
WITH CUTANEOUS MANIFESTATIONS
 THE CLASSIC SKIN LESIONCONSISTS OF
CONCENTRIC ERYTHEMATOUS RINGS
SEPARATED BY RINGS OF NEAR NORMAL
COLOR
 OTHER TYPE OF MANIFESTATIONS INCLUDE
MACULES, PAPULES,VESICLES, BULLAE AND
URTICARIAL PLAQUES

35.  EM PRESENTS AS ULCERATIVE DISEASE
VARYING FROM APHTHOUS TYPE
LESIONSTO MULTIPLE WIDE SPREAD
ULCERS
 LIPS BUCCAL MUCOSA, PALATE AND
TONGUE ARE MOSTLY AFFECTED
 FROM MILD DISCOMFORTTO SEVERE
PAIN IT MAY EVEN LEAD TO
HEADACHE, HIGH BODY TEMPERATURE
AND LYMPHADENOPATHY
 STEVENS-JOHNSONS SYNDROME A
MAJOR FORM OF EM IS
CHARACTERISED BY CRUSTING
ULCERATON AT VERMILION BORDER
THAT MAY CAUSE IMMENSE PAIN.

36.  THE MICROSCOPIC
PATTERN OF EM CONSISTS
OF EPITHELIAL
HYPERPLASIA AND
SPONGIOSIS
 EPITHELIAL NECROSIS IS
SEEN
 CONNECTIVE TISSUE
CHANGES USUALLY
APPEAR AS INFILTRATES
OF LYMPHOCYTES AND
MACROPHAGES IN
PERIVASCULAR SPACES
AND IN CONNECTIVE
TISSUE PAPILLAE.

37.  IT AFFECTS SKIN OR MUCOSA. ERYTHEMIA ,WHITE LESIONS,VESICLES OR
ULCERS MAY BE SEEN. HISTORY OF DRUG INGESTIONS IS IMPORTANT
I. ALENDRONATE ( BISPHOSPHONATE )
II. METHOTREXATE ( CHEMOTHERAPY )
III. NSAIDS ( NICORANDIL )
IV. RECREATIONAL DRUGS ( COCAINE )
 THIS IS CAUSED BY POTENTIALLY ANY DRUG VIA STIMULATON OF IMMUNE
SYSTEM.
 REACTIONS SUCH AS ANAPHYLAXIS OR ANGIOEDEMA MAY REQUIRE
EMERGENCY CARE; AND HIGHLY VARIABLE CLINICAL PICTURE CAN MAKE
DIAGNOSIS DIFFICULT
 THE PATHOGENESIS OF DRUG REACTIONS MAY BE IMMUNOLOGIC OR
NONIMMUNOLOGIC

38.  ORAL MANIFESTATIONS MAY
BE ERYTHEMATOUS,
VESICULAROR ULCERATIVE.
 THEY MAY ALSO MIMIC
LICHEN PLANUS SO,THEY ARE
KNOWNAS LICHENOID DRUG
REACTIONS.
 THE NONSPECIFIC FEATURES
INCLUDE SPONGIOSIS,
APOPTOTIC KERATINOCYTES,
LYMPHOID INFILTRATES,
EOSINOPHILS AND
ULCERATION.

39.  LESIONS ARE CAUSED BY DIRECT CONTACTWITH
FOREIGN ANTIGEN; ERYTHEMA,VESICLES AND
ULCERS MAY BE SEEN
 ITS CAUSED BY POTENTIALLY ANY FOREIGN
ANTIGEN THAT CONTACTS SKIN OR MUCOSA;
CINNAMON IS FREQUENTLY CITED IN ORAL CONTACT
STOMATITIS
 THE IMMNUNE RESPONSE IS PREDOMINANTLY T-
CELL MEDIATED
 PATCH TESTIN G MAY BE HELPUL FOR DIAGNOSIS;
HISTORY IS IMPORTANT.

40.  CONTACT ALLERGY IS FREQUENTLY
SEEN ON SKINAND ITS
UNCOMMON INTRAORALLY.
 MATERIALS CAUSING INTRAORAL
ALLERGY ARETOOTHPASTE,
MOUTHWASH, CANDY, TOPICAL
ANTIMICROBIALS, TOPICAL
STEROIDS, IODINE, DENTURE BASE
MATERIAL ETC
 THIS CONDITION PRIMARILY
AFFECTS ATTACHED GINGIVAAS
BRIGHT BILATERAL BAND
 MICROSCOPICALLY, EPITHELIUM
AND CONNACTIVE TISSUE SHOW
INFLAMMATORY CHANGES
 BLOOD VESSELS MAY BE DILATED
AND EOSINOPHILS MAY BE SEEN.

41.  CLINICAL FEATURES INCLUDE INFLAMMATORY LESIONSOF LUNG, KIDNEY
AND UPPER AIRWAY; MAYAFFECT GINGIVAWHEN INTRAORAL.
 THE HEAD AND NECK MANIFESTATIONS ARE SINUSITIS, RHINORRHEA,
NASAL STIFFNESS AND EPITAXIS.
 INTRAORAL LESONS CONSIST OF RED, HYPERPLASTIC,GRANULAR
LESONS OF ATTACHED GINGIVA.
 KIDNEY INVOLVEMENT CONSISTS OF FOCAL NECROTIZING GLOMERULITIS
AND THE FINAL OUTCOME IS RENAL FAILURE.
 THIS IS A RARE DISEASE OF MIDDLEAGE.
 THE CAUSE IS POSSIBLY IMMUNE DEFECT OR INFECTION.
 IT MAY BECOME LIFE THREATING AS A RESULT OFTISSUE DESTRUCTION
IN ANY OF 3 INVOLVED SITES.

42.  THE BASIC PATHOLOGIC
PROCESS IS
GRANULOMATOUS WITH
CHARACTERISTIC
NECROTIZINGVASCULITIS
 NECROSIS AND
MULTINUCLEATED GIANT
CELLS MAY BE SEEN IN
THE GRANULOMATOUS
AREAS
 DIAGNOSIS MAY BE MADE
BY EXCLUSION OF OTHER
DISEASES PARTICULARLY
MIDLINE GRANULOMA.

43.  THIS IS RARE BUT DESTRUCTIVE, NECROTIC,
NONHEALING LESIONS OF NOSE, PALATEAND
SINUSES.
 BIOPSY SHOWS NONSPECIFIC INFLAMMATION
DISTINCT FROM WEGENER’S GRANULOMATOSIS
 MIDLINE GRANULOMA REPRESENTS NK/T-CELL
LYMPHOMA
 PROGNOSIS IS POOR; DEATH MAY FOLOWWHEN
ERODED INTO MAJOR BLOODVESSELS

44.  MIDLINE GRANULOMA ISA UNIFOCAL
DESTRUCTIVE DISEASE INTHE MIDLINE
OF ORONASAL REGION.
 OTHER DISEASES THAT PRODUCE THIS
KIND OF LESIONS ARE WEGENER’S
GRANULOMATOSIS, INFETIOUS DISEASE
AND CARCINOMA.
 MICROSCOPICALLY THIS PROCESS
APPEARS AS ACUTE AND CHRONIC
INFLAMMATION IN PARTIALLY
NECROTICTISSUE WITH ANGIOCENTRIC
INFLAMMATION AS COMMON FINDING.

45.  THIS DISEASE IS RARE AND PRESENTS AS RECURRENT
INFECTIONS IN VARIOUS ORGANS.
 MOSTLY OCCCURS IN MALES
 IT’S A GENETIC DISEASE (X-LINKED)
 THIS IS CAUSED BY THE DEFECT IN NICOTINAMIDE ADENINE
DINUCLEOTIDE PHOSPHATE OXIDASE COMPLEX THAT
RESULTS IN ALTERED NEUTROPHIL AND MACROPHAGE
FUNCTION RESULTING IN INABILITY TO KILL BACERIA AND
FUNGI
 MANIFESTATIONS APPEAR DURING CHILDHOOD DUE TO
MORE FREQUENT X-LINKED INHERITANCE PATTERN.

46.  THE CLINICAL FEATURES INCLUDE ORAL ULCERS
WITH PERIODICITY; INFECTIONS, ADENOPATHY;
PERIODONTAL DISEASE
 THIS IS CAUSED BY MUTATIONS IN NEUTROPHIL
ELASTASE GENE
 CYCLIC NEUTROPENIA RESULTS IN RARE BLOOD
DYSCRASIA
 FEVER, MALAISE, ORAL ULCERS, CERVICAL
LYMPHADENOPATHY AND INFECTIONS CAN
OCCUR

48.  THIS IS SEXUALLY TRANSMITTED BY A SPIROCHETE-
TREPONEMA
 CLASSIFICATION:
1. PRIMARY (CHANCRE)- SINGLE, INDURATED NONPAINFUL ULCER
ATTHE SITE OF SRIROCHETE ENTRY, SPONTANEOUSLY HEALS IN
4-6WEEKS
2. SECONDARY- MACULOPAPULAR RASH ON SKIN, ORAL
ULCERS COVERED BY MEMBRANE(MUCOUS PATCHES)
3. TERTIARY- GUMMAS, CARDIOVASCULAR AND CNS LESIONS
4. CONGENITAL- HUTCHINSON TRIAD(DEAFNESS, INTESTINAL
KERATITIS, DENTAL ANOMALIES)

49.  PRIMARY AND
SECONDARY FORMS ARE
HIGHLY INFECTIOUS.
 SECONDARY FORM
DEVELOPS IN 2-10WEEKS.
 LATENCY PERIODS ARE
SEEN BETWEEN PRIMARY
AND SECONDARY STAGES
AND BETWEEN
SECONDARY AND
TERTIARY STAGES.

50. OTHER
INFEC-
TIONS
CLINICAL FEATURE CAUSE SIGNIFICANCE
GONORRHEA GENITAL LESIONSWITH RARE
ORAL MANIFESTATIONS;
ERYTHEMAOR ULCERS
N.gonorrhea MAY BECONFUSEDWITH
OTHER ULCERATIVE
DISEASES
TUBERCULOSIS INDURATED,CHRONIC ULCER
THAT MAY BEPAINFUL-ONANY
MUCOSAL SURFACE
M.tuberculosis INFECTIOUSORAL LESIONS
AREALWAYS RESULTOF
LUNG LESIONS
LEPROSY SKIN DISEASEWITH RARE
NODULESOR ULCERS
M.leprae COMMON IN SOUTHEAST
ASIA, INDIA, SOUTHAMERICA
ACTINOMYCOSI
S
TYPICALLYSEEN IN MANDINLE,
WOOD HARD NODULEWITH
SULFURGRANULES
A.israelii INFECTION FOLLOWS ENTRY
THROUGH SURGICAL SITE,
PERIODONTAL DISEASEOR
OPEN ROOT CANAL
NOMA NECROTIC, NONHEALING ULCER
OF GINGIVA OR BUCCAL MUCOSA;
RARE;AFFECTSCHILDREN
ANAEROBES IN PATIENT
WHOSE SYSTEMIC
HEALTH IS
COMPROMISED
OFTENASSOCIATEDWITH
MALNUTRITION; MAY RESULT
INTISSUE DESTRUCTION

51.  DEEP FUNGAL INFECTIONS ARE CHARACTERISED
BY PRIMARY INVOLVEMENT OF THE LUNGS.
 ORAL INFECTIONS FOLLOW IMPLANTATION OF
INFECTED SPUTUM IN ORAL MUCOSA.
 ORAL LESIONS ARE USUALLY PRECEDED BY
PULMONARY INFECTION.
 PRIMARY INVOLVEMENT OF ORAL MUCOUS
MEMBRANE IS UNLIKELY MODE OF INFECTION.

52. BL

53.  THE BASIC
INFLAMMATORY
RESPONSE IN A DEEP
FUNGAL INFECTION IS
GRANULOMATOUS.
 MACROPHAGES AND
MULTINUCLEATED GIANT
CELLS DOMINATE THE
HISTOLOGIC PICTURE
 PECULIAR TO
BLASTOMYCOSIS IS
PSEUDOEPITHELIO-
MATOUS HYPERPLASIA
ASSOCIATED WITH
SUPERFICIAL INFECTION

55.  THIS IS CAUSED BY SPOROTHIX SCHENCKII AND
RESULTS FROM INOCULATION OF SKIN OR MUCOSA
BY CONTAMINATE SOIL ORTHRONY PLANTS.
 LESIONS APPEAR AT SITE OF INOCULATION AND
SPREAD ALONG LYMPHATIC CHANNELS.
 THE INFLAMMATORY RESPONSE IS
GRANULOMATOUS.
 CENTRAL ABSCESSES MAY BE FOUND IN SOME OF
GRANULOMAS AND OVERLING EPITHELIUM EXHIBITS
PSEUDOEPITHELIOMATOUS HYPERPLASIA.

56.  PHYCOMYCOSIS (MUCORMYCOSIS) IS
CAUSED BY GENERA MUCOR AND
RHIZOPUS.ASPERGILLOUS IS UBIQUITOUS IN
THE ENVIRONMENT
 THE ROUTE OF INFECTION ISTHROUGH
GASTROINTESTINALTRACT OR RESPIRATORY
TRACT.
 IN HEAD AND NECK, LESIONS ARE MOST
LIKELYTO OCCUR IN NASAL CAVITY,
PARANASAL SINUSESAND OROPHARYNX.

57.  ACUTE AND CHRONIC
INFLAMMATORY
INFILTRATE IS SEEN IN
RESPONSE TO FUNGUS
 CHARACTERISTIC
NECROTIC WALLS
CONTAINING THROMBI
AND FUNGI MAY BE
EVIDENT
 THE FUNGUS CONSISTS
OF LARGE PALE
STAINING NON -SEPTATE
HYPHAETHAT TEND TO
BRANCH AT 90
DEGREES.

58.  TREATMENT IS CAUSE RELATED
 SYMPTOMATIC IF UNDERLYING CAUSE IS
UNKNOWN OR NOT CORRECTABLE
 MOST ULCERSWILL HEAL COMPLETELY
WITHOUT ANY INTERVENTION
 REMOVAL OF LOCAL IRRITATING CAUSE
 ADDRESSING UNDERLYING FACTORS, DRY
MOUTH