THE DIAGNOSTIC SEQUENCE
Sequence Summary
1. Detection and preliminary examination of the lesion
2. Examination of the patient
3. Re-examination of the lesion
4. Classification of the lesion
5. Listing possible diagnosis
6. Differential diagnosis
7. Working Diagnosis
8. Final Diagnosis
1. Detection and Preliminary Examination of the lesion
In some instances the patient will have come to you for the diagnosis of a lesion which they have discovered in their own mouths. In such an instance it is wise to take a short preliminary look at the lesion first in order to get some idea about it's appearance. such preliminary information will guide the dental personnel to the correct questions to ask the patient.
On other occasions the lesion will be detected during your careful systematic examination of the oral cavity.
2. Data Obtained From The Examination of The Patient
A. History
1. Chief Complaint (CC)
2. History of Present Illness (HPI)
3. Past Medical History (PMH)
4. Past Dental History (PDH)
5. Family History (FH)
6. Social and Personal History (S & PH)
7. Review of Systems (RoS)
B. Clinical Examination
1. Inspection
2. Palpation
3. Percussion
4. Auscultation
5. Aspiration
C. Radiographic Examination
often identifies whether lesion originated in soft tissue or bone
D. Various Laboratory Tests
white blood count and differential counts: infections, leukemia,
hyperparathyroidism etc.
3. Re-examination of the Lesion
Now it's a suitable time to return to the lesion and to examine it fully both clinically and radiographically.
4. Classification
You will be able to decide in almost all cases if the lesion originated in soft tissue or bone. This is very helpful in the elimination of possibilities at this early stage. For instance, if there are no radiographic changes in the bone, then this is almost certain proof that the lesion originated in soft tissue. Thus, perhaps 500 lesions have been eliminated by this one decision. Then the soft tissue lesion should be classified into major categories according to clinical appearance: eg. white, red ulcerated, exophytic. These each correspond to a chapter heading to the book.
In a similar manner if the lesion is bony in origin then it should be classified as (a) totally radiolucent (b). mixed (radiolucent/radiopaque) or (c). radiopaque. The lesion is then placed in the correct subcategory which will be a chapter heading in the "Bony Lesions" section of the book.
5. List of Diagnostic Possibilities
When all of this data is available the diagnostician needs to sit down and draw up a list which includes all the possible disease entities that this lesion could be. An extensive list may be found at the beginning of each chapter.
For example if the lesion is white, then the list at the beginning of the chapter "White lesions should be referred to for suitable possibilities.
6. Differential Diagnosis
The diagnostician next review each possibility, weighs it in the light of all the clinical or radiographic data and assigns it to a position int he list depending on the probability of it being the final diagnosis. The list is thus rearranged so that the most likely possibility is at the top and the least likely is at the bottom. This rank process requires that the diagnostician possesses a pretty thorough knowledge of the symptoms and signs of all these diseases. It is particularly important to know differentiating features.
The following categories of data are helpful to consider during this stage.
a. Chief Complaints From Oral Diseases
b. H.P.I. (see addendum)
c. Relative incidence
extremely important, must know if a lesion is common, uncommon or rare must be able to grossly rank each clinical or radiographic group of similar lesions according to frequency of occurrence in the general population.
Uncommon or rare lesions should neverbe assigned a high ranking unless there is special evidence that points to the rare diagnosis.
d. Peak age of Incidence
In which age group does a certain lesion most commonly occur.
Young
fibrous dysplasia, Ewing's sarcoma, adenomatoid odontogenic tumor, early odontoma
Paget's disease - Old Age
Leukoplakia - 40-70 y/o
squamous cell carcinoma 40-80 y/o
malignant salivary tumor - 40-80 y/o
chondrosarcoma - 40-80 y/o
lichen planus - over 40 y/o
cementomas - over 30 y/o
Other
osteogenic sarcoma (of the jaws) - 20-30 y/o
candidosis - extremes of life
ameloblastoma - 20-50 y/o
ameloblastoma in follicular cyst - 21 y/o
fibrous dysplasia - 5-30 y/o
adenomatoid odontogenic tumor - 5-20 y/o
e. Sexual Frequency
Lesions more common in males
a. squamous cell carcinoma
b. leukoplakia
c. erythema multiform
d. all oral cancers but metastatic ca, and minor salivary gland tumors
e. osteomyelitis
Lesions more common in females
a. cementomas
b. lichen planus
c. metastatic ca
d. primary hyperparathyroidism (7/1)
e. pyogenic granuloma
f. metastatic carcinoma and minor salivary gland tumors
f. Racial Consideration
More Common in blacks
a. leukoedema
b. melanoplakia
c. sickle cell anemia
d. cementomas
e. diffuse cementosis (gigantiform cementomas)
More Common in whites
a. lichen planus
b. infectious mononucleosis
c. benign mucous membrane pemphigoid
g. Age, Race & Sex
ie. diffuse cementosis - black, females over 30 y/o
h. Frequent Locations
Some lesions are more commonly found in one jaw
(a). mandible maxilla
osteomyelitis compound odontoma
ameloblastoma incisive canal cyst
primordial cyst palatal tori
cementoma Paget's disease (20/3)
traumatic bone cyst chondrosarcoma
lingual tori adenomatoid odontogenic tumor
(b). most frequent regions
mucocele - lower lip
minor salivary tumor - posterolateral hard palate
ranula - floor of mouth
pyogenic granuloma - gingivae, tongue
peripheral odontogenic fibroma - interdental papilla
snuff or chewing tobacco lesions - vestibule
leukoedema - buccal mucosa
median rhomboid glossitis - dorsal surface of tongue
cementoma - apices of lower anteriors
odontomas - supracoronal location, molar and incisors
ameloblastomas - third molar and angle
primordial cyst - third molar region
thyroglossal cyst - midline of neck
branchial cyst - lateral neck
traumatic bone cyst - premolar/first molar (mandible)
Note: You may choose to order some additional tests at this stage to help differentiate between entities.
7. Working Diagnosis, Impression, Tentative Diagnosis
The diagnostician further examines the top two or three entities on the differential diagnosis list, does further workup and evaluation if necessary, perhaps asking more definite questions in the history until all are ruled out except one or two entities. These entities are the working diagnosis or tentative diagnosis or clinical impression. These will direct or dictate your next step which may be a surgical exploration with a biopsy. Before the biopsy is done the clinician may choose to do a last test or two such as an aspiration of the mass. This is an excellent test to rule out vascular tumors and the nasty surprise that greets the surgeon when he encounters an unexpected vascular tumor at surgery.
8. The Surgical Procedure
a. Exploratory
b. Incisional Biopsy
c. Frozen Section
d. Excisional Biopsy
9. Final Diagnosis
Usually from microscopy
10. Further patient management and prognosis
1. Geographic Locations
a. Southeastern U.S. - greater use of snuff and chewing tobacco give rise to more frequent leukoplakias + carcinomas
b. India - palatal cancer - reverse smoking
c. Mediterranean countries - Thalassemia
d. Africa - Burkitt's tumor
Addendum to Lecture on Diagnostic Sequence
RANKED CHIEF COMPLAINTS FROM ORAL DISEASES
A. Pain
1. Inflammation of any etiology
2. Mechanical Pressure on nerve endings
3. Some tumors - Infected or traumatized
- central malignant tumors of bone
- cylindroma
- amputation neuroma
4. Psychosomatic
5. Neuralgias
6. Systemic diseases referring pain to oral cavity
B. Sores
1. Inflammation and/or ulcer from any etiology excepting early malignant ulcer- usually painless.
C. Bleeding- Oral
1. Gingivitis and periodontal disease
2. Traumatic incidents including surgery
3. Reactive proliferations - are vascular
- usually subjected to trauma
4. Erosions
5. Some tumors - hemangiomas
tumors with rich blood supply
erosive tumors (malignant)
6. Defects of vascular hemostasis
D. Burning Sensation
(Thinned or eroded mucosa)
1. Geographic Tongue
2. Psychological
3. Erosive Lichen Planus
4. Avitaminosis
5. Anemias
E. Drainage- usually no pain
1. Chronic abscess with sinus tract
2. Ruptured retention phenomenon - mucocele, ranula
3. Cyst with sinus tract
4. Fistulas (a). antro-oral, (b). oral to skin (trauma or infection or malignancy
5. Major salivary gland fistulous tracts
F. Swellings
1. Inflammation and/or infection
2. Cysts
3. Retention phenomenon
4. Reactive proliferations
5. Tumors
G. Loose Teeth
1. Periodontal disease
2. Trauma
3. Normal resorption of deciduous teeth
4. Periapical pulpal lesions mostly resorb surrounding bone sometimes resorb roots too.
5. Malignant tumors
6. Benign tumors which can resorb roots chondromas, myxomas, hemangiomas.
H. Recently teeth don't bite right or recently some teeth are out of line
1. Periodontal disease
2. Trauma - possible fractured jaw
3. Periapical abscess
4. Cysts - spread
5. Tumors of the teeth-bearing areas of the jaw
6. Fibrous dysplasia
I. Delayed eruption of a tooth
1. Malpositioned - impacted
2. Cyst
3. Odontome
4. Sclerosed bone
5. Tumor
6. Maldevelopment
7. Systemic-hyperthyroidism - several
J. Too Little Saliva
mumps
1. Local inflammation of salivary glands {
postradiation
2. Dehydration states
starvation
3. Drug induced - atropine-probanthine
4. Psychosomatic
5. Autoimmune disease - eg Sjorgen's syndrome
Mikulicz's syndrome
K. Too much saliva
1. Psychomatic
2. Post denture insertion - foreign body
3. Insufficient freeway space
Massess - History of Present Illness (onset and course)
1. Mass becomes larger just before or during eating-salivary retention phenomenon
2. Slow growing mass (months - years) reactive hyperplasia
chronic infection
benign tumor
3. More rapidly growing mass (weeks - couple of months) malignancies
4. Rapidly expanding mass (hours - days)
- abscess-painful
- infected cyst - painful
- retention phenomena- painless
- aneurysm-painless
- hematoma-painless-stings on digital pressure
5. Mass with accompanying fever - infection - Hodgkin's disease
1. Mechanical Traumatic Lesions
toothbrush-usually a single episode
a. erythematous macules - cheek biting
- sharp teeth
- foreign objects
- ill-fitting dentures
- oral sex - palate + tip of tongue
- normal prominence prone to trauma-tori
b. Inflammatory hyperplasias (elevated lesions)
usually chronic application of low grade irritant-calculus, bony
spicules, etc.
See section on Exophytic Lesions for specific information on the following lesions:
pyogenic granuloma
hormonal tumor
epulis fissuratum
papillary hyperplasia
peripheral giant cell granuloma
pulp polyp
epulis granulomatosum
2. Erythema Migrans (migratory glossitis, geographic tongue)
a. Clinical
white annular lesions with atrophic red centers; pattern migrates over dorsum of tongue; varies in intensity; may spontaneously disappear; occasionally painful; common
b. Etiology, Pathogenesis and History
Cause is unknown
c. Treatment/Prognosis
None; symptomatic treatment for painful lesions; is a completely benign condition; not premalignant; may spontaneously regress after wks./mos./yrs.
3. Burns
will be red or white (necrotic) depending on severity
history will indicate the correct diagnosis
4. Chemical injury Note: Allergy
will be red or white (necrotic) depending on severity
history will indicate the correct diagnosis
aspirin, tylenol, etc.
5. Viral Infections
a. recurrent herpes - unilateral cluster of small vesicles - hard palate
or attached gingiva (see section on mucosal ulcers for further information)
b. Herpangina - Coxsackie virus (soft palate)
1. Etiology, Pathogenesis and History
Cause by a Coxsackie virus; early lesions are vesicles which then ulcerate
2. Clinical
multiple painful ulcers develop in posterior oral cavity and pharynx; lesions (ulcers) are preceded by vesicles; children are most common affected; seasonal occurrence; rare except in epidemics
3. Treatment/Prognosis
supportive; herpangina is a self-limiting disease with recovery occurring in less than a week
6. Bacterial Infections
a. odontogenic - if staph, early stage only - later stage may be yellowish
(pus)
b. Actinomycosis
c. Ludwig's angina - streptococcus (non pus producing)
7. Capillary Hemangiomas (See exophytic section for more specific information)
this variety is usually red - especially portwind stains (Sturge-Weber Syndrome)
Sturge Weber: 1. Portwine stain
2. Oral (gingiva) hemangioma
3. Calcification of some vessel of the brain.
4. Epilepsy
Cavernous hemangiomas are usually blue in color
8. ulcers with inflammation surrounding them
aphthous ulcers (see section on mucosal ulcers for more details on this entity)
9. Early purpuric areas
due to local trauma only - must investigate possibility of a systemic bleeding problem
petechial and ecchymotic patches
early stages are red
later - blue - brown - green - yellow
10. Denture Stomatitis
In theory just the mucosa in contact with the denture base is red.
In practice inflammation is almost always limited to the mucosa under the denture.
NOTE: If multiple papules - changes diagnosis to papillary hyperplasia
Causes:
a. secondary candial infection - acrylic impregnated with Candida
b. ill-fitting appliance - slippage
- too much pressure
c. allergy to denture base material - probably very rare
11. Erythroplakia
meaning of term parallels that of "leukoplakia"
i.e. leukoplakia is white (keratin formation)
erythroplakia is red (no kerating formation)
speckled leukoplakia or speckled erythroplakia has a mix of both
microscopic spectrum is similar to leukoplakia in that it can range from minimal amount of atypia to carcinoma-in-situ, to invasive carcinoma
clinically erythroplakia is a velvety red patch in a case where all the other red lesions have been ruled out. Note - Exophytic Squamous Cell
12. Fungal Infections
a. acute atrophic Candidosis
same etiological factors as necrotic (white) variety but in this case minimal necrosis combined with an erosion or thinning of the surface epithelium + underlying inflammation gives red appearance.
lesions may be solitary or multiple and widely disseminated areas may be present.
b. Histoplasmosis, etc.
13. Solitary or Herald spots of generalized oral mucositides e.g. In some instances these generalized conditions commence as a single lesion-later they may develop into a full blown case.
a. erythema multiforme (Discussed with Generalized Red Conditions)
b. erosive lichen planus (See White Lesions and Generalized Red)
14. Bald Tongue
smooth beefy red appearance - papillae are lost example of atrophy of surface epithelium
a. median not congenital at all
probably healed phase of traumatic or candidal lesion
b. partly or completely bald
may be found in certain anemias and vitamin deficiencies
GENERALIZED RED ORAL CONDITIONS
Synonyms - Stomatitis, Oral Mucositis
1. Recurrent aphthous Stomatitis
a. same pathogenesis, history, clinical and histopathology as "garden variety" of aphthous ulcers except:
i. when 3 or 4 or more ulcers are present at the same time we call it aphthous stomatitis
ii. he ulcers may be widely dispersed in the mouth but keratinized (fixed) mucosal surfaces are generally not affected.
iii. patients suffer recurrent bouts perhaps a month or two apart
b. Treatment consists of:
i. tetracycline rinses 4 to 6 times per day
ii. systemic cortisone if necessary
2. Erosive lichen planus
a. Etiology, Pathogenesis and History
i. same as other varieties of lichen planus but erosive type is more severe-loss of epithelium in places
ii. cause is unknown; may be precipitated by stress; may be a hyperimmune condition mediated by T cells (immunological data is accumulating)
b. Clinical Features
i. painful ulcers + erosions - usually several surfaces may be involved including the tongues and lips
ii. fortunately small traces of keratotic areas (i.e. Wickham's stria) are frequently present and this aids greatly in establishing the diagnosis
iii. skin lesions are occasionally present and are purple pruritic papules
seen in middle age with females more commonly affected; buccal mucosa most common site
c. Histopathology
i. the erosive areas usually present with a non-specific loss of epithelium with underlying inflammation; any keraotic areas will show classic pathology related to the white lesions of lichen planus such as “saw-tooth” rete pegs, band-like infiltration of lymphocytes, etc.
ii. if the surgeon is able to include a keratotic region in the biopsy this may permit a definitive microscopic diagnosis
iii. several other oral mucositides will give similar histological picture
d. Treatment
i. high doses of cortisone for 1 week
ii. patient instructed to use when the attack first appears in attempt to abort or prevent a severe exacerbation
NOTE: Lichenoid drug reaction is an occasional reaction to drugs (e.g. diuretics, etc.) that will produce clinical lesions identical to lichen palmus. This entity is not well understood but it is usually stated that lichenoid drug reaction responds very poorly to cortisone. Treatment is to withdraw the causative drug. Then very slowly the lesions disappear taking perhaps several months to disappear completely.
3. Erythema Multiforme
a. Etiology, Pathogenesis and History
i. cause is unknown; ? hypersensitivity; may follow ingestion of drug or an infection such as herpes labialis or Mycoplasma pneumonia
ii. lesions may be recurrent, especially in the fall and spring; some cases become chronic
b. Clinical Features
i. minor, major (Stevens-Johnson syndrome) and toxic epidermal necrolysis; the minor form is more common and will be the main topic in this discussion
ii. sudden onset; painful widespread, superficial ulcers; usually self-limited; young adults; may also have “target”, “bull’s eye”, “iris” lesions of skin;
iii. like name implies-may see several different lesions e.g. blebs, large ulcers, large macules, stripped epithelium but all these are sequential - i.e. appear as red macule than perhaps as a bleb and then as a denuded area of the mucosa; perhaps only one or two lesions in some cases; in other cases, many of the oral surfaces are severely involved
c. Histopathology
i. non-specific oral ulcerations if bullae are present usually located at c.t. junction
d. Treatment
i. generally, symptomatic; steroid usage is controversial; soothing anesthetic mouth rinses with antihistamines may ease symptoms; allergy tests
NOTE: Stevens-Johnson's Syndrome is a variant of erythema multiforme involving the skin, oral cavity, eyes and genitalia. Toxic epidermal necrolysis is considered by some authorities to be the most serious for of erythema multiforme.
4. Primary Herpetic Gingivostomatitis(For more details concerning this entity see the section on Mucosal Ulcers)
a. Etiology, Pathogenesis and History
i. herpes simplex virus - may be type 1 or type 2 (genital type)
ii. frequently it is the primary infection which presents as a “generalized” red condition
1. remember may cases of herpes simplex infection are subclinical; in other cases perhaps just a solitary lesion develops at site of inoculation (6-12 hrs propagation of virus)
2. occasionally patient gets full blown i.e. a gingivostomatitis
3. a one-time attack - at the most two
iii. Clinical Features
iv. Erythema of many oral surfaces usually including gingiva; small vesicles distributed over erythematous areas soon rupture and so are succeeded by small circular ulcers; patient generally has a fever of maybe as high as 103 or 104; painful cervical lymph nodes are common
v. Treatment
1. Supportive: mild soft diet, aspirin, antihistamine + kaopectate rinse,
a. tetracycline rinses to combat secondary bacterial infection; antivirals such as acyclovir are occasionally useful
5. Xerostomia
a. Causes - idiopathic
i. drug therapy
ii. post-radiation - fibrosis of salivary glands
iii. autoimmune disease
1. Sjögrens (Sicca) syndrome
2. Mikulicz's disease, etc.
iv. History of case will usually clearly indicate cause
v. Sicca Syndrome - "Siccus" means "dry"
1. dry mouth (xerostomia)
2. dry eyes (xeropthalmia)
vi. Sjögren’s Syndrome
1. dry mouth - (Xerostomia)
2. dry eyes (xeropthalmia)
3. rheumatoid joint diseas
b. Clinical Features of Xerostomia
i. severity depends on degree of reduction of saliva;
ii. ranges from a mild mucositis to frank ulceration and stripping;
iii. pain may range from a slight burning to mild to severe pain;
iv. salivary pool in floor of mouth is missing
c. Treatment
i. varies with cause
ii. glycerine mouth rinses; artificial saliva, drug therapy
6. Polycythemia (erythremia)
a. is a chronic, sustained elevation in the number of erythrocytes and level of hemoglobin; there are several forms of polycythemia both primary and secondary
b. the entire mucosa is deep red or purple; laboratory tests are extremely helpful in determining an increase in RBCs, hemoglobin concentration and hematocrit values
7. Atrophic (erythematous) Candidiasis
a. Etiology, Pathogenesis and History
i. same as pseudomembranous type (usually Candida albicans) only infection is milder thus not severe enough to produce necrosis of tissue; poor oral hygiene and ill-fitting dentures are often predisposing factors
b. Clinical features
i. various erythematous patches on mucosal surfaces; pain ranges from mild discomfort to moderate pain; may be seen as hyperemic area under a denture, as an angular cheilitis, or generalized throughout the mouth
c. Histopathology
i. cytology smear shows pseudohyphae
d. Treatment/Prognosis
i. check for underlying systemic disease or other cause; nystatin or other antifungal; improve oral hygiene; ?? perhaps requires a new denture??
8. Rarities
a. cicatricial (benign mucous membrane) pemphigoid
i. Clinical
1. multiple painful ulers preceded by bullae; lesion may heal with scar formation; positive Nikolsky’s sign; may affect any mucous membrane; when limited to attached gingiva may be termed desquamative gingivitis (gingivosis); more common in middle-aged and older women
ii. Cause
1. autoimmune, antibodies directed against basement membrane antigens, laminin 5 and BP 180
iii. Treatment/Prognosis
1. topical or systemic steroids; runs a protracted course; ocular scarring can lead to symblepharon formation and blindness; may be debilitating but rarely causes death itself
b. Pemphigus variants
i. Clinical
1. multiple painful ulcers preceded by vesicles or bullae; positive Nikolsky’s sign; more common in middle aged patients; progressive disease; remissions and/or control with therapy; 2-3 cases per million population
ii. Cause
1. autoimmune; antibodies directed against desmosome-associated protein, desmoglein 3
iii. Treatment/Prognosis
1. systemic steroids; occasionally immunosuppressive drugs; disease may be fatal if not treated or with treatment (significant morbidity occurs from steroid therapy); oral lesions may be first manifestation of disease (50% of time); prognosis improved if treated early
c. radiation mucositis
d. chemotherapy mucositis
e. Reiter's Syndrome
f. Behcet's Syndrome
g. Lupus Erythematosus
i. Clinical
1. painful erythematous and ulcerative lesions on buccal mucosa, gingiva and vermilion of lip; white (keratotic) areas may surround lesions; chronic discoid type generally affects skin and mucous membranes only; in systemic type (SLE) the skin lesions may be erythematouos with a scale; classic sign of SLE is butterfly rash across bridge of nose; patients also have cardiovascular, kidney and joint lesions as well as hematologic abnormalities; more common in middle-aged women
ii. Cause
1. immune defect; patient has numerous autoantibodies especially ANAs
iii. Treatment/Prognosi
1. treated by steroid and immunosuppressive drug therapy; SLE has guarded prognosis while discoid presents mainly cosmetic and discomfort problems
h. Epidermolysis bullosa
RED TONGUE LESIONS
1. Geographic Tongue (Erythema Migrans)
a. Ectopic on buccal mucosa
2. Median Rhomboid Glossitis
NORMAL - linea alba
- Filiform and Fungiform papillae
- Attached gingiva and anterior hard palate (masticatory mucosa)
- Skin graft - history is diagnostic
- Leukoedema
(a). Etiology and History
cause is unknown but can be considered a variation of normal
cause - probably related to mastication;
patient is unaware of its presence
(b). Clinical features
50% of Whites and 90% of African-Americans; uniform (milky) opacification to wrinkled, white opalescent. Stretching mucosa will cause it to disappear
Location - complete surface of buccal mucosa
Age - present in a very high percentage of adults
(c). Microscopic appearance
hyperparakeratosis
ballooning of prickle cells
(d). Treatment
None required after recognition of the lesion; recognize entity as a normal variant
Remains indefinitely; no ill effects
Major Types of White Lesions
A. Keratotic - white material cannot be easily scraped off.
B. Necrotic - white material can be easily removed, leaving a raw bleeding surface.
C. Vesiculobullous - will be covered under "Generalized Mucositides".
A. Keratotic White Lesions (not readily removed)
1. Spectrum of "Leukoplakia Type" Lesions
a. Pathogenesis
- A defense mechanism to chronic irritation.
tobacco- Cigar, Pipe - heat
Cigarettes - tar
- combustion products
- paper
Smokeless tobacco Snuff, chewing tobacco, Beetle Nut
Hot Spicy Foods
Mechanical - dentures, teeth
Material alba
Actinic radiation
Thermal extremes - ice cubes, hot beverages
Note: a combination of heavy smoking and heavy alcohol consumption is believed to be associated with an increased incidence of squamous cell carcinoma
of the oral cavity.
b. Types: (1). Reversible-lesion will disappear after irritant is withdrawn
(2). Irreversible-lesion persists after irritant is withdrawn
c. Histopathology
(1). Hyperkeratosis, parakeratosis or both
(2). Keratosis + acanthosis
(3). Keratosis + acanthosis + basal layer hyperplasia
(4). Keratosis + acanthosis + basal layer hyperplasia with minimal atypicalities + lymphocytes in sub-basal area
(5). Keratosis + acanthosis + moderate atypicalities + lymphocytes
(6). Keratosis _ acanthosis + severe atypicalities, basement membrane intact + lymphocytes. Carcinoma-in-situ (intra-epithelial carcinoma).
d. Idiopathic Leukoplakia: Clinical Features
- M/F = 2/1
-Asymptomatic (painless) white patch, any shape, borders may be distinct or indistinct; cannot scrape off white material
-Will most frequently be a single lesion - occasionally multiple or disseminated.
-80-90% of lesions are found in patients over 40 y/o
-Less serious lesions will disappear when irritant is removed (reversible).
-The more serious lesions will remain (irreversible) and 6-10% are already or will develop into an invasive squamous cell carcinoma;
(5% are malignant; 5% become malignant).
-Cracks, fissures, ulcerations, bleeding areas and induration in a white patch are ominous sings in the absence of mechanical trauma.
* - floor of the mouth lesions, ventral surface and lateral borders of the tongue have a much greater malignant potential - up to 42%.
* - Erythroplakia: (will be discussed with red lesions)
Speckled Leukoplakia (erythroleukoplakia)
these lesions are often carcinoma-in-situ or already invasive carcinomas histopathologically
Differential Diagnoses of speckled leukoplakia
1. cheek chewing 3. erosive lichen planus
2. candidiasis 4. nicotine stomatitis
e. Treatment and Prognosis
(I). homogeneous lesions where the suspicious index is low remove irritant and re-examine in two weeks. If lesion has disappeared examine periodically - if it has gotten smaller re-examine in another two weeks. If it has not disappeared excise completely and send for microscopic study. Close follow-up is mandatory.
(II). heterogeneous lesions such as speckled leukoplakias (erythroleukoplakia) have a high suspicion index and should be excised completely quite soon without a waiting period. Close follow-up is mandatory.
Note - Hairy leukoplakia - seen most often in homosexual males may be a prodromal sign of AIDS
2. Nicotine Stomatitis (smoker's palate)
i. Pathogenesis and History - almost all patients are pipe smokers - most are males
ii. Clinical Features - Asymptomatic, generalized opacification of the palate, often segmented into small sections with linear borders and with pinpoint red dots in centers. The red dots represent the orifices of minor salivary gland ducts. Location - limited almost exclusively to palate
iii. Histopathology
iv. Treatment and Prognosis - discontinue pipe smoking
- almost never becomes malignant
3. Snuff Dipper's Lesion (also Chewing Tobacco)
a. Pathogenesis and History
history of prolonged habit - watch for use in students (grade school to college) also in older patients. Cause: chronic irritation from snuff or chewing tobacco
b. Clinical Feature - lesion occurs where product is applied.
Early lesion may be inflamed - later red and white - then white wrinkled (parboiled). When white often described as asymptomatic white folds. Location in vestibles (usually buccal or labial of the mandible) - frequently causes gingival recession.
Sex - male - greater occurrence
c. Treatment and Prognosis - less serious lesions will disappear within two to four weeks after use is stopped. Biopsy those lesions that look suspicious. Increased risk for development of verrucous and squamous cell carcinoma after years of use. Lesions that are or become malignant are usually low-grade but may be high grade.
4. White exophytic squamous cell carcinoma - discussed in more detail under exophytic lesions, basically an exophytic tumor with enough surface keratin to give it a white color. These may be red portions too. Basically the lesion has a rough surface.
5. Erythema Migrans (Geographic Tongue;Migratory Glossitis)
(a). Pathogenesis and History
cause unknown, psychological factors play a role, affects 1 to 2% of the population.
(b). Clinical Features
White annular lesions with atrophic red centers; patterns change from week to week (migrates over dorsum of the tongue) and cases may go into remission for a time (varies in intensity and may spontaneously disappear); very occasionally painful (usually asymptomatic)
(c). Treatment and Prognosis
Make correct diagnosis
None, usually required
Symptomatic treatment in painful cases - bland diet
6. Peripheral Scar Tissue
(a). Pathogenesis and History
history of surgery at site. Scar tissue is unusual in the oral cavity because of rich vascularity which promotes good healing.
(b). Clinical Features
firm pale pink line or patch
Location
at site of previous surgery: eg root resection
(c). Treatment and Prognosis
correct identification
7. Lichen Planus (Keratotic type)
(a). Pathogenesis and History
mucocutaneous disease
cause unknown but there is a psychological component.
(b). Clinical Features
65% - women
the majority of patients are over 40 years old
Bilateral white striae (Wickham’s); buccal mucosa most frequent site;
painless (asymptomatic except when erosions are present) white lattice-like pattern but may be plaque like with feathered edges, or be doughnut shaped or have a floral design. Skin lesions are occasionally present where they appear as purple pruritic papules most common seen on forearm and lower leg.
(c). Differential Diagnosis
(a). lichenoid drug reaction
(b). biting & sucking trauma
(c). galvanic lesion
(d). Microscopic
Classic type: saw tooth rate ridges, narrow band of inflammation just beneath epithelium.
(e). Treatment
For keratotic type no treatment is necessary except periodic follow up.
Steroids helpful with symptomatic type; may regress; rarely associated with malignant change
8. White hairy tongue
(a). Pathogenesis and History
Elongation of filiform papillae
Cause-unknown but may follow antibiotic or corticosteroid use
possible more common in patients with malignancy
(b). Clinical Features
More common in men
Location - dorsal surface of tongue
(c). Treatment and Prognosis
Improve oral hygiene; proper brushing of tongue will produce a remission in slight to moderate cases; identify contributing factors; benign process which may be cosmetically objectionable.
9. Verruca Vulgaris, Papilloma and Condyloma Acuminatum
(a). Etiology and History
Papillomavirus is cause of verruca vulgaris and condyloma acuminatum
Etiology of papilloma is uncertain
(b). Clinical Features
All may appear as painless, exophytic, rough surfaced lesions with a cauliflower-like appearance
Papillomas have a predilection for the tongue, palate, uvula, floor, etc.
Verruca and condylomas occur at site of inoculation
Papillomas and condylomas are more common in young adults, adults (most between the ages of 21 and 50) while verruca are more common in children and young adults
(c). Histological Features
(d). Treatment and Prognosis
Oral lesions are treated by excision with microscopic study
Papillomas rarely occur and there is no known malignant potential
Verruca are of little significance but may present a cosmetic problem if multiple
Condyloma acuminatum are acquired through autoinoculation or sexual contact and recurrences are common
10. Verrucous Carcinoma
(a). Pathogenesis and History
chewing tobacco and snuff; HPV present in some lesions
low grade - minimal invasion - seldom metastatic
(b). Clinical Features - Broad-based, exophytic, indurated lesions which may be white to pink in color and have a fissured or pebbled surface
Location: labial and buccal vestibule and buccal mucosa
Age: 60-70 y/o - males 4/1
(c). Histological Features
(d). Treatment and Prognosis - much better than for squamous cell carcinoma
- surgical excision; radiation may have a role
- 76% - 5 year cure rate
- can transform to squamous cell carcinoma though
11. Chronic Hyperplastic Candidiasis
occasionally a low grade candidal infection will produce a hyperkeratotic lesion and as such will be a white lesion which cannot be scraped off.
12. White Sponge Nevus
(a). Etiology, Pathogenesis and History
Hereditary - autosomal dominant either present at birth or manifests at puberty
(b). Clinical Features - buccal mucosa usually involved and bilaterally, almost the entire mucosa may be involved in some cases, rough white appearance
(Asymptomatic, bilateral, dense, shaggy, white to gray, gneralized opacification primarily affecting the buccal mucosa but other mucosal surface may be involved)
(c). Histological Feature
(d). Treatment and Prognosis
Recognize the condition and make the correct diagnosis
Remains indefinitely with no ill effect
13. (White) Hairy Leukoplakia
(a) Etiology, Pathogenesis and History
Caused by opportunistic Epstein-Barr virus (EBV); more common in
immunodeficient/immunosuppressed patients especially those infected with
HIV
(a) Clinical features: asymptomatic filiform to flat patch on lateral surface of tongue; may appear on buccal mucosa; often bilateral
(a) Treatment and Prognosis
There is no specific treatment; pt. should be evaluated for AIDS;
Seen in @0% of HIV-infected patients with a marked increase in those who develop AIDS; may affect other immunosuppressed pts; rare in pts. who are immunocompetent
B. NECROTIC WHITE LESIONS: (Sloughing Pseudomembranous Non-Keratotic White Lesions)
Note: Sloughing white lesions are generally the result of coagulation of mucosal surface by various agents, such as heat, chemicals or
microorganisms. The white sloughing tissue can usually be stripped from the surface quite readily leaving a denuded bleeding surface and inducing a burning painful sensation.
1. Materia Alba
2. Trauma
Crushing types of trauma will cause a crushing injury which will, be comprised mostly of necrotic white material at the region of impact. The history is usually definitive.
3. Chemical Burns
(a). Pathogenesis and History
Here again the history will indicate the correct diagnosis.
(b). Clinical Features
whitish lesion which can be scraped off.
Location - if aspirin burn, the lesion will be on cheek near the offending tooth.
(c). Histopathology
necrotic material on the surface
(d). Treatment and Prognosis
advise patient to swallow analgesics in the future.
4. Pyogenic Granuloma
This lesion will be discussed in detail in the exophytic lecture.
The lesion occurs on the gingiva, tongue or cheeks due to mechanical
trauma. It is an inflammatory hyperplasia type lesion. Trauma to the surface of the lesion causes a white necrosis which can be scraped off leaving a raw bleeding surface.
5. A.N.U.G. (Vincent's)
(a). Pathogenesis and History
1. anaerobic fusiforms and spirochetes
2. lowered systemic resistance - psychological stress - run down
3. lowered local resistance - poor hygiene - pockets - erupting teeth
Patient complains of pain, bad taste and odor
(b). Clinical Features
ulcers of ging.-initially the interdental papillae is involved only, are blunted by necrotic process and covered with grayish white membrane
Age - 7-35 y/o - painful lymphadenopathy
(c). Histopathology
(d). Treatment and Prognosis
A. Local
1. H2O2 mouthwashes
2. Penicillin
3. eliminate pockets after acute phase has passed
B. Systemic
increase resistance
6. Candidiasis (Moniliasis)
(a). Pathogenesis and History - yeast like fungus - normal component of oral cavity in the majority of individuals, a saprophyte - for disease need:
1. change in bacterial flora
2. greatly lowered resistance
(b). Clinical Features
Age - the extremes of life
(c). Lab Tests - smear - see pseudohyphae
(d). Histopathology
(e). Treatment and Prognosis
Nystatin
7. Diffuse Gangrenous Stomatitis and/or Gingivitis
a). Pathogenesis and History
A very severe systemic disease such as acute leukemia or advanced malignancy must be present to lower resistance enough to permit this condition to occur. The resistance is so low that necrosis of the tissue occurs.
b). Clinical Features
in some instances there is a single region of necrosis in other cases many areas of the mucosa are necrotic.
c). Treatment and Prognosis
H2O2 mouth washes, antibiotics
Hopefully the M.D. can treat the systemic disease successfully.
8. Rarities - See Text
A. Normal Oral Exophytic Structures
1. Accessory tonsilar tissue
2. Buccal fat pads
3. Circumvallate papillae
4. Foliate papillae
5. Genial tubercles
6. Lingual tonsilar tissue
7. Palatal rugae
8. Palatal tonsil
9. Papilla Palatini
10. Stenson's papillae
11. Sublingual caruncle
12. Tongue
13. Uvula
B. Exophytic Lesions
1. Lesions which project above the normal surface contour. They may have originated (a) on the surface or (b) beneath the surface epithelium.
2. When we find an exophytic lesion on the oral mucosa overlying bone we must determine whether it is peripheral in origin (i.e. originating in the mucosa) or whether it is a central lesion (i.e. originating in bone and extending through the mucous membrane by growth and expansion). A careful digital and X-ray examination will usually reveal whether the lesion in question is peripheral or central. If the lesion and mucosa can be moved over the overlying bone and a radiograph shows no bony involvement, then we are relatively safe concluding that such is a peripheral lesion. Remember though, that in some regions of the oral cavity the mucosa is normally bound tightly to bone, e.g. anterior hard palate and alveolar gingiva. Occasionally it is difficult to identify the tissue of origin because lesions originating in mucosa may invade the underlying bone and in these cases it may be difficult to reconstruct the sequence of events. A biopsy will often do this for us.
3. The general rule states that rough surfaced lesions have their origin in the surface epithelium while smooth surface lesions are generally slow growing lesions that have originated beneath the surface epithelium.
4. Previously we categorized these lesions according to etiology (developmental, inflammatory, tumor and metabolic) but now have attempted to arrange these entities in order of frequency of occurrence.
1. Tori-Exostosis
a. Etiology, Pathogenesis and History
cause not known-but there appears to be a genetic component and questions have been raised about environmental factors
b. Clinical Features
firm, smooth, maybe bosselated covered with normal mucosa
location - palate - 20-25% F/M=2/1; lingual mandible - 7-10%; may be bilateral
Eoxtoses are seen on the buccal aspect of alveolar bone
Seen mostly in adults
c. If seen on Radiograph the Radiographic findings:
completely radiopaque
smooth contours
d. Histological
mostly composed of dense bone
e. Treatment and Prognosis
May not require treatment but excise if: (1) ulcerated repeatedly,
(2). speech, (3). prosthesis, (4). psychological
2. Inflammatory (fibrous) Hyperplasias
This whole group of lesions is similar in pathogenesis. A chronic mechanical irritation is present which produces "proud" flesh or granulation tissue. At first the lesion appears quite red because of the very generous vascularity but later when fibrous tissue forms and the vascularity decreases the lesion may take on a normal mucosal pink color or even a lighter pink. Decisions often must be made whether the lesion should be excised or whether it will shrink in size if the irritant is removed one can expect a great reduction in size and perhaps complete disappearance. If the percentage of fibrous tissue is high then there will be very little regression in the size after the irritant is eliminated and surgical excision will very likely be necessary.
Note: The fibromas of the oral cavity are probably seldom true tumors but develop from existing inflammatory hyperplasia lesion and should really be termed inflammatory fibrous hyperplasia.
Lesions of Inflammatory Hyperplasias
a. Fibroma - inflammatory fibrous hyperplasia
b. Pyogenic granuloma
c. Hormonal tumors
d. Epulis fissuratum
e. Parulis
f. Inflammatory papillary hyperplasia (multiple papillomatosis)
g. Peripheral giant cell granuloma
h. Pulp Polyp
i. Epulis granulomatosum
j. Myxofibroma
k. Peripheral odontogenic fibroma
(peripheral fibroma with calcification)
a. Fibroma (peripheral, traumatic, irritation)/fibrous hyperplasia
Clinical: firm “tumor”; color same as surrounding tissue or lighter; usually asymptomatic; may be sessile or pedunculated
Cause: reaction to chronic irritation or trauma
Treatment/Prognosis: excision; recurrence not expected if source of irritation removed
a. Pyogenic granuloma
Clinical: asymptomatic red “tumor” found primarily on gingiva but on any skin/mucosal surface where trauma has occurred
Cause: reaction to chronic irritation or trauma
Treatment/Prognosis: Excision is treatment of choice; may recur if
excision is incomplete or source of irritation/trauma not removed
b. Hormonal tumors: “tumors” histologically identical to pyogenic granulomas are seen in patients who are going through puberty or are pregnant
c. Epulis fissuratum
Clinical: tumor-like hyperplasia of fibrous connective tissue that develops in association with the flange of an ill-fitting denture; typically presents as
single or multiple folds of firm hyperplastic tissue in the alveolar vestibule; early lesions may be erythematous and may be ulcerated while older ones are usually the color of the surrounding tissue
Cause: reaction to chronic irritation/trauma from an ill-fitting denture
Treatment/Prognosis: surgical removal with a remaking (or relining) of the denture
d. Parulis
Clinical: Red tumor-like (yellow if pus present) occurring usually on the buccal gingiva and often asymptomatic; more common in children and
young adults
Cause: sinus tract from periapical or periodontal abscess
Treatment/Prognosis: treatment of the periapical or periodontal condition
e. (Inflammatory) papillary hyperplasia
Clinical: painless papillomatous (cobblestone) lesion of the hard palate seen overwhelmingly in denture wearers; usually red due to inflammation
Cause: soft tissue reaction to poorly fitting denture with a probable fungal overgrowth
Treatment/Prognosis: excision with construction of new denture; may regress (somewhat) with denture removal; antifungals may help
g. Peripheral giant cell granuloma
Clinical: asymptomatic red tumor-like lesion of the gingiva; composed of fibroblasts and mutinucleated giant cell; most common in adults in areas where the deciduous teeth had been; may produce saucer-like radiolucency due to superficial erosion of bone particularly in edentulous areas
Cause: usually associated with trauma or chronic irritation
Treatment/Prognosis: excision is treatment of choice; will remain indefinitely if not treated
h. See text for discussion of the remainder of this list
3. Mucocele-Ranula
a. Etiology, Pathogenesis and History
For the purpose of this discussion a ranula can be considered a mucocele of the floor of the mouth resembling a “frog’s belly”
These lesions usually arise because of traumatic severance of salivary gland excretory duct(s) but similar lesions occur as the result of a blockage of the duct(s)
b. Clinical Features
dome or nodular shaped, light bluish to pink in color if deep, rubbery, fluctuant
those related to severance of the duct may occasionally be tender;
most frequently seen on the lower lip and these lesions are more common in children and adolescents
mucocele-most common on lower lip
ranula - floor of mouth-involves sublingual gland.
c. Histopathology
d. Treatment and Prognosis
excision is treatment of choice; recurrence is to be expected if the contributing salivary gland is not removed or if adjacent ducts are severed
4. Hemangiomas, Lymphangiomas and Varicosities
a. Hemangioma- tumor or tumor-like lesion composed of blood vessels of varying size
Clinical: red/blue lesion that is poorly defined and commonly blanches when compressed; may be part of the Sturge-Weber syndrome, Rendu-Osler-Weber syndrome or hereditary hemorrhagic telangiectasia; most common in children
Cause: some are developmental, some are congential neoplasms; some are due to abnormal vessel morphogenesis
Treatment/Prognosis: some lesions involute while others require removal via surgery, sclerosing agents, cautery, etc.
a. Lymphangioma
Clinical: spongy, diffuse, painless mass composed of lymphatic vessels; red/blue in color and most frequently seen in the tongue but may also effect other tissues such as the neck; some can become quite large; most common in children
Cause: developmental
Treatment/Prognosis: excision is treatment of choice as sclerosing agents do not work as well as in hemangiomas
5. Central exophytic lesions
6. Verruca Vulgaris - Papilloma - Condyloma Accuminatum
See the section covering White Lesions to fill in the blanks of the following areas
a. Pathogenesis and History
b. Clinical Features
location
age
c. Histopathology
d. Treatment and Prognosis
7. Exophytic squamous cell carcinoma
See text and White Lesions section for more details of squamous cell carcinoma
8. Verrucous carcinoma
a. Etiology, Pathogenesis and History
usually due to use of chewing tobacco or snuff; HPV found in some lesions
b. Clinical Features
Broad-based, exophytic, indurated lesions usually found on buccal mucosa; most common in men; rough white and or pink, broad based, little vertical dimension, may also be seen on the
palate, vestibule, tongue.
c. Histopathology
benign looking appearance - maybe little evidence of malignancy in cells.
d. Treatment and Prognosis
These slow growing lesions require wide excision, close follow up, 5 year cure rate is 75%-metastasis is uncommon; generally speaking these lesions have a better prognosis than the usual squamous cell carcinoma as the growth pattern is more expansile rather than invasive
9. Minor salivary gland tumors
a. Pathogenesis and History
usually a slow growing mass
b. Clinical features
smooth dome-shaped mass covered by normal appearing mucosa
location - posterior-lateral hard palate
- retromolar area
age 30-70
c. Histopathology
many histologic types
d. Treatment and Prognosis
complete excision, close follow up.
10. Peripheral Benign Mesenchymal Tumors
lipomas
myomas
peripheral nerve tumors
11. Nevus and melanoma
12. Peripheral metastatic tumors
13. Peripheral malignant mesenchymal tumors
14. Rarities - See Text
MUCOSAL ULCERS
Erosion - a shallow crater in the epithelial surface-only the superficial part of the epithelial lining is lost-will appear red because of (1) loss of keratin, (2), underlying inflammation.
Ulcer - a deeper crater in the mucosa or skin which extends through the entire thickness of the epithelium and involves the underlying connective tissue
Ulcer Classification:
A. Short Term - disappears within three weeks
Persistent - persists beyond three weeks after the elimination of etiological factor.
B. Primary - present first as ulcers - i.e. traumatic ulcer
Secondary - present first as another type of lesion and secondarily ulcerates i.e., vesicles and blebs.
NOTE: Due to contamination with oral bacteria and juices the majority of ulcers are accompanied by a tender or painful lymphadenopathy. Hence, the presence of a painful lymphadenopathy is of little diagnostic aid.
1. Traumatic Ulcers (short or persistent)
a. Pathogenesis and History
Painful ulcers covered by yellow fibrin membrane; diagnosis usually evident from appearance when combined with history.
In almost all cases the patient can identify the traumatic agent and when it happened.
1. mechanical
dentures, sharp edge of tooth, foreign object, toothbrush, biting habit
2. thermal
hot food, hot instruments, handpiece
3. medicinal
aspirin, tylenol, turpentine
b. Clinical Features
Ulcerative lesions covered by yellow fibrin membrane; pain almost always present; ulcers of tongue may be persistent location
location
tongue, lips, gingiva, palate, mucobuccal fold.
Ulcers of lip usually have crusted surface
any shape or size, almost any location.
c. Histopathology
nonspecific picture: epithelium missing, inflammation of underlying
connective tissue.
d. Treatment and Prognosis
1. eliminate causative agent
2. symptomatic treatment; coat ulcer. with Kenalog in Orabase
3. if doesn't disappear in three week-excisional biopsy
2. Herpetic Ulcer (Recurrent) (Short)
a. Etiology, Pathogenesis and History
Causative agent is Herpes simplex virus type I (occasionally type II)
Primary herpetic lesions usually affect children under the age of 5 yrs.; while Secondary (Recurrent) lesions are seen in patients who have had previous herpes lesions and these patients are usually adults or young adults
b. Clinical Features
Appear as multiple, small, painful ulcers preceded by vesicles
In Primary disease, the lesions may appear on any oral mucosal surface with the gingiva generally involved; perioral and skin lesions may occur
In Secondary herpes simplex infection lesions are common on the lips and intraorally the palate and attached gingiva are usually involved.
Prodromal symptoms such as burning, pain or tingling may occur
Lesions need to be differentiated from recurrent aphthous ulcers
Help: in distinguishing Recurrent Herpes simplex infection from recurrent
aphthous ulcers (See page 166 in your textbook)
Look for dissimilar features in:
1. location
2. appearance of initial and mature lesions
3. number of lesions
4. size of lesions
5. site of recurrence
6. early histopathology
c. Blood workup
serology - negative, w.b.c. normal
d. Histopathology
non-specific ulcer (early lesion (vesicle) would have specific histology)
e. Treatment and Prognosis
Self-limiting disease which heals in about 2 weeks without scaring
Symptomatic treatment may help such as Kenalog with Orabase
3. Recurrent Aphthous Ulcer (short)
a. Pathogenesis and History
uncertain pathogenesis-allergy, microbial, endocrine, autoimmune
recurrent painful ulcers lasting 7-14 days
b. Clinical Features
Recurrent, painful ulcers seen mainly on the tongue, vestibular mucosa, floor of mouth, and faucial pillars; not found on skin, vermikion of lip, attached gingiva or hard palate. There maybe multiple ulcers but don't form a cluster formation as does recurrent herpetic lesions - a scattered distribution
Three types: Minor (most common), Major and Herpetiform; aphthae also associated with Behcet’s syndrome, etc.
Important distinguishing features include:
1. location
on loose (non-keratinized) surfaces
2. age
wide range
3. again see your textbook, page 166
c. Histopathology
nonspecific ulcer
d. Treatment and Prognosis
Painful nuisance disease which is rarely debilitating except for the major type; symptomatic remedies include:
(1) tetracycline mouthwashes
(2) cover with kenalog and Orabase before meals and before bed (H.S.)
4. Ulcers Resulting from Odontogenic Infection
a. Pathogenesis and History
(1) from a chronic alveolar abscess
(2) from rupture of a space infection
History of pain & swelling related to a tooth
b. Clinical Features
1. location of sinus opening
buccal or lingual surface of alveolar ridge, palate too
2. age most are in children under 14 years.
c. Radiologic
see evidence of infection - radiolucency around apex
place g.p. cone up tract and take x-ray
d. Histopathology
nonspecific - some polymorphs present
5. Sloughing pseudomembranous ulcers (short or persistent)
refer to previous lecture
1. drug burns
2. crushing trauma
3. Candidiasis (moniliasis)
4. ANUG
6. Generalized Mucositides and Vesiculobullous Diseases (short or persistent)
Generalized Mucositides:
a. Erosive lichen planus
b. Erythema multiform
c. Primary herpetic stomatitis
d. Stevens-Johnsons Syndrome may commence as a
e. Behcet's syndrome
7. Squamous Cell Carcinoma (persistent)
a. Pathogenesis and History
use of tobacco and alcohol; hx. of previous irradiation; uv light (lip)
patient is usually unaware of the lesion (earliest presenting feature is an asymptomatic red lesion/erythroplakia.
b. Clinical Features
painless ulcer with indurated border - red velvety base
1. location
lower lip, tongue (ventral & Lateral), floor, gingiva
buccal, soft palate
2. age
over forty
Remember: squamous cell carcinoma may have many clinical appearances, ie.
red, white, red & white, exophytic, etc.
c. Histopathology
ulcer with malignant epithelial fingers invading into c.t.
increased number of mitotic figures (some atypical), keratin pearls, pleomorphism, hyperchromatism, etc.
d. Treatment and Prognosis
surgery and/or irradiation and/or chemotherapy
radical neck
Overall 5-year survival rate is now 55%; prognosis better if found in early stages; poor prognosis with metastases
NOTE: Basal Cell Carcinoma (Rodent ulcer)
on face superior to line drawn from corner of mouth to tragus of ear locally malignant very rarely metastasize
8. Syphilis(chancre and gumma) - (persistent)
a. Pathogenesis and History
Treponema pallidum (motile spirochete)
dark field
hx. of oral intercourse with infected partner
lesion develops at site of inoculation
Read about Primary, Secondary, Tertiary and Congenital Syphilis
b. Clinical Features (chancre)
A chancre is the primary lesion of syphilis and usually appears as an indurated, nonpainful ulcer which on occasions may be tender; it appears at the site of inoculation
The ulcer usually has a wide base, may have a coppery colored, narrowed border
1. location
lips, tip of tongue, tonsil region, soft palate
2. age
no age group is immune
3. Mucous patches (ulcers covered by a membrane) are seen in Secondary Syphilis while the Gumma is the lesion of the Tertiary stage
c. Blood Workup
Serology - will become positive two or three weeks into chancre stage if not treated.
once positive may or may not remain positive for life
R.P.R. - screen test: F.T.S. - specific
d. Histopathology
if silver stains used, will see T.P. as black ~~~
e. Treatment and Prognosis
Penicillin is still the drug of choice
9. Ulcers in Blood Dyscrasias (persistent)
a. Pathogenesis and History
A number of symptoms of the particular systemic disease may occur;
small traumatic lesion in mucosa becomes secondarily infected due to decreased resistance of host. Sickle cell ulcer due to infarct.
b. Clinical Features
Non-specific, painful, ulcers often with lymphadenopathy
1. location
gingiva, tongue, buccal mucosa
c. Blood Workup
sickle cell prep
RBC WBC differential
d. Histopathology
nonspecific
e. Treatment and Prognosis
1. control systemic disease
2. H2O2 mouthwash
3. antibiotics
10. Ulcers in Uremia (persistent)
a. Pathogenesis and History
kidney failure - increased B.U.N. - patient may be on dialysis
1. bacterial breakdown of urea to ammonia
2. mouth breathing in acidosis
b. Clinical Features
1. location
usually gingival
2. age
c. Blood Workup
RBC. WBC. differential
d. Histopathology
nonspecifice.
a. Treatment and Prognosis
1. control uremia
2. H2O2 mouthwash
3. antibiotics
4. prognosis will depend on systemic disease control
11. Traumatized Tumors (persistent)
a. Pathogenesis and History
tumors originating in the tissues beneath the surface epithelium are
characteristically non-ulcerated in early stages. Trauma due to chewing or incisional biopsy will frequently produce a persistent ulceration.
b. Clinical Features
a nodular, domeshaped or nodular growth
ulcerated surface-tender but usually not very painful
c. Histopathology
picture of tumor with ulcerated epithelial surface
d. Treatment and Prognosis
excisional biopsy
12. Minor Salivary Tumors (Types prone to ulceration) - (persistent)
a. Pathogenesis and History
those containing pooled fluid are prone to rupture-low grade mucoepidermoid carcinoma, Warthin's tumor
b. Clinical Features
1. location
posterior-lateral hard palate and retromolar region
2. age: 30-60
c. Histopathology
many varieties; depends on particular salivary gland tumor
d. Treatment and Prognosis
excisional biopsy or referral
13. Rarities - See Text
BLUISH-BROWNISH-BLACK CONDITIONS
Introduction
I. Color derived from
a. accumulation of colored material
b. refractive phenomenon with colorless fluids
II. Colored material
A. Exogenous
pigments and metals etc. which are ingested
1. heavy metals
lead, bismuth
2. commercial dyes
3. Vegetable pigments
carotene
B. Endogenous
pigments or metals which normally occur in body but due to some
pathological process are deposited in increased amounts
1. Melanin
2. blood pigments
3. biological metals - iron
III. Refractive phenomena (bluish)
bluish color due to the fact that the colorless fluid which is pooled just under the surface alters the reflection and resorption of light. In some cases the resultant color is so blue that the observer is certain that it is a pigmented condition, or even bluish blood.
Examples:
A. Salivary retention phenomena
mucocele
ranula
mucus producing salivary tumor
B. superficial cyst (non-keratinizing)
C. Lymphangioma
IV. Factors influencing color of lesions
A. amount of material present
B. depth of normal tissue covering colored material or refractive fluid
V. Melanoplakia (Physiologic Pigmentation)
a. Pathogenesis and History
normal intraoral pigmentation in African-Americans
mild to moderate amounts may be present in Caucasians, particularly of
Mediterranean origin
b. Clinical Features
Symmetric distribution; does not change in intensity; does not change the surface
morphology; various interesting shapes and designs; constant appearance
c. Histopathology
increased melanin deposits in basal cell layer
no increase in the number of melanocytes
d. Treatment and prognosis
none needed; may biopsy if suspicion index is high that it is another lesion such as a melanoma
SPECIFIC LESIONS
A. Distinct circumscribed types (most are single lesions)
1. Varicosity/varix: abnormal venous dilatation
a. Pathogenesis and History
local-very common on ventral surface of the tongue in older people; if generalized-may be associated with congestive heart failure
NOTE: Phlebectasia linguae (caviar tongue)
2. Amalgam tattoo
a. Pathogenesis and History
soft tissue abraided during restorative procedure-silver or mercury from filling comes in apposition to it and stains reticulin fibers permanently.
usually no "chunk" of amalgam is present in the tissues
b. Clinical Features
asymptomatic gray/blue pigmented macule in tissue near where amalgam filling was placed (gingiva, tongue, palate or buccal mucosa; consistency same as surrounding tissue - does not blanch or change; no associated inflammation; if large enough piece may be seen radiographically
c. Histopathology
reticulin fibers are stained black
d. Treatment and Prognosis
none require; if suspicion index is high for melanoma, excise and submit for microscopic study; amalgam tattoos remain indefinitely with little change
3. Black hairy tongue
a. Etiology, Pathogenesis and History
Elongation of the filiform papillae creates what is known as hairy tongue; the cause of hairy tongue is unknown but poor hygiene, and antibiotic/corticosteroid use have been suggested
debris and microorganisms may irritate filiform papillae and cause retention of keratin, then the keratin hairs stain according to whatever color substance they are exposed to
b. Clinical features
hairy appearance on mid-posterior of dorsal surface of the tongue due to elongation of the filiform papillae
c. Histopathology
elongated filiform papillae (keratin retention)
d. Treatment and Prognosis
clip- if "hairs" are long enough
institute proper brushing of the tongue to improve hygiene; identify
any contributing factors
4. Mucocele
See section on Exophytic Lesions and Textbook for more information
a. Etiology, Pathogenesis and History
severed duct of minor salivary glands
saliva is deposited and pools in the tissue-usually superficially
b. Clinical features
bluish nodular or dome-shaped rubbery mass, fluctuant,
vast majority occur on lower lip - few on cheek and retromolar area, yield thick, clear fluid (mucin) on aspiration
c. Histopathology
roundish mass of mucin surrounded by c.t. + macrophages, lymphocytes
d. Treatment and prognosis
excision + microscopic study
5. Ranula
See section on Exophytic Lesions and textbook for more information
a. Pathogenesis and history
blocked or severed duct of section of sublingual glands
may appear then disappear (ruptured) and then recur
b. Clinical features
bluish fluctuant mass in floor of mouth
usually unilateral but may involve both sides; resembles a “frog’s belly”
c. Histopathology
usually no epithelial lining
d. Treatment and prognosis
surgical excision; marsupialization may be used but lesions often recur and if it recurs, excise gland on the involved side (which could have been done in the first place)
6. Hemangioma
a. Etiology, Pathogenesis and history
congenital, neoplastic or traumatic
dilatation and/or increased number of capillaries
b. Clinical features
Red/blue lesion that usually blanches when compressed; extent of lesion usually difficult to discern; see association with Sturge-Weber and Rendu-Osler-Weber syndromes and hereditary hemorrhagic telangiectasia
c. Histopathology
dilated blood spaces lined with endothelium
fibrous septae vary in number and thickness
d. Treatment and prognosis
excision after careful workup-perhaps angiograms
if large or in delicate region-hospitalize;
sclerose with sclerosing solutions is another modality
7. Lymphangioma
a. Pathogenesis and history
congenital-increased number of lymphatic vessels
not common in the oral cavity
b. Clinical features
dorsal or lateral surface of tongue is primary intraoral site
surface usually papillary
if superficial-light blue cast
aspirated fluid will froth easily when shaked
(high lipid content)
c. Histopathology
dilated lymphatic vessels
d. Treatment and Prognosis
excision
8. Melanotic macule of Lip or Oral Cavity (Labial or Oral Melanotic Macule
a. Etiology, Pathogenesis and History
Cause is unknown but post-inflammatory and trauma mentioned
congenital; like a large freckle (ephelis) but more heavily stained.
b. Clinical Features
flat oral pigmentatikon less than 1 cm in diameter; on lower lip or in oral cavity-gingiva, buccal mucosa, palate; borders may be smoothly circumscribed or ragged, does not blanch;
remains constant in size and appearance year after year
c. Histopathology
d. Treatment
If suspicion index is high, excise and send for microscopic study.
If not examine periodically
9. Early Hematoma
a. Etiology, Pathogenesis and History
Expect trauma or bleeding diathesis
bleeding and pooling of blood beneath tissues
b. Clinical Features
bluish nodular or dome shaped, rubbery
stinging sensation on pressure (dissection of tissues)
c. Treatment and Prognosis
if large, may have to hospitalize-airway
attempt to aspirate, then pressure
antibiotic coverage
10. Late hematoma
a. Etiology, Pathogenesis and History
Blood has clotted at this point
b. Clinical Features
feels very firm
c. Treatment and Prognosis
antibiotics
11. Petechia, ecchymosis (purpura)
a. Etiology, Pathogenesis and History
bleeding into the tissue - less quantity than in hematoma-trauma or systemic disease
b. Clinical features
does not blanch
petechiae-pinpoint
ecchymotic patches-larger
c. Treatment and prognosis
if findings are more spectacular than degree of trauma would indicate work up patient for systemic disease
12. Superficial Cyst
a. Etiology, Pathogenesis and History
exclude keratin forming cysts here. They will appear white if superficial.
b. Clinical features
on alveolus - bluish nodular mass-fluctuant
usually dentigerous or residual
c. Histopathology
non-keratinizing cyst
d. Treatment and Prognosis
enucleation
13. Peripheral giant cell granuloma
discussed previously under exophytic lesions
one clinical example
14. Pigmented fibroma
just represents a fibroma that has developed in an melanoplakia patch
15. Ephelis (freckle)
rare in oral cavity
common on lips
16. Melanoma
a. Etiology, Pathogenesis and History
malignant tumor of melanocytes; uv light may be carcinogenic and cause skin lesions; cause intraorally is unknown
b. Clinical features
may appear at first as an insignificant spot
bluish black - firm macule or nodule
macule-usually very low grade slow growing
nodular-usually highly malignant
most common on the palate and gingiva intraorally
c. Histopathology Note Kaposi's Sarcoma (AIDS)
malignant nevus cells
d. Treatment and prognosis
wide excision; oral 5-year survival rate is around 20%; unpredictable metastatic behavior; some type have a poorer prognosis, ie. nodular melanoma, which has only a vertical growth phase
17. Mucus-producing minor salivary gland tumors
uncommon
mucoepidermoid tumor - most frequent
posterior-lateral hard palate-most frequent site
may be mistaken for a mucocele
18. Heavy metal lines
rare today
a clinical example or two
lead, bismuth
19. Nevus
a. Etiology, Pathogenesis and History
Cause is unknown; due to nests f nevus cells; congenital hamartoma
b. Clinical features
Elevated pigmentations but may be flat; firm-does not blanch; often non-pigmented in the oral cavity; while common on skin are uncommon intraorally; intramucosal most common type; blue nevus is more common on palate
c. Histopathology
nevus cells in tissue
d. Treatment and prognosis
for oral nevi, it is suggested that all are excised to rule out melanoma
20. Von Recklinghausen's disease(neurofibromatosis)
a. Etiology, Pathogenesis and History
hereditary condition seen in about 1 of every 3,000 live births;
several types; type 1 is most common accounting for about 85-90%
of cases; type 1 is autosomal dominant however 50% of cases have no family history and are probably new mutations
b. Clinical features
multipe neurofibromas may appear anywhere in the body although most appear as multiple nodules on skin; patients may also present with cafe' au lait (coffee with milk) spots on skin; Crowe’s sign (axillary freckling) and Lisch nodules (brown pigmented spots on iris); oral lesions occur by of the soft tissues and within bone (mandibular canal)
c. Treatment and prognosis
there is no specific therapy and treatment often is directed toward prevention or management of complications; surveillance is important in case one of neurofibromas becomes malignant (this occurs in about 5 % of the cases)
21. McCune-Albright's Syndrome
a. Etiology, Pathogenesis and History
is a syndrome that includes: polyostotic fibrous dysplasia, cutaneous melanotic pigmentations and endocrine abnormalities
a. Clinical Features
polyostotic fibrous dysplasia (fibrous dysplasia of two or more bones)
the skin/mucosal pigmentations appear as cafe' au lait spots
the most common endocrine abnormality is precocious puberty in girls (acromegaly, hyperparathyroidism and hyperprolactinemia are also known to occur)
22. Puetz-Jegher's Syndrome
a. Etiology, Pathogenesis and History
is a condition that is inherited as an autosomal dominant trait
patients manifest ephelides/melanotic macules and intestinal polyposis
b. Clinical Features
multiple pinpoint melanin pigmentations around lips and other body orifices; intestinal polyposis; polyps are regarded as hamartomas with very limited neoplastic potential; polyps most common in small intestine where they may produce evidence of obstruction and other symptoms such as abdominal pain, rectal bleeding and diarrhea
23. Rarities - see text
B. GENERALIZED TYPES OF BLUISH, BROWNISH AND BLACK CONDITIONS
1. Cyanosis
2. Addison's disease
3. Chloasma gravidarum
4. Hemochromatosis
5. Argyria - silver
6. Rarities - see text
1. Cyanosis
a. Etiology, Pathogenesis and History
is caused by a substantial rise in the proportion of reduced hemoglobin to oxygenated hemoglobin in the blood;
may be localized (tourniquet applied to arm/cold fingers) or generalized (respiratory deficiency, cardiovascular disease, or abnormal hemoglobin metabolism)
b. Clinical
localized or generalized bluish cast of skin (easier seen in light-skinned patients); if the cyanosis has persisted as a chronic condition, clubbing of the fingers can occur
2. Addison’s disease
a. Etiology, Pathogenesis and History
is primary adrenal cortical insufficiency which may result from:
adrenal gland infection, autoimmune disease affecting the gland or idiopathic causes; with reduced cortisol there is an increase in ACTH and MSH; increased ACTH and MSH both result in stimulation of melanocytes which leads to a diffuse (focal) pigmentation of the skin and mucous membranes
a. Clinical
either a diffuse or focal pigmentation of the skin and mucous membranes may be observed; other signs/symptoms include: weakness, weight loss, nausea, vomiting and hypotension
3. Chloasma gravidarum
is the tanned mask seen on the cheeks, nose and infraorbital areas of pregnant, light-skinned women during late pregnancy; occasionally the oral mucosa may become diffusely brown; this disappears after delivery
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