D2 Fall PAR 8 Flashcards
Erythematous Definition
Red in color due to dilation and congestion of capillaries, increased blood flow; implies injury, infection, or inflammatory process
“Red” does NOT always mean erythematous
Fibroma
(aka irritation fibroma, traumatic fibroma, hyperplastic scar)
reactive fibrous hyperplasia (connective tissue)
people 40-60 years old
most are 1.5cm or less
smooth surfaced papule/nodule
similar color to surrounding tissue
common at buccal mucosa along line of occlusion
MUST BIOPSY
Epulis Fissuratum/Inflammatory Fibrous Hyperplasia
fibrous hyperplasia developing because of an ill-fitting removable prosthesis (denture or partial)
IFH can also occur WITHOUT a prosthesis because of inflammatory factors like plaque and calculus– cannot call this epulis fissuratum
firm and fibrous
usually on FACIAL ASPECT
Good prognosis when the ill-fitting prosthesis is fixed
Bumps on the Gums– 4 P’s
- Pyogenic Granuloma
- Peripheral ossifying fibroma
- Peripheral giant cell granuloma
- Peripheral odontogenic fibroma
Pyogenic Granuloma
Anywhere on oral mucosa
LOCAL IRRITANT causes granulation tissue response
may have rapid/alarming growth rate
- smooth or lobulated mass
- pedunculated
- Very vascular (red/blue color, may blanche with pressure)
- compressible, spongy
- surface frequently ulcerated
several mm to several cm
PREGNANT WOMEN common– may resolve after delivery
May recur if local irritant isn’t removed
Peripheral Ossifying Fibroma
ONLY ON GINGIVA/EDENTULOUS ALVEOLAR RIDGE
TEENS AND YOUNG ADULTS
- nodular mass
- varying degrees of calcified material (“ossifying”)
- pedunculated or sessile
- reactive
- red/pink color
- often ulcerated
Most are less than 2 cm
Tx: excision to periosteum
Recurrence rate is low, 8-16%
Peripheral Giant Cell Granuloma
Reactive lesion caused by LOCAL IRRITATION or TRAUMA
ONLY ON GINGIVA/EDENTULOUS ALVEOLAR RIDGE
- Red/Purplish nodular mass
- most less than 2cm
- may or may not be ulcerated
ANY AGE
Tx: excision to underlying bone
10-18% recurrence rate
Recurrent Aphthous Stomatitis
likely IMMUNOLOGICAL
- HIV
- HLA types
- trauma, food, stress
Tx: Topical corticosteroids
- augmented betamethasone dipropionate 0.05% gel
- clobetasol propionate 0.05% gel
can use elixirs/syrups with corticosteroids for ulcerations that are hard to reach
Three types: (detailed in other cards)
1. Minor recurrent aphthous stomatitis
2. Major recurrent aphthous stomatitis
3. Herpetiform recurrent aphthous stomatitis
All three forms are on UNATTACHED GINGIVA
MINOR Recurrent Aphthous Stomatitis
Ulcer with yellow-white membrane
Erythematous halo
Small (3-5mm)
Unattached mucosa, usually on the ANTERIOR
MAJOR Recurrent Aphthous Stomatitis
Can be associated with HIV or other immunocompromised states
Larger (up to 3cm) and longer duration (2-6 weeks)
usually a deeper ulcer– may SCAR once healed
Unattached mucosa, usually on the POSTERIOR
HERPETIFORM Recurrent Aphthous Stomatitis
Numerous, small lesions
NON-KERATINIZED unattached mucosa
Herpes Simplex Virus
Self limiting (resolves itself if not immunocompromised)
Primary infection that can be reactivated (secondary infection)
Most orofacial infections caused by HSV-1 (remainder by HSV-2)
Primary HSV infection usually ages 2-4 (TODDLERS)
80-90% asymptomatic
The symptomatic cases are called ACUTE HERPETIC GINGIVOSTOMATITIS
Spread by saliva and direct contact with active perioral lesions
Multiple vesicles and ulcers ANYWHERE ON SKIN OR ORAL CAVITY
Unattached AND attached mucosa
Quickly rupture and leave shallow, painful ulcers
HSV remains latent in regional ganglia, and can be reactivated by…
- UV light
- physical trauma
- upper resp. tract infection
- pregnancy and menstruation
- immunosuppression
Herpes labialis
Cold sore/fever blister
Secondary HSV form
prodromal signs and symptoms 6-24 hrs before lesions develop
Vesicles rupture and crust within 2 days– minimal risk for infection after lesions crust
Intraoral Secondary HSV
KERATINIZED MUCOSA bound to bone in immunocompetent patients (attached gingiva and hard palate)
Less intense symptoms
Healing in 7-10 days
Treatment for acute herpetic gingivostomatitis
must treat within first 3 symptomatic days to be effective
Systemic valacyclovir (preferred) or acyclovir
Treatment for herpes labialis
initiation of treatment during prodromal period has maximum benefit
systemic valacyclovir, acyclovir, or penciclovir cream
Treatment for recurrent intraoral herpes
usually no treatment necessary
Chlorhexidine rinse with or without valacyclovir/acyclovir
Candida albicans (general microbiology)
Most common fungal infection in humans
common dimorphic yeast
yeast form = commensal
hyphae = pathogen
yeast can undergo transformation to hyphae form, producing germinative or “germ tubes”
Candida hyphae never penetrate deeper than the keratin layer
Microabscesses may be seen on superficial spinous layer
acanthosis often present (benign thickening of stratum spinosum)
chronic inflammation of the connective tissue
Candidiasis Spectrum of Disease
(most mild to most serious):
- Carrier state
- superficial mucosal/cutaneous infection
- localized invasive candidiasis
- disseminated candidiasis
Candida infections are more prevalent in…
(remember it is opportunistic)
- infants
- pts who had recent abx tx
- pts on corticosteroids
- immunodeficiency
- people with RPD
- pregnancy
- overweight/diabetes
- zinc or iron deficiency
- hypothyroid conditions
Candida Diagnosis
often clinical signs and symptoms are enough
Culture– may not distinguish between carrier and infection
Exfoliative cytology
Biopsy usually NOT NEEDED
Candidiasis Treatment
Superficial oral mucosal infections can be treated with milder topical or systemic antifungals:
- clotrimazole 10mg troches
- nystatin oral susp. (100,000 units/mL)
- fluconazole 100mg tablets
Life threatening infections:
- IV amphotericin B
Erythematous candidiasis
Common on TONGUE
area of redness, variable borders
diffuse atrophy of dorsal tongue papillae, particularly after broad-spectrum antibiotics… causes “burning sensation”
2 forms of erythematous candidiasis:
- central papillary atrophy
- denture stomatitis
4 types of Oral Candidiasis
- Erythematous candidiasis
(two types– central papillary atrophy and denture stomatitis) - Angular cheilitis
- Acute pseudomembranous candidiasis
- Hyperplastic candidiasis
Central Papillary Atrophy
One of the 2 types of Erythematous Candidiasis
previously called “median rhomboid glossitis”
Most caused by chronic candidiasis
Well-defined area of redness, mid-posterior dorsal tongue
Usually asymptomatic
Denture Stomatitis
One of the 2 types of Erythematous candidiasis
May be called “chronic atrophic candidiasis”
Denture is often contaminated with candida organisms, but NO INVASION OF MUCOSA is seen
Erythema of palatal denture-bearing area
Usually asymptomatic
Angular Cheilitis
Usually related to candidiasis, but may have other cutaneous bacterial microflora
Redness, cracking of corners of the mouth
Often waxes and wanes
Usually required topical anti-fungal therapy
Treatment for angular cheilitis
Angular cheilitis with intramural candidiasis:
- clotrimazole troches– have pts lick corners of mouth while using troches
Isolated or severe: topical anti fungal creams
- 1%/1% iodoquinol/hydrocortisone
- nystatin/triamcinolone cream
- OTC 1% clotrimazole
Pseudomembranous Candidiasis
Also called “thrush”
White “curdled milk” or “cottage cheese-like” plaques that CAN BE WIPED OFF and leave an erythematous base
BUCCAL MUCOSA
PALATE
TONGUE
May be asymptomatic
- burning or unpleasant taste occasionally noted
Hyperplastic Candidiasis
also known as “candidal leukoplakia”
White patch that CANNOT be rubbed off
ANTERIOR BUCCAL MUCOSA
May be problematic because a true leukoplakia may have superimposed candidiasis (leukoplakia is premalignant and you may not recognize it due to the candida growth)
should resolve with anti fungal therapy
Leukoplakia
white patch or plaque that cannot be characterized as any other disease
considered PREMALIGNANT (most common precancerous oral lesion–may transform to SCC)
Well-defined with crisp margins
May be homogenous, variably thick, or speckled
Common areas: “soft areas”
- lateral/ventral tongue
- floor of mouth
- soft palate
hyperkeratosis with or without acanthosis
most do NOT show dysplasia
Possible etiologies of leukoplakia (there are 3)
- tobacco smoking
- sanguinaria (blood root) [this is a flower]
- betel nut use
Alcohol is NOT necessarily associated with leukoplakia
5 Lesions that ARE NOT LEUKOPLAKIA:
“Frick, This is Not A Leukoplakia”
Frictional keratosis
Tobacco pouch keratosis
Nicotine stomatitis
Amalgam reactions
Lichen Planus
Prognosis and Tx of Leukoplakia
BIOPSY MANDATORY (premalignant.. duh)
Tx: clinical monitoring, excision, laser ablation
Small risk of transformation to SCC
Follow-up appt is essential, with or without removal
Recurrences COMMON (1/3 of patients)
Proliferative Verrucous Leukoplakia (PVL)
More than 1 precancerous lesion in the mouth OR a single lesion greater than 3cm
no definite etiology
OLDER FEMALES (mean age = 67)
Malignant transformation in more than 70% of patients
almost guaranteed recurrence (87-100%)
Prognosis is GUARDED
Management:
- 3-6 month recall with excellent documentation
- biopsy at least every 12-18 months, sooner if it changes or a new lesion appears.
Erythroplakia
Red patch that cannot be clinically or pathologically diagnosed as any other condition
MUCH MORE DYSPLASIA upon biopsy than leukoplakia
- 90% of erythroplakia shows dysplasia (CIS)
Same etiology as SCC (tobacco, alcohol)
OLDER MALES
Same locations as leukoplakia (very soft areas)
- floor of mouth
- ventral tongue
- soft palate
Well-demarcated velvety, red plaque
May be adjacent to areas of leukoplakia
Epithelial atrophy with lack of keratin production
Chronic inflammation
BIOPSY and close follow-up are MANDATORY
Tx depends on how severe the dysplasia is
Recurrence, developing separate lesions, and malignant transformation are all common
Most common oral cancer? Most common demographic for this cancer?
Oral Squamous Cell Carcinoma
Most common in BLACK MALES
OSCC Risk Factors
Tobacco (especially combustible)–75-85% have OSCC association
Alcohol (not directly a carcinogen here, but works synergistically with tobacco)
Betel quid
Radiation
Plummer Vinson Syndrome
- iron deficiency anemia
- glossitis
- dysphagia
Immunosuppression
High-risk HPV strains
- not a major risk factor for oral cavity cancer
- associated more with OROPHARYNX cancers (base of tongue, tonsillar pillars, back of throat)– usually attributed to HPV16
** 20-25% of OSCC present with NO IDENTIFIABLE RISK FACTORS
How long is OSCC usually present before pt seeks medical attention?
4-8 months
longer (8-24 months) in lower socioeconomic classes
denial, lack of pain, and insufficient education play a role
OSCC has highly varied features that may include:
exophytic (growing out from tissue)
endophytic (growing down into tissue
ulcerated
erythroplakic
leukoplakic
** it doesn’t have all these features at once, these are just possible appearances
SCC of the LIP
Cause: chronic UV light
MALES (usually light skinned with outdoor occupations)
Slowly growing, indurated (hardened) ulceration
Verrucous Carcinoma
first reported as a smoke-less tobacco related lesion
SCC is much more common, even among smokeless tobacco users
May be associated with proliferative verrucous leukoplakia (PVL)
MALES older than 55
white, warty plaque
mandibular vestibule
buccal mucosa
hard palate
VERY RARE METASTASIS
GOOD PROGNOSIS
- up to 20% have foci of SCC
Branchial Cleft Cyst (Cervical Lymphoepithelial Cyst)
arise from remnants of the branchial clefts–95% from the 2nd arch
swelling ANTERIOR to the sternocleidomastoid
more likely on the LEFT side
Fixed position on the neck (doesn’t move around)
stratified squamous epithelial lining
lymphoid tissues present in wall, with germinal center formation
Recurrence is RARE
Thyroglossal Duct Cyst
CHILDREN 10-12
Fluctuant midline swelling from foramen cecum to suprasternal notch
80% located BELOW the HYOID BONE
Cysts often move up and down upon swallowing
columnar and/or stratified squamous epithelial lining
Often with thyroid tissue present in cyst wall
TX: Sistrunk Procedure (removal of cyst with midline segment of hyoid bone and muscle… less than 10% recurrence)
Mucocele (Mucous Extravasation Phenomenon)
blockage or rupture of salivary gland duct and spillage of mucin into surrounding tissue
usually children or young adults
usually by local trauma, like a lip bite
Usually on lower lip, followed by floor of mouth (ranula), anterior ventral tongue, buccal mucosa, and palate
RARE in upper lip– submucosal nodule in upper lip is probably a neoplasm– not a mucocele!!
Dome shaped submucosal swelling 2mm to several cm in size
Bluish translucence to normal color
Fluctuant or firm on palpation
Ranula
Mucocele that is on the floor of the mouth
Sialolithiasis
Salivary stone
- calcified structures that develop within salivary ductal system
Etiology: deposition of calcium salts around nidus of debris (bacteria, etc)
usually SUBMANDIBULAR gland duct– because duct is long and has a tortuous uphill course
Increased pain and swelling at mealtime
Firm (rock-hard) mass in floor of mouth or cheek
Smooth surfaced radiopaque mass, can see concentric rings on radiograph
Surrounded by salivary duct epithelium
Pleomorphic Adenoma (Benign Mixed Tumor)
MOST COMMON salivary gland tumor
arises from ductal epithelium and myoepithelial elements
ADULT FEMALES
slowly growing, rubbery-firm mass
If in the parotid gland, it is usually the superficial lobe
If in a minor salivary gland, it is usually seen in the palate or upper lip
well circumscribed, encapsulated tumor
tumors may be completely composed of myoepithelial cells
GOOD PROGNOSIS with adequate surgical excision
small amount will undergo malignant transformation
Papillary Cystadenoma Lymphomatosum (Warthin Tumor)
BENIGN tumor of PAROTID
almost exclusively in the parotid gland (slow growing in tail of parotid)
strong association with SMOKING
OLDER MALES
very small percent is bilateral
relatively low recurrence rate
VERY RARE malignant transformation
Mucoepidermoid Carcinoma
Most common MALIGNANT salivary gland tumor
mucous and squamous differentiation
Wide age range, but peak is in pt’s 30s
FEMALES
parotid and minor salivary glands of the palate most common
may present as intraosseous jaw tumor
Low grade– very good prognosis
High grade– bad prognosis
Children have better prognosis than adults
Intraosseous Mucoepidermoid Carcinoma
MALIGNANT
central tumor, possibly arising from entrapped, ectopic salivary gland tissue or odontogenic epithelium
histologically identical to soft tissue tumor (mucoepidermoid carcinoma)
MIDDLE AGED FEMALES
MANDIBLE more common
Swelling, pain, paresthesia
Unilocular or multilocular radiolucency
GOOD PROGNOSIS–90% cure rate
Dentigerous Cyst
Cyst originating around the crown of an unerupted tooth
MOST COMMON DEVELOPMENTAL ODONTOGENIC CYST
usually MAND. 3RD MOLARS
other common sites:
- maxillary canines
- maxillary 3rd molars
- mandibular 2nd premolars
usually PERMANENT TEETH
may cause root resorption of adjacent teeth
usually between ages 10-30
Well-defined, unilocular radiolucency around crown of unerupted tooth
Odontoma
type of mixed odontogenic tumor
MOST COMMON ODONTOGENIC TUMOR
Developmental anomaly (hamartoma)
Compound and complex types
composed mostly of enamel and dentin, variable amounts of pulp and cementum
KIDS AND TEENS (median is 14)
asymptomatic and small, but some can be 6+ cm in size
may cause clinical expansion
Radiograph: calcified mass or tooth-like structures surrounded by well-defined, narrow radiolucent border
EXCELLENT PROGNOSIS
Ameloblastoma Radiograph Characteristics
Well-defined, multilocular radiolucency, but could be unilocular
Resorption of roots of adjacent teeth
Buccal and lingual expansion
Common association with unerupted tooth
