WHITE LESIONS

Appear on the oral mucosa as a result of trauma, infection, immunomediated

diseases or neoplasm, and most lesions appear white for increasing thickness of the
epithelium (caused by hypertrophy, hyperplasia, edema and hyperkeratinosis) or
decreasing submucosal vascularity.
Localized lesions result mainly from trauma while wide lesions from systemic,
immune or hereditary diseases.
some of the white lesions are considered to be premalignant conditions (in these
cases biopsy is obligatory).
White lesions are subdivided in 2 groups:
- painful white lesion : chemical burn, Lichen Planus, Lichenoid reactions and
Lupus Erythromatosus
- rarely painful (painless) white lesions : Dyskeratosis congenital, Leukoplakia,
Nicotinic stomatitis, Pyostomatitis vegatens, skin and mucosa graft, Squamous cell
carcinoma, oral submucosa fibrosis, white sponge nevus, pseudomembranous
Candidiasis and chronic hyper plastic Candidiasis
Squamous-cell carcinoma

DIAGNOSIS:
- Squamous-cell carcinoma
DIFFERENTIAL DIAGNOSIS: X

CLINICAL FORMS:
- may develop everywhere in the oral cavity, most common location in the tongue,
lip, floor of the mouth and retromolar area.
- clinical presentation of oral SCCA is varied: lesion may appear flat (macular), raised
(plaque-like), exophytic (growing outward) or ulcerated (showing surface erosions.
- the surface texture can range from smooth to irregular
- induration (firmness or hardness) and fixation (immobility or palpable adherence to
underlying structures) indicate infiltration of the cancer into deeper tissues
- these lesions are mostly spread by lymphatics and blood stream and can destroy
the bone and invade the nerves.
- usually pain indicates malignancy but the lack of it doesn’t exclude malignancy
- signs of cancer are: difficulty or pain in chewing and swallowing (dysphagia and
odynophagia), ear pain (otalgia), alteration of speech, trismus, cervical lymph node
enlargement (adenopathy), tooth mobility and persistent lesions
ETIOLOGY AND CONTRIBUTING FACTORS:
-tobacco and alcohol, sun exposure, viruses (HPV), dietary factors, illness (erosive
Lichen Plans, iron deficiency), immunosuppression.
tobacco : the major risk, combustion products result in damage to epithelium (high
dosage=high damage: 11-20 cigarettes daily enhances the malignant formation),
with disruption of DNA repair mechanisms and potential genetic mutation that can
lead to malignancy
alcohol : risk factor in moderate to heavy drinkers (5-8 drinks per day)
the combined use of both produces a synergistic effect: one substances
enhances the effect of the other one
- sun exposure: risk factor for lip cancer (lower lip is common affected) due to UV
damage
RELEVANT DIAGNOSTIC TEST:
- biopsy investigation
TREATMENT PLAN AND PROGNOSIS:
- the treatment depend on: cell type, degree of the differentiation, site and size of
primary lesion, the presence of bone involvement, presence of metastases and the
ability to preserve oropharyngeal functions (speech, swallowing and esthetic).
- surgery and radiation therapy
Lichen Planus
Chronic mucocutaneous T-cell mediates inflammatory condition
DIAGNOSIS:
- Lichen Planus/oral lichen planus (OLP)
DIFFERENTIAL DIAGNOSIS:
- in a variation of reticular form there is a plaque-like changes that can be similar to
Lukoplakia
CLINICAL FORMS:
- oral sensitivity to: tooth paste, acid substances, alcohol, spicy or salty food and
abrasive food
- there are 3 clinical distinct presentations
reticular lesions: also know as Wickham’s striae, they are white mucosal change due
to hyperkeratosis, distinctive characteristic of OLP commonly seen in skin lesion.
erytomatous lesion: associated with reticular changes caused by thinning or atrophy
of the epithelium with inflammation of the underlying connective tissue
erosive/ulcerative lesion: most severe form almost always associated with reticular
and erytromatous changes, consisted of extensive ulcerative lesions.
- any intramural site can be affected, the most common are buccal mucosa and
lateral tongue and these lesion are commonly bilateral, the gingiva and alveolar
mucosa are also common sites and when the lesion is only in these areas and
erythema or ulcer are present the clinical condition is called desquamative gengivitis
(the causes of desquamative gingivitis are: 50% mucous membranous pemphigoid,
25% are OLP and the other 25% are other vesicle-bollous disorders as pemphigus
vulgaris and linear IgA disease.
- the disease extent and severity can change over the time and it is correlated with
stress and illness; most serious complication of OLP is malignant transformation to
squamous-cell carcinoma
ETIOLOGY AND CONTRIBUTING FACTORS:
- immune system has a primary role in the development of this disease
- a lot of risk factors: tobacco, alcohol, oral hygiene, local trauma, diabetes mellitus
-recently it has been found from Japan and some Mediterranean countries a
correlation between OLP and HCV
- lichenoid hypersensitivity reactions can be caused by:
antihypertensive and non-steroidal antinflammatory drugs
amalgam restorations (silver fillings) and cinnamon flavored products
RELEVANT DIAGNOSTIC TEST:
- when the lesion is bilateral the clinical appearance is enough
- biopsy in suspicious areas avoiding ulcer zone
TREATMENT PLAN AND PROGNOSIS:
- limited lesion are treated with topical gel, while more extensive or difficult to reach
areas are treated with rinse.
- with desquamative gingivitis is used custom fabricated tray to apply medication
Leukoplakia

DIAGNOSIS:
- Leukoplakia/OL
DIFFERENTIAL DIAGNOSIS:
- lichen planus, pseudomembranous candidiasis and white sponge nevus
CLINICAL FORMS:
- white lesion that cannot be classified as any other lesion divided into:
homogeneous: white well-demarcated plaque with same pattern on the entire lesion,
that can be smooth or rough (cracked mud); the demarcation is very distinct,
different from OLP where the white components have more transition to normal oral
mucosa with peripheral erytromatous zone.
non homogeneous: white patches or plaque intermixed with red tissue elements, for
that also called erythroleukoplakia or speckled leukoplakia, also if the surface texture
contain verrocous or papillary the leukoplakia is non homogeneous
- both types can develop in all site ov the oral mucosa but non-smokers have high
percentage to have it in the border of the tongue (this area and the floor of the mouth
have high risk of malignancy).
-where the withe component is predominated by papillary projections (similar to
papillomas) it is referred to verruciform leukoplakia: this type of leukoplakia has more
aggressive proliferation pattern and it is also called proliferative verrucous
leukoplakia (PVL).
ETIOLOGY AND CONTRIBUTING FACTORS:
- tobacco and alcohol that increase the risk for squamous cell carcinoma
RELEVANT DIAGNOSTIC TEST:
- clinical observation of withe lesion that cannot be explained as other cause such a
trauma (if trauma is suspected the causative agents should be removed like sharp
cusp of restoration)
- biopsy essential for suspicious malignancy (after 2 weeks without healing)

TREATMENT PLAN AND PROGNOSIS:

- local application of vit.A
- systemic intake of vit. A
- cold-knife surgical excision, laser surgery for eradication of the lesions
Hairy Leukoplakia

DIAGNOSIS:
- Hairy Leukoplakia/Oral hairy leukoplakia (OHL)
DIFFERENTIAL DIAGNOSIS:
- chronic lateral trauma of the tongue
CLINICAL FORMS:
- frequently on lateral borders of the tongue but can also in the dorm and in the
buccal mucosa, clinical appaearance is vertical white folds oriented as a palisade
along the borders of the tongue, but can also be present as elevated white plaque
that cannot be scraped off
-OHL is asymptomatic so symptoms can occur when the lesion is super infected
with Candida
ETIOLOGY AND CONTRIBUTING FACTORS:
-strongly associated with Epstein-Barr virus (EBV) and with low levels of CD 4+ T
lymphocytes, so OHL is associated with immunosuppressive patients (rarely OHL
is seen in healthy people)
- in HIV patient the presence of OHL is very high
RELEVANT DIAGNOSTIC TEST:
- clinical observation
- histopathology examination
- detection of EBV
TREATMENT PLAN AND PROGNOSIS:
- antiviral medication, but not always indicated because the disorder is not
associated with subjective symptoms
- OHL is not related to increased risk of malignant transformation
Oral Candidiasis (main species are C.Tropicalis, Albicans and Glabrata) most
common opportunistic infection affecting oral mucosa, and a number of
predisposing factors have the capacity to convert Candida from the normal
commensal form (saprophytic stage) to a pathogenic organism (parasitic stage).
C.Albicans is usually a weak pathogen and it is said that affects very young, very
old and very sick.
And it is divided in primary (restricted to oral and peri oral sites) and secondary
(systemic mucocutaneous) infection.
Classification of primary candidiasis: acute (pseudomembranous candidiasis and
erythematousous candidiasis) and chronic form (chronic plaque-type and nodular
candidiasis, denture stomatitis, angular cheilitis and oral candidiasis associated with
HIV)
DIAGNOSIS:
- Oral Candidiasis
DIFFERENTIAL DIAGNOSIS:
- erythematous candidiasis with erytheroplakia, distinguishable because the candida
has diffuse border instead sharp demarcation
- chronic plaque-type and nodular candidiasis with Leukoplakia
CLINICAL FORMS:
- pseudomembranous candidiasis: recognized as the classical oral candidiasis
and is typically presents with loosely attached membranes (cottage cheese
appearance) comprising fungal organisms and cellular debris, which leave inflamed
and sometimes bleeding area if the pseudomembranous is removed
- erythematous candidiasis: it can be see as successor of pseudomembranous
type but can also emerge de novo, usually present on the dorm of the tongue and
palate in patient using inhalation steroids
- chronic plaque and nodular candidiasis: white plaque that may be
indistinguishable from Leukoplakia, and also there is a correlation between this types
of candida and dysplasia and also it is present an association with malignancy
transformation
ETIOLOGY AND CONTRIBUTING FACTORS:
- local factors: denture wearing, smoking, inhalation steroids, hyperkeratinosis,
imbalance of oral microflora and quality and quantity of saliva
- general factors: immune and endocrine disorders, immunosuppressive drugs,
chemotherapy
- hospitalized patients have higher risk
RELEVANT DIAGNOSTIC TEST:
- clinical appearance or biopsy to distinguish from leukoplakia
- PCR
- microbial growth on agar
TREATMENT PLAN AND PROGNOSIS:
- antifungal and predisposing factors should be removed (the removable denture)
Oral Candidiasis associated with HIV
More than 90% of acquired immunodeficiency syndrome patients have had oral
candidiasis during the course of their HIV infection, and the most common types of
oral candidiasis in conjunction with HIV are pseudomembranous, erythematous and
angular cheilitis and chronic hyper plastic candidiasis
DIAGNOSIS:
- Oral Candidiasis
DIFFERENTIAL DIAGNOSIS:
- look above
CLINICAL FORMS:
- look above
ETIOLOGY AND CONTRIBUTING FACTORS:
- look above
RELEVANT DIAGNOSTIC TEST:
- look above
TREATMENT PLAN AND PROGNOSIS:
- look above
Linea Alba

DIAGNOSIS:
- Linea Alba/Frictional hyperkeratosis
DIFFERENTIAL DIAGNOSIS:
- Lichen Planus
CLINICAL FORMS:
- literally meaning “white line”, commonly seen as horizontal white streak along the
buccal mucosa at the level of the occlusal plane bilaterally and conforms to the
configuration of the teeth in that area, it can also be seen in other common
traumatized areas such edountulus alveolar ridge spaces, lips and lateral aspect of
the tongue
ETIOLOGY AND CONTRIBUTING FACTORS:
- focal hyperkeratosis results from chronic frictional trauma of the tissues rubbing
against the adjacent teeth
RELEVANT DIAGNOSTIC TEST:
- based on clinical appearance
TREATMENT PLAN AND PROGNOSIS:
- identify the causative factors and eliminate them
Cheek biting

DIAGNOSIS:
- Cheek biting
DIFFERENTIAL DIAGNOSIS:
- oral hairy Leukoplakia
CLINICAL FORMS:
- similar to line alba but the friction zone is frayed with ulcerations or redness,
chronic chewing lesions of the tongue (morsicatio linguarum)
ETIOLOGY AND CONTRIBUTING FACTORS:
- hyperkeratosis from frictional trauma more accentuated than line alba caused by
chronic cheek chewing
RELEVANT DIAGNOSTIC TEST:
- clinical appearance or biopsy if there is any doubt
TREATMENT PLAN AND PROGNOSIS:
- attempt to remove source of irritation after which lesion should resolve in 1-3 weeks
Nicotinic Stomatitis

DIAGNOSIS:
- Nicotinic Stomatitis/Smoker’s keratosis
DIFFERENTIAL DIAGNOSIS: X

CLINICAL FORMS:
- initially the inflammation is erythematous then become white for the progression
epithelia hyperplasia and hyperkeratosis
- palate exhibits a cracked or wrinkled appearance, with metaplasia of minor salivary
gland duct orefices
- any mucosa covered by a denture will be spared if the prothesis is worn while
smoking
ETIOLOGY AND CONTRIBUTING FACTORS:
- direct irritations pf the palatal mucosa from hot tobacco smoke can lead to
inflammatory changes
RELEVANT DIAGNOSTIC TEST:
- based on clinical appearance
- biopsy only with presence of ulceration or focal erythroplakia
TREATMENT PLAN AND PROGNOSIS:
- lesion is reversible with the smoking cessation