Aetiology and epidemiology 

• Snuff (particulate, finely divided, or shredded tobacco) appears to much more likely cause oral lesions than chewing tobacco 
• Tobacco-containing preparations are generally of a higher pH (alkaline) and often mixed with other ingredients e.g. betel nut, lime, camphor, spice 

Pathology 

• Oral mucosa responds with inflammation and keratosis 
• Altered cell signalling and subsequent cell damage have been demonstrated 
• Dysplastic changes may follow with a risk of malignant change 

Clinical features 

• White asymptomatic lesions develop in the immediate area where the tobacco was placed, most commonly mucobuccal fold mandible 
• Mucosa develops a granular to wrinkled appearance 
• Advanced cases, a heavy folded character may be seen 

Histology

• Slight to moderate parakeratosis 
• Superficial epithelium may demonstrate vacuolisation or oedema 
• Slight to moderate chronic inflammatory cell infiltrate 
• Epithelial dysplasia may develop 

Diagnosis

• Clinical presentation, history  
• Biopsy not necessarily required unless lesions persistent after discontinuation of smokeless tobacco use 

Management

• Discontinuation of smokeless tobacco use  

Dental implications

• These patients will have acceleration of periodontal disease

Overview

Benign, however reverse smokers keratosis is potentially malignant (see oral cancer)

• Found in pipe and cigar smokers

Pathology

The smoke causes inflammation of tissues especially tissue surrounding the minor salivary gland ducts.

Clinical Features

• Palatal mucosa is initially erythematous due to the inflammation followed by white and crazed appearance due to the resulting keratosis 
• Red spots appear due to blockage of minor salivary ducts caused by surrounding tissues being inflamed

Histology

• Epithelial hyperplasia, hyperkeratinization 
• Chronic inflammatory cell infiltration of sub epithelial connective tissue 
• Excretory ducts show squamous metaplasia 

Diagnosis

• Clinical features and history are so distinctive there is no need for biopsy 

Treatment

• Smoking cessation will resolve the lesion

Potentially-malignant (High risk) (see oral cancer)

Clinical Features

• Soft white plaque in sublingual surface with wrinkles 
• The plaque typically extends from the anterior floor of the mouth to the under surface of the tongue 
• Irregular but well-defined outline – often butterfly shaped 
• Common in western population due to a combination of alcohol and smoking. Alcohol increases the permeability of the non keratinised tissue on the floor of the mouth- making tissues more susceptible to carcinogenic attack.  

Diagnosis

• Diagnosed through clinical sign 
• Doesn’t have distinct histological features but use the appearances stated above for diagnosis
• Biopsy may be indicated 

Overview

Potentially-malignant (see oral cancer)

• This is a chronic complex potentially malignant condition (1% transformation risk) of the oral cavity which can develop into squamous cell carcinoma.
• Common in south east asian population (Betal nut/areca nut)
• It leads to a progressive inability to open the mouth, resulting in difficulty eating and consequently nutritional deficiencies. 
• Characterised by inflammation and progressive fibrosis of the submucosal tissues (lamina propria and deeper connective tissues) 
• It results in marked rigidity and eventual inability to open the mouth (Trismus)  
• Most commonly affects the buccal mucosa but can involve any part of oral cavity and pharynx 

Overview

Potentially-malignant (see oral cancer)

• Very common cause of white patches. 
• Lichen planus itself isn’t a serious condition and it’s not contagious. However it can be potentially-malignant (1% or less). This is a chronic inflammatory disease of the skin and lining of the mouth, mainly affecting patients middle-aged or over. 
• Lichen planus (LP) is an inflammatory autoimmune type of disease, but it differs from classic autoimmune disorders in having no defined auto-antibodies
• More common with females.   
• Lichen plan can be oral or cutaneous (read further down)

Cause

• The aetiology isn’t completely understood 
• Many patients afflicted with LP have a conscientious type of personality with obsessive-compulsive traits and suffer mild chronic anxiety, suggesting neuro-immunological mechanisms may be at play.  
• Stress has been held to be important in LP, patients tend to be anxious and depressed. 

Complications

• Lichen planus is a potentially malignant lesion (1%) and can lead to squamous cell carcinoma. 
• Patient with LP should be strictly followed up to allow early diagnosis of a potential malignant lesion 

Histology

• Hyperkeratinisation 
• Mononuclear infiltration of T-cells to form a typical band like appearance subepithelial 
• Destruction of the basal layer due to hydropic degeneration (accumulation of water in cells) 
• Formation of Civatte bodies (due to apoptosis of basal cells)  
• ‘Saw tooth profile’ of rete ridges i.e. shaped like a saw (rete ridges are epithelial extensions that project into underlying connective tissue in skin or mucous membranes) 

Diagnosis

Through clinical signs however biopsy can be taken to confirm diagnosis (histopathology)

Treatment

• Treatment is only to alleviate symptoms and not to treat the patch 
• Prognosis for LP is 50% of patients will clear in 9 months and 85% by 18 months, however oral LP lasts longer than cutaneous LP and often reoccurs 
• Treatment focuses on relieving the intense itch 
• Diet modification (avoid spicy/acidic food) 
• Topical anaesthetic – Benzydamine hydrochloride 
• Topical corticosteroids are used and can come in many forms:
  • Lozenges:  Hydrocortisone   
  • Soluble tablets:  betamethasone (dissolved in water)
  • Inhalers:  beclomethazone from aerosol  
  • Paste:  triamcinolone dental paste.    

• As symptoms improve less potent topical steroids are used in order to minimise the side effects 
• If symptoms don’t relieve then an injection of steroid can also be given 
• Anti-histamines may be given to relieve itch 
• If there is severe or extensive oral involvement, if LP fails to respond to topical medications, or if there are extraoral lesions, specialist referral may be indicated. 

Oral Lichen Planus

• Usually found on buccal mucosa and on the side of the tongue and are bilateral. Can also be found on gums (known as desquamative gingivitis) and palate. 
• Oral lesions are often bilateral  
• There a 7 types of clinical manifestations:

TYPE	FEATURES
Plaque-like	White lesion similar to leukoplakia.
Atrophic	Diffuse red lesions simulating erythroplasia . Painful and can cause difficulty eating/speaking.
Papular	many small pimples forming a rash-like lesion
Reticular	Network of raised white lines  called wickham’s striae. Often have an erythematous background. Asymptomatic.
Erosive	Radiant red keratinised mucosa with a network appearance often covered in a yellow lesion.
Bullous	Subepithelial bullae (blood filled blisters) . Rare.
Annular	Circular rays of white lines

Cutaneous Lichen Planus

Clinical features

• Can affect any part of the body especially the flexural aspects of wrists, legs and lumbar region 
• Shiny purple papules on skin 
• Wavy white lines known as Wickham’s striae (visible in the purple papules) 
• Hyperpigmentation (go darker) of the purple papules over time 
• Itching at the site affected 
• Blisters  

Lichenoid Reaction

The term lichenoid reactions refer to a lesion almost identical histologically as well as clinically to lichen planus. Often dental material and drugs are the cause of the reaction. 

Clinically present as reticular, erosive or bullous lesions with wickham’s striae. 

Clinical features and histology are identical to lichen planus. The main distinguishing factor is that unlike lichen planus, lichenoid reactions are unilateral in appearance.

Drugs causing lichenoid reactions:

• NSAID’s 
• Anti hypertensives, e.g, ACE inhibitors and beta blockers 
• Anti malarial 
• Anti diabetics 

Underlying conditions causing lichenoid reactions:

• Stress 
• Diabetes 
• Hep C 
• HIV 
• Graft vs host disease 

Restorative materials causing lichenoid reactions:

• Amalgam – caused by the release of mercury
• Gold 

Removal of the cause will resolve the lesion

• Consider replacing the amalgam with another restorative filling e.g. composite
• Treat underlying condition
• Discuss with the GP options of prescribing alternate medication

It has a potential for malignant transformation so must be reviewed long term.

• Yellow spots normally on the buccal mucosa due to concentrated sebaceous glands 
• Completely normal, no cause for concern and no treatment required 

Benign

• Common benign congenital white/grey lesion on the buccal or labial mucosa 
• Most commonly found bilaterally
• Common in people of Africa or Asian descent 
• Asymptomatic  
• Leukoedema lesions disappear when stretched helping differentiate it from other white lesions 
• Cause is unknown although it is thought to be caused by intracellular oedema of the superficial epithelial cells  
• No treatment required 

Some forms can be potentially malignant

• Developmental anomaly  – X-linked and autosomal, both dominant and recessive forms are recognised 
• Patients undergo premature aging and have a predisposition to malignancy 
• Manifestations appear in first 10 years of life
• Most common type is white sponge nevus
• Although white sponge nevus is benign, other forms of inherited dyskeratoses can be pre-malignant so they should be referred for specialist care

Pathology

• X-linked dyskeratosis encodes a protein called dyskerin, which is abnormal 

Clinical features

• Affect the oral mucosa as well as nails
• Reticulated skin hyperpigmentation of the upper chest and dysplastic nail changes are characteristic 
• Rapidly progressing periodontal disease, thrombocytopenia and aplastic anaemia may also be seen

Histology

• Hyperkeratosis with epithelial atrophy 
• Varying severity of dysplasia

Diagnosis

History, clinical presentation and biopsy 

Management

• Careful observation and biopsy of suspicious areas to detect any malignant change 

White sponge nevus:

• Most common form of inherited dyskeratoses
• Found on buccal mucosa
• Thick white patch
• Can affect the genital and rectal mucosa
• Benign
• No treatment required 

Potentially malignant (See oral Cancer)

• Leukoplakia s defined as “a white patch or plaque that cannot be characterised clinically or pathologically as any other disease and which is not associated with any physical or chemical causative agent except the use of tobacco” 
• Leukoplakia cannot be scraped off  
• It has variable histology depending on what type it is  

Risk Factors

Aetiology is unknown but risk factors include:

• Smoking
• Chewing tobacco
• Alcohol
• Betel nuts
• HIV
• Candida albicans

Leukoplakia can be divided into 2 categories:

Homogeneous:	Uniformly white, slightly elevated compared to surrounding mucosa, has a wrinkled surface, and with clear demarcated margins. They have a reduced risk of malignant transformation.
Non- homogenous:	Mixture of red and white lesions with a predominately white surface. The surface text cam be flat or nodular. They have a greater risk of malignant transformation.
	-Speckled:   White flecks/fine nodules of an atrophic erythematous base   Can be considered as a transition between lekoplakia and erythroplasia
	-Nodular:
	-Verrucous [Warty]

Overview

Common condition in patients with an already fissured tongue. It often runs in the family as genetic plays a large part.

Found in 1-2% of patients

Clinical Features

• Found on the dorsum of the tongue
• Normally asymptomatic, sometimes patient complain of soreness
• Red depapillated map-like areas which can change in shape
• Red areas are often surrounded by white/yellow margins

Geographic tongue Via @all_things_oral_medicine

Diagnosis

• Mainly through clinical features due to its distinct appearance
• Blood examination may be performed to distinguish from a depapillated tongue of glossitis

Management

• Reassurance – treatment isn’t required usually
• Can prescribe zinc sulphate or topical salicyclic acid in 70% alcohol

Aetiology and epidemiology 

Occurs in two forms: systemic and discoid 

1. Systemic lupus erythematosus (SLE):  
   • usually in women under 30 years and affects most systems of the body 
   • when salivary glands are affected, it forms the connective tissue component of secondary Sjogren’s syndrome 
   • Patients have high titres of circulating antinuclear factor 
2. Discoid lupus erythematosus (DLE):
   • More frequent in women than men, usually 30’s/40’s 
   • Any area of the skin is involved, lesions more common in the ear 
   • Oral lesions develop in 15% 

Pathophysiology 

• Chronic autoimmune disorder characterized by the production of antinuclear autoantibodies 
• Immune complexes (type III hypersensitivity) are formed and deposited along the basement membrane, leading to basal cell damage 

Clinical features

• White, striated, keratotic and erythematous patches which resemble lichen planus 
• Butterfly rash of SLE 

Histopathology 

• Basal cell destruction 
• Basement membrane thickening 
• Lymphocytic infiltrates in the superficial connective tissues and in a perivascular distribution 
• IgG and IgM along basement membrane 

Diagnosis 

• Serological evidence of autoantibodies is important for diagnosis – several method, most frequent being indirect immuno-fluorescence 

Management 

• Topical steroid 

Dental implications

• Many suffer from xerostomia: consequences include increased caries risk and fungal infections

Dental Updates: Oral Medicine – White Patches:
https://www.dental-update.co.uk/issuesSingleIssueArticle.asp?aKey=833

Scully, C. (1999). Handbook of oral disease. London: Martin Dunitz.

Jordan, R. and Lewis, M. (2004). A colour handbook of oral medicine. New York: Thieme

Cawson. R A, Odell. E W. (2008). Cawson’s Essentials of Oral Pathology and Oral Medicine. 8th Edition