Managing oral mucosal disease

The management of patients with the common oral mucosal conditions of recurrent aphthous stomatitis and lichen planus in primary care dentistry and medicine

22 May, 2015 / clinical
 Professor John Gibson and Alexander Crighton  

Oral mucosal conditions are common and can be worrying and troublesome for patients. With demands on waiting lists in secondary care and the desire of some dental practitioners in primary care to take on “special interests”, now is the time to challenge the need to refer so many patients with oral mucosal disease into a secondary care setting?

Perhaps also now is the time to augment the relationship between doctor and dentist in the primary care setting to ensure that patients receive a first-class, joined-up service with a reduced need for onward referral? With this construct in mind, we offer management regimes for patients with oral mucosal disease in a primary care setting and invite referral of patients with more serious or sinister disease into secondary care, along with those who do not respond promptly to the regimes proposed in this paper.

We hope that this paper will serve as an aide-memoire in your practice or clinic.


Recurrent aphthous stomatitis (RAS)

RAS is the commonest inflammatory oral mucosal disease, said to affect 20 per cent of the adult population. It comes in three main forms: Minor (85 per cent), Major (10 per cent) and Herpetiform (5 per cent) and may be indicative of underlying systemic disease.

RAS is primarily a disease of exacerbation and remission, commonly occurring in late childhood or adolescence and remaining into adulthood. It is an easy diagnosis to make from the history alone – essentially any recurring ulcers of the oral mucosa are likely to be aphthous in type. Appearance may clinch the diagnosis – ulcers are round or oval in shape, with a red, inflammatory border and a yellow fibrinous base.

We are seeing less cases of RAS due to deficiencies of iron, folate and vitamin B12, but more due to the Koebner effect of mucosal damage due to trauma from tooth clenching/grinding and tongue thrusting. These habits are thought to be part of a person’s outworking of stress and seem to be ever more common in our stressful world.


Clinical tip

Patients who develop RAS in adulthood should be viewed with some concern as there is almost always an important underlying cause such as deficiency or hypersensitivity.


Case

A 54-year-old man developed RAS with no background of the condition. He was referred promptly by his dentist and blood tests revealed a picture of iron deficiency. Further investigations revealed an early bowel tumour which was readily resected. His iron deficiency resolved and his mouth ulcers settled.


What to ask

Patients with RAS should be asked about the following:

  • What sites are involved?
  • Frequency of episodes?
  • Number of ulcers in each episode?
  • Size of ulcer(s)?
  • How long do the ulcer episodes last?Other systems involved? (e.g. eyes, genitalia, skin)
  • Other symptoms? (e.g. swelling of joints or upset lower gut)
  • Related to stress/stressful events?
  • Aware of tooth clenching/grinding or tongue thrusting?
  • Use of toothpaste containing Sodium Lauryl Sulphate (SLS)?
  • Dietary consumption of fizzy drinks (benzoates)?
  • Use of prescribed drugs? (e.g. Nicorandil, NSAIDs).

Examination

  • Presence (confirmatory appearance) of ulcer(s)
  • Size of ulcer
  • Type of ulcer: minor, major, herpetiform
  • Any evidence of trauma, cheek biting/chewing, tongue-thrusting?

Investigations

  • Liaise with patient’s medical practitioner to request the following blood tests:
  • FBC (with the inflammatory markers PV or CRP if systemic disease suspected)
  • Levels of folate, ferritin, vitamin B12
  • Coeliac antibody screen (TTG)
  • ANA antibody if any history or suggestion of autoimmune disease.

RAS has both person-specific and environmental factors involved in its aetiology (see below).


Factors that cause RAS

PERSON SPECIFIC

  • Genetic
  • Nutritional (e.g. deficiencies in folate, iron or vitamin B12)
  • Hormonal (e.g. menstrually related)
  • Associated systemic diseases

ENVIRONMENTAL

  • Dietary factors causing hypersensitivity reactions (e.g. benzoates in fizzy drinks)
  • Trauma (Koebner phenomenon)
  • Possibly others, yet to be identified (e.g. viral/bacterial)

A relatively “new” syndrome associated with RAS is PFAPA which particularly occurs in children, adolescents and young adults. PFAPA is an acronym for: Periodic Fever, Aphthous stomatitis, Pharyngitis and cervical Adenitis.

It is said to respond promptly to high dose oral corticosteroids but also, interestingly, to tonsillectomy. Patients suspected of this condition should be referred to secondary care (oral medicine, paediatrics or ENT) for assessment.


Clinical tip: remember all the ‘20s’

  • RAS affects up to 20 per cent of the UK population
  • Up to 20 per cent of sufferers have an underlying haematinic deficiency (e.g. iron, folate, vitamin B12)
  • A further 20 per cent may have an “allergic” (hypersensitivity) basis (e.g. benzoates in fizzy drinks or colophony in chewing gum).

Management of patients with recurrent aphthous stomatitis

  1. Identify and eliminate sources of trauma (consider soft occlusal splint if bruxist or tongue thrusting)
  2. Review with blood results
  3. If deficiency identified, discuss with GP regarding possible cause and onward referral
  4. If coeliac antibody positive, or any possibility of Crohn’s disease or OFG, refer to consultant gastroenterologist
  5. Once cause of deficiency established, consider replacement therapy via GP: review three months
  6. If consumer of fizzy drinks, consider diet advice regarding empirical benzoate avoidance
  7. Change to an SLS-free toothpaste
  8. If Behcet’s Syndrome is possible (in view of skin, eye or genital lesions), or you are concerned about another systemic disease, liaise with GP and refer to appropriate specialist for opinion (e.g. oral medicine, dermatology, ophthalmology or gynaecology)
  9. Consider referral for patch testing if you practice in an area where this service is routinely provided
  10. Topical therapies:
    a. Chlorhexidine gluconate (0.2 per cent) mouthwash twice daily for 28 days initially
    b. Benzydamine hydrochloride mouthwash up to three times daily as required
    c. Gengigel
    d. Gelclair or Aloclair
    e. Topical steroid therapy (see Appendix 1).
  11. Should the patient fail to respond to the above regime, then refer to secondary care (oral medicine).

Lichen planus and lichenoid tissue reactions

Lichen planus (LP) is another common oral mucosal disease, affecting approximately 1-2 per cent of the population. Increasingly, LP is considered to be an autoimmune disease.

Autoimmune diseases arise in part from our genetic make-up and in part from an environmental factor – most of which are yet to be identified. Interestingly, LP is increasingly seen in conjunction with other autoimmune disorders, such as hypothyroidism.

There is often confusion in the literature about terminology – is it lichen planus or a lichenoid tissue reaction? For avoidance of doubt, we suggest that where the condition is deemed to have no obvious cause (and therefore likely to be autoimmune in origin), the term oral lichen planus (OLP) is used.

Where a causative or contributory factor is identified, we suggest that the term lichenoid tissue reaction (LTR) is used. Such factors may be stress, drug reactions and dental materials, such as amalgam and even gold.

Clinical varieties of OLP and LTRs

  • Reticular (striated)
  • Erosive
  • Plaque
  • Atrophic
  • Papular
  • Bullous
  • Desquamative gingivitis.

Clinical tip

Many drugs have been identified as contributing to LTRs, including: beta-blockers, diuretics, NSAIDs, oral hypoglycaemics, anti-epileptics, lithium, ACE-inhibitors, chloroquine and certain vaccines.


Case

A 48-year-old woman complained bitterly of discomfort when eating her favourite dish of Indian origin. Her GDP identified striated lesions on a red background on the buccal mucosae bilaterally and on the left ventro-lateral surface of her tongue. She had been started on a beta-blocker for anxiety several months previously.

The GDP discussed with the GP the possible role of this drug and the patient was happy to stop the medication. Her symptoms lessened over the subsequent weeks and the lesions disappeared completely within three months. The patient was delighted to be able to visit her local curry house again.


Patients with OLP/LTR should be asked:

Do you have any itchy skin lesions (purple papules, red spots or white, lacey lesions) – particularly at the wrists, on the shins; or do you have any white or red areas on the genitals?

Examination

  • Presence (confirmatory appearance) of OLP/LTR?
  • Extent of condition – localised or more generalised?
  • Relation to old amalgam (or other) restorations?
  • Any evidence of trauma, cheek biting/chewing, tongue thrusting (Koebner effect)?
  • Record clinical type of OLP/LTR.

Lichen planus is a mucocutaneous disorder which can affect the oral mucosa, genital mucosa and skin. Patients should be asked specifically about the possibility of lesions at sites outside the mouth. This is particularly important with regard to identifying those patients who might have vulvo-vaginal-gingival syndrome or peno-gingival syndrome, as both appear to have increased risk of genital, and possibly oral, malignancy.

The presence of extra-oral LP will also influence management options and may move the patient more quickly to a secondary care environment for combined oral medicine/dermatology management.

Once again, the Koebner phenomenon is important in OLP (and in LTRs) and mucosal trauma should be reduced by careful assessment of the dentition, restorations and prosthesis. Mucosal trauma due to tooth clenching or grinding should also be sought and eliminated.

SLS-containing toothpastes and mouthwashes tend to irritate the oral mucosa of patients with OLP and LTRs and should be changed to SLS-free variants. Indeed, the question should be asked: are proprietary mouthwashes required at all for anyone?

Smoking is considered to increase the risk of the patient’s OLP or LTR transforming to oral squamous cell carcinoma and so patients with OLP/LTR must be encouraged to stop smoking and understand fully the risks in maintaining the habit.


Clinical tip

What to do?

  • Asymptomatic, reticular: review
  • Symptomatic, reticular: biopsy, treat and review
  • Other types: biopsy, treat and review
  • Smokers: biopsy all types
  • Local lesion: remove amalgam
  • Widespread lesions: consider patch testing.

Investigations

  • If the patient’s OLP/LTR is causing symptoms and is of a non-reticular variant, liaise with the GP to exclude contributory systemic factors by way of blood tests: check FBC, folate, ferritin, vitamin B12.
  • If the patient also has hypertension (from history), liaise with the GP to check random blood glucose to exclude Grinspan’s Syndrome – a triad of OLP, hypertension and Type 2 diabetes mellitus.
  • In a secondary care setting if the patient is of mainland European, Middle Eastern or Far Eastern origin, it may also be worth considering checking liver function tests and Hepatitis C serology as there is an apparent link in certain ethnic groups between OLP and Hepatitis C viral infection.
  • In a secondary care setting if the patient has the bullous variant, check indirect immunofluorescence serology to exclude other bullous disorders.
  • Also, a biopsy should be taken from a representative area (or areas) for routine histopathology, especially if a smoker. Where different variants of the condition co-exist, biopsies should be taken from different sites. Where bullous lesions are evident or reported, peri-lesional biopsy tissue should be sent for direct immunofluorescence.

If a patient has asymptomatic, reticular OLP/LTR and is a non-smoker, then no referral to secondary care is required. Instead, such patients should be advised of the diagnosis, the possibility of skin or genital lesions and the small risk of subsequent oral squamous cell carcinoma. The importance of maintaining a smoke-free status should be emphasised, alongside the advice to ensure that alcohol consumption is within recommended limits. Such patients should be placed on regular six monthly review, but also advised to return for further assessment/advice if any changes within the mouth occur in the interim period.

If a patient has symptomatic OLP/LTR of any variant (including reticular), then referral to secondary care is advised – with a biopsy likely to exclude any super-added fungal infection or dysplasia. Similarly, a smoker with any variant of OLP/LTR (including reticular) should be referred to secondary care for assessment and consideration of biopsy.

Management

  1. Identify and eliminate sources of trauma
  2. Change to an SLS-free toothpaste
  3. Maximise oral hygiene to eliminate irritation from plaque
  4. Advise to stop smoking, if required. Support quit attempt, via GP or local smoking cessation services
  5. If chronology of drug use fits with onset of symptoms/signs, consider liaising with prescribing GMP or hospital specialist to request changing to structurally unrelated drug. This should be pursued where a patient has symptoms
  6. If lesions are localised and related to an obvious cause (e.g. old amalgam restoration), consider the replacement of the restoration with a non-mercury containing restoration (e.g. composite, porcelain or gold) or cover the tooth/restoration with an appropriate crown. This should be pursued where a patient has symptoms
  7. If the lesions of OLP/LTR are extensive and the patient has symptoms, a trial of a systemic anti-fungal drug (e.g. fluconazole or itraconazole) at conventional dose for two weeks or so may be worthwhile
  8. If other systems are involved or, from symptoms, potentially involved, a referral to the appropriate hospital specialist should be instituted (e.g. dermatology, gynaecology)
  9. Topical therapies:a. Chlorhexidine gluconate 0.2 per cent mouthwash twice daily for 28 days initially
    b. Benzydamine hydrochloride mouthwash up to three times daily
    c. Gingigel
    d. Gelclair or Aloclair
    e. Aloe vera mouthwash
    f. Topical steroid therapy (see Appendix 1).
  10. Should the patient fail to respond to the above regime, then refer to secondary care (oral medicine).

Helpful references and resources:

The British Society for Oral Medicine www.bsom.org.uk/clinical-care-chooser/soft-tissue-conditions/
The Scottish Dental Clinical Effectiveness Programme (SDCEP) www.sdcep.org.uk/published-guidance drug-prescribing/
Oral and Maxillofacial Medicine: the basis of diagnosis and treatment (Third Edition) Scully, C. Churchill Livingstone, 2013

APPENDIX 1

Topical corticosteroid therapies:

Hydrocortisone mucoadhesive buccal tablets: 2.5mg (as sodium succinate) Dissolve one tablet slowly in the mouth up to four times daily.
Beclometasone dipropionate puffer: 50g: apply two puffs two to three times daily directly to the oral mucosa. NB: Advise patient to shake inhaler prior to use to mix steroid and propellant. Useful for one or two lesions.
Betamethasone sodium phosphate: 500g (0.5mg) tablet. One tablet to be dissolved in water and used as a mouthwash for two minutes, and expectorated, two to three times daily for seven to 10 days initially, and then intermittently as required. NB: Advise patient not to swallow solution. Useful for multiple/widespread lesions.

Notes

Use therapies as soon as lesions appear
Use therapy for as little time as possible and make steroid-free episodes regular occurrences
Where therapy is likely (or confirmed) to be long-term and/or involving systemic steroids too, discuss with GP about when to arrange bone density scan and consider osteoporosis prophylaxis.

ABOUT THE AUTHORS

John Gibson is professor of medicine in relation to dentistry and honorary consultant in oral medicine at Glasgow Dental Hospital and School

Alexander Crighton is consultant in oral medicine and honorary senior lecturer in medicine in relation to dentistry at Glasgow Dental Hospital and School

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