2: Differential diagnosis by signs and symptoms


Differential diagnosis by signs and symptoms

This chapter discusses the main signs and symptoms of diseases affecting the orofacial region. Specific diseases are discussed in Chapter 3.

Pain is by far the most common symptom affecting the orofacial region (see Pain, page 89). The other most common signs and symptoms of orofacial disease fall into a limited number of categories, namely:

• Coloured lesions
• Bleeding
• Soreness
• White lesions
• Ulceration
• Lumps/swelling
• Tooth mobility
• Halitosis

This can be remembered by the mnemonic Could Be Someone We Usually Love To Hear.



• Bleeding may arise from wounds or from the gingival margins, or may be into the tissues – where it appears as petechiae or ecchymoses (purpura).
• Gingival bleeding is usually due to plaque-induced inflammation – gingivitis or periodontitis.
• Gingival bleeding may be aggravated by, and purpura caused by, disorders of haemostasis or drugs interfering with haemostasis.
• Purpura in the mouth is seen mainly at areas of trauma – usually at the occlusal line and junction of the hard and soft palates.
• Bleeding of the lips may be seen where there is a lip fissure, or in erythema multiforme or some types of pemphigus.
• Vascular anomalies such as telangiectasia or angiomas may bleed if traumatized.


Box 2.1   Main causes of gingival bleeding

Platelet defects

Causes may include:

• Gingivitis (plaque-induced) – by far the most common cause (Figure 2.1)
Figure 2.1 Gingivitis – the common cause of gingival bleeding.
• Thrombocytopenia (low blood platelet numbers)

image aplastic anaemia
image idiopathic (this means ‘of unknown cause’ but actually it is autoimmune) thrombocytopenic purpura
image leukaemia (Figure 2.2)
Figure 2.2 Leukaemia may present with gingival bleeding, swelling and/or ulceration.
• Medications that impair haemostasis: anticoagulants, platelet aggregation inhibitors, chemotherapy, some herbal supplements
• Factitial or traumatic injury.

Oral bleeding occasionally arises from a vascular anomaly (Figure 2.3).

Figure 2.3 Hereditary haemorrhagic telangiectasia may chronically bleed.
Figure 2.4 Algorithm for bleeding gums diagnosis.

Burning mouth


• Burning mouth (glossodynia) is a common complaint.
• The cause is not usually known but it may be a nerve hypersensitivity.
• Burning mouth is not inherited.
• Burning mouth is not infectious.
• Burning mouth may occasionally be caused by some mouth conditions, dry mouth, deficiencies, diabetes or drugs.
• Burning mouth has no long-term consequences.
• Burning mouth typically affects the anterior tongue bilaterally but may affect other sites such as palate and/or lips.
• Oral examination is important to exclude organic causes of similar discomfort – such as erythema migrans (geographic tongue), candidosis, glossitis and lichen planus (Figure 2.5).
Figure 2.5 Burning mouth caused by lichen planus.

• In the absence of a recognizable organic cause (Figure 2.6), the condition is termed ‘burning mouth syndrome (BMS)’ and the underlying basis may be psychogenic. These patients may also suffer taste disturbances.
Figure 2.6 Burning mouth syndrome (no lesions discernible apart from mild tongue furring).
• Blood tests, biopsy or other tests may be required.
• Burning mouth syndrome may be controlled by some psychotropic drugs or B vitamin.


Box 2.2   Main causes of burning mouth sensation

Erythema migrans
Lichen planus
Haematinic (iron, folate, vitamin B12) deficiency

Causes may include (alphabetically):

• Allergies (including oral allergy syndrome)
• Bruxism/tongue thrusting
• Candidosis
• Dermatoses such as lichen planus
• Dry mouth and drugs such as angiotensin-converting enzyme (ACE) inhibitors, proton pump inhibitors (PPIs) and protease inhibitors (PIs)
• Erythema migrans (geographic tongue)
• Fissured tongue
• Gastric reflux, and glossitis such as caused by haematinic deficiency, such as

image B complex deficiency
image folate deficiency
image iron deficiency
image vitamin B12 deficiency
• Hormonal (endocrine) problems such as diabetes and hypothyroidism.

Once these causes are excluded, the condition is termed ‘burning mouth syndrome’, when the cause may be psychogenic, and include:

• Anxiety states
• Cancerophobia

• Depression
• Hypochondriasis.

A normal-appearing tongue may be seen in psychogenic causes, and with a burning sensation caused by deficiency states, drugs (e.g. captopril and other ACE inhibitors, proton pump inhibitors) and diabetes mellitus.

This section deals only with a normal-looking but burning tongue.

Burning mouth syndrome

Common, especially in middle-aged females.

Typical orofacial symptoms and signs: invariably persistent burning sensation with no organic disease.
Main oral sites affected: anterior tongue (occasionally palate or lip).
Aetiopathogenesis: see above.
Gender predominance: female.
Age predominance: middle age or older.

Extraoral possible lesions: often psychogenic complaints or anxiety.
Main associated conditions: few profess anxiety about (for example) cancer or sexually shared disease; some admit this on specific questioning.
Differential diagnosis: differentiate from organic causes.
Investigations: blood picture, glucose, thyroid hormone and haematinic assays to exclude organic causes; psychiatric investigation for depression.
Main diagnostic criteria: clinical.
Main treatments: treat any organic cause. Topical anaesthetics and oral distractors such as sucking on ice chips or sugarless candy, and chewing sugarless gum may be temporarily effective. Otherwise, B vitamins, topical capsaicin, psychotherapy (cognitive-behavioural therapy; CBT) or antidepressants are all occasionally helpful.
Figure 2.7 Algorithm for burning mouth diagnosis.

Desquamative gingivitis


• Desquamative gingivitis is not a disease entity but a clinical term for persistently sore, glazed and red or ulcerated gingivae.
• The usual complaint is of persistently sore gingivae in many areas.
• Lichen planus or pemphigoid are the most common causes.


Box 2.3   Main causes of desquamative gingivitis

Lichen planus

Fairly common, it is almost exclusively a disease of middle-aged or older females.

Typical orofacial symptoms and signs: soreness or stinging, especially on eating spices or citrus foods, or taking acidic drinks. Gingivae are red and glazed (patchily or uniformly), especially labially and in several sites. Gingival margins and edentulous ridges tend to be spared. Erythema is exaggerated where oral hygiene is poor.
Main oral sites affected: facial gingivae.

Aetiopathogenesis: lichen planus or mucous membrane pemphigoid, and rarely pemphigus or other dermatoses (skin disorders) (Figures 2.82.10).
Figure 2.8 Desquamative gingivitis: associated with lichen planus.
Figure 2.9 Desquamative gingivitis: associated with lichen planus.
Figure 2.10 Desquamative gingivitis: associated with pemphigoid.
Gender predominance: female.
Age predominance: adult.
Extraoral possible lesions: cutaneous, mucosal or adnexal lesions of dermatoses may be associated.
Differential diagnosis: differentiate mainly from acute candidosis, chronic marginal gingivitis, and occasionally from plasma cell gingivitis.
Investigations: biopsy with immunostaining.
Main diagnostic criteria: clinical and histology.
Main treatments: improve oral hygiene; topical corticosteroids, or systemic dapsone as appropriate. Corticosteroid creams used overnight in a polythene splint may help. Frequent dental cleanings and periodontal maintenance are important for disease control.

Dry mouth (hyposalivation and xerostomia)


• Xerostomia is a frequent, and the most common, salivary complaint but is not synonymous with hyposalivation.
• Xerostomia is a subjective complaint of oral dryness, and objective evidence of hyposalivation is far less common.
• Hyposalivation (hyposialia) is a reduction in saliva production – usually defined as an unstimulated whole salivary flow rate <0.1 ml/min.
• Causes of hyposalivation are often iatrogenic (doctor-induced), particularly with drugs (medications) or cancer therapy.
• Hyposalivation may also be caused by dehydration, or diseases affecting the salivary glands.
• Xerostomia has similar causes to hyposalivation and, additionally, may be psychogenic.
• Saliva helps swallowing, talking, and taste, and protects the mouth. Where saliva is reduced there is a risk of dental caries and tooth wear, halitosis, altered taste, mouth soreness and infections.

• Hyposalivation presents with obvious dryness (Figure 2.11) or frothy scant saliva (Figure 2.12), or with complaints of difficulties with speech, swallowing or denture retention; of soreness; or of complications such as candidosis, caries or sialadenitis.
Figure 2.11 Dry mouth, and lobulated tongue which may follow chronic hyposalivation.
Figure 2.12 Dry mouth manifesting as frothy saliva.


Box 2.4   Main causes of dry mouth sensation

Irradiation of salivary glands
Sjögren syndrome

Causes of hyposalivation may include:

• Iatrogenic

image drugs (medications) with anticholinergic or sympathomimetic effects, such as tricyclic antidepressants, phenothiazines and antihistamines
image irradiation of major salivary glands
image cytotoxic agents, bone marrow transplantation and chronic graft-versus-host (GvHD) disease
• Non-iatrogenic

image dehydration, e.g. uncontrolled diabetes, diabetes insipidus, diarrhoea and vomiting, hypercalcaemia, severe haemorrhage
image salivary gland disorders

a. amyloidosis or other deposits
b. cholinergic dysautonomia
c. cystic fibrosis
d. ectodermal dysplasia
e. HCV infection
f. HIV infection
g. IgG4 syndrome
h. salivary gland aplasia
i. sarcoidosis
j. Sjögren syndrome.

Causes of xerostomia may ALSO include:

• Psychogenic states

image anxiety states
image bulimia nervosa
image depression
image hypochondriasis.

Figure 2.13 Algorithm for dry mouth diagnosis.

Halitosis (oral malodour)


• Oral malodour is a common subjective complaint but often far more obvious to the sufferer than others.
• Malodour ‘if real’ can be measured with a gas chromatography or a halimeter, but objective evidence for it by measuring volatile sulphur compounds (VSCs) in the breath by halimetry or smelling the breath is far less common.
• Malodour is common on awakening or if there is infrequent eating or starvation, and is then sometimes called ‘physiological’.
• It is usually caused by diet, habits, dental plaque or oral disease.
• Oral malodour is to be anticipated in smokers, after eating odiferous foods such as garlic or durian, or drinking excess alcohol or coffee.
• Oral malodour is common where there are oral infections.
• Malodour can sometimes be caused by sinus, nose or throat conditions.
• Oral malodour occasionally arises from metabolic disorders but it is only rarely caused by more serious disease.
• In the absence of an identifiable malodour or a defined organic cause, the complaint of malodour may be psychogenic in origin.
• It often significantly improves with oral hygiene and tongue-brushing.
• It may also be helped by:

image regularly eating yoghurts or ingesting certain probiotics
image finishing meals with apples, carrots or celery
image chewing spearmint, tarragon, eucalyptus, rosemary, or cardamom
image avoiding habits such as smoking and odiferous foods, and avoiding foods such as eggs, legumes, certain meats, fish and foods that contain choline, carnitine, nitrogen and sulphur.


Box 2.5   Main causes of halitosis (oral malodour)

Odiferous foods
Poor oral hygiene

Causes may include:

• Starvation
• Lifestyle habits

image habits

a. alcohol
b. amyl nitrites
c. solvent misuse
d. tobacco
image volatile foodstuffs

a. durian
b. garlic
c. highly spiced foods
d. onions
• Drugs (see also Chapter 4): amphetamines, aztreonam, cytotoxic drugs, disulfiram, melatonin, mycophenolate sodium, nicotine lozenges, nitrates and phenothiazines
• Oral sepsis

image dental or periodontal sepsis (Figure 2.14)
Figure 2.14 Halitosis caused by periodontitis.
image dry socket
image food impaction
image hyposalivation
image necrotizing ulcerative gingivitis
image oral malignancy
image osteochemonecrosis (bisphosphonates, denosumab, bevacizumab)
image osteomyelitis
image osteoradionecrosis of the jaw
image pericoronitis
image ulceration
• Oesophageal disease

image pouch
image reflux
• Sinusitis
• Nasopharyngeal disease

image foreign body
image infection
image neoplasm

• Pharyngeal disease

image foreign body
image infection (e.g. tonsillitis, tonsillolith)
image neoplasm
image pouch
• Systemic disease

image acute febrile illness
image metabolic disorders

– diabetic ketoacidosis
– hepatic failure
– renal failure
– trimethylaminuria
image Psychogenic (delusional)

– neuroses
– psychoses

Figure 2.15 Algorithm for halitosis diagnosis.

Mucosal blisters


• A blister, if solitary, may be due to saliva extravasation into the tissues (mucocele).
• Blisters may be due to a subepithelial split, seen mainly in sub-epithelial immune blistering diseases (e.g. pemphigoid) (Figure 2.16).
Figure 2.16 Blistering in pemphigoid.
• Blisters due to intraepithelial vesiculation are less common and caused particularly by pemphigus, and readily break to form erosions.
• Blisters rarely are caused by blood extravasation into the tissues (purpura) (Figure 2.17).
Figure 2.17 Blood blisters in purpura.


Box 2.6   Main causes of oral blisters

Angina bullosa haemorrhagica
Trauma (mucosal burn)

Causes may include:

• Infections

image enteroviruses such as Coxsackie viruses and ECHO viruses
image herpes simplex virus
image herpes varicella-zoster virus
• Mucoceles
• Purpura, and angina bullosa haemorrhagica (localized oral purpura)
• Burns
• Cysts
• Skin diseases

image dermatitis herpetiformis
image epidermolysis bullosa (congenita and acquisita)
image erythema multiforme and Stevens–Johnson syndrome
image intraepidermal IgA pustulosis
image lichen planus (superficial mucoceles)
image linear IgA disease
image pemphigoid (usually mucous membrane pemphigoid)
image pemphigus (usually pemphigus vulgaris)
image Sweet syndrome
• Drugs
• Paraneoplastic disorders
• Amyloidosis.

Mucosal brown and black lesions


• Mucosal brown and black lesions are common.
• Most mouth pigmentation is inherited. The most common cause of multiple oral brown lesions is racial or ethnic pigmentation, common in people of colour but also seen in some Caucasians and most noticeable on the facial gingivae, or other keratinized areas such as the dorsum of tongue or palate.
• Most pigmented lesions affect only the mouth but they are occasionally seen elsewhere or associated with other conditions.
• Otherwise, the cause is usually embedded amalgam, inflammation, or drugs or social habits.
• The most common cause of single oral brown lesions are naevi (Figure 2.18) or melanotic macules.
Figure 2.18 Hyperpigmentation: naevus.
• Oral post-inflammatory pigmentation (pigmentary incontinence) is the common cause of multiple oral brown lesions associated with chronic inflammatory disorders (oral lichen planus and lichenoid lesions, pemphigus, or pemphigoid).

• The most common cause of single oral grey or black lesions is an amalgam tattoo, where amalgam has become embedded during restorative dental procedures (Figures 2.19, 2.20). A graphite tattoo from a pencil broken in the mouth is uncommon.
Figure 2.19 Hyperpigmentation: amalgam tattoo.
Figure 2.20 Hyperpigmentation: amalgam tattoo (radiographic view).
• Rare causes of brown or black lesions include drugs (Figure 2.21) or endocrinopathies such as Addisonian hypoadrenalism (Figure 2.22) and neoplasms such as malignant melanoma and Kaposi sarcoma.
Figure 2.21 Hyperpigmentation: drug-induced (antimalarials, minocycline and others can be responsible).
Figure 2.22 Hyperpigmentation: in hypoadrenocorticism (Addison disease).
• Solitary brown or black lesions may raise concern about the possibility of melanoma.
• Features suggestive of melanoma include (ABCDE):

Assymetry in shape
Border irregular
Colour variations or changes
Diameter (large size)
Elevation above mucosa
• Imaging, biopsy or other investigations may be indicated to differentiate the causes.
• Pigmented lesions are often removed by surgery for histopathological examination.
• There are usually no long-term consequences.


Box 2.7   Main causes of mucosal brown or black lesions

Melanotic macule
Amalgam tattoo

Causes may include:

• Racial
• Food/drugs

image beetroot
image betel nut
image chlorhexidine
image liquorice
image tobacco
image systemic drugs, such as minocycline, certain antimalarials and chemotherapeutic agents
• Hormonal

image pregnancy (chloasma)
image Addison disease
image Albright syndrome (fibrous dysplasia)
• Others

image Kaposi sarcoma
image leukoplakia with pigmentary incontinence
image lichen planus with pigmentary incontinence
image melanoacanthoma
image melanoma
image melanotic macule
image naevus
image Peutz–Jeghers syndrome.

Table 2.1

Features of most important isolated hyperpigmented oral lesions

Lesion Usual age of presentation Morphology Colour Main locations Approximate size Other comments
Amalgam tattoo >5 years Macular Grey or black Floor of mouth, mandibular and maxillary gingivae <1 cm May be confirmed by radiography
Graphite tattoo >5 years Macular Grey or black Palate <0.5 cm May be revealed by radiography
Kaposi sarcoma >young adult Macular becoming nodular Red, purple or black Palate, gingivae Any Mainly in HIV/AIDS
Melanoma Any Macular becoming nodular Brown, grey or black Palate, gingivae Any Rare
Melanotic macules Any Macular Brown or black Lips, gingivae <1 cm Usually benign
Mostly in Caucasians
Naevi 3rd–4th decade Raised Blue or brown Palate <1 cm Usually benign
Purpura Any Macular Red, purple or brown Palate, buccal or lingual mucosa Any Usually traumatic and resolves spontaneously


Black or brown hairy tongue

Common, especially in adult men.

Typical orofacial symptoms and signs: persistent brown or black hairy appearance of tongue.
Main oral sites affected: central dorsum of tongue, mainly posteriorly but extending anteriorly.
Aetiopathogenesis: unknown. Smoking, foods such as liquorice, drugs (e.g. iron salts, chlorhexidine, bismuth) and poor oral hygiene (proliferation of chromogenic microorganisms may predispose.
Gender predominance: male.
Age predominance: adult.
Extraoral possible lesions: none.
Main associated conditions: none.
Differential diagnosis: candidosis.
Investigations: history of use of offending agents.
Main diagnostic criteria: clear-cut clinically.
Main treatments: improve oral hygiene; discontinue any drugs responsible; scrape or brush tongue (in evenings with cold water); suck dry peach stone (yes!).
Figure 2.23 Algorithm for hyperpigmentation diagnosis.

Mucosal erosions (see also mucosal ulceration)


• Mucosal damage may lead to inflammation and/or partial-thickness loss of epithelium, both of which appear red, or to loss of most of the epithelium, which then may initially appear red but becomes covered with a yellowish fibrinous slough. Full-thickness loss of epithelium typically causes a grey or yellow lesion (an ulcer).
• Patients often present with a mix of these appearances; mucositis is the term applied to widespread oral erythema, ulceration and soreness.
• Any of the causes of mucosal blisters may result eventually in erosions.


Box 2.8   Main causes of mucosal erosions

Systemic disease (blood, infections, gastrointestinal, skin)
Malignant lesions
Local causes (e.g. burns)

Causes may include:

• Any of the causes of mucosal blisters (may result eventually in erosions).
• Erosions are especially seen after burns, caused by drugs (Figure 2.24) and lichen planus (Figure 2.25).
Figure 2.24 Erosion showing fibrinous slough.
Figure 2.25 Erosions induced by lichenoid adverse drug reaction. Erosions are yellow: the white lesions are lichenoid.
• Mucositis, and sometimes bleeding, is common after chemo- or radio- or chemoradio-therapy, and graft-versus-host disease (GvHD). Sometimes called mucosal barrier injury, mucositis is common during the treatment of cancer but also in the conditioning prior to haematopoietic stem cell transplantation (bone marrow transplants).

Mucosal fissures or cracks


• Fissures are common on the dorsum of the tongue (Figure 2.26) when they are usually of genetic basis and, as there is no break in the epithelium, they are symptomless unless, as is common, there is an associated geographic tongue (erythema migrans) (Figure 2.27).
Figure 2.26 Fissured tongue in a patient with Crohn disease.
Figure 2.27 Fissured tongue in a patient with erythema migrans (geographic tongue).
• Fissures otherwise are often associated with epithelial breaks and are seen mainly on the lip, usually at the commissures (angular cheilitis or stomatitis), rarely elsewhere (lip fissure).


Box 2.9   Main causes of mucosal fissures

Angular stomatitis
Lip fissure
Any cause of lip swelling (e.g. Crohn disease)

Causes may include:

• Angular stomatitis
• Lip fissure
• Down syndrome
• Crohn disease or orofacial granulomatosis (OFG)
• Actinic cheilitis.

Angular stomatitis (perleche; angular cheilitis)

Common, especially in older edentulous patients who are denture-wearers.

Typical orofacial symptoms and signs: symmetrical erythematous fissures on skin of commissures (Figures 2.28, 2.29), and (very rarely) commissural leukopakia intraorally.
Figure 2.28 Angular stomatitis (cheilitis) causing fissuring at commissures.
Figure 2.29 Angular stomatitis causing fissuring at commissures.
Main oral sites affected: commissures, bilaterally.
Aetiopathogenesis: usually due to infection with Candida albicans. Staphylococcus aureus and/or streptococci may also be cultured from lesions. Patients may have denture-related stomatitis or other forms of intraoral candidosis. Other causes include lip incompetence, especially from orthodontic appliances, iron deficiency, hypovitaminoses (especially B), malabsorption states (e.g. Crohn disease), HIV infection and other immune defects.
Gender predominance: none.
Age predominance: older.
Extraoral possible lesions: none usually.
Main associated conditions: see aetiopathogenesis.
Differential diagnosis: see aetiopathogenesis.
Investigations: occasionally, blood picture and haematinic assays; investigations for diabetes and other immune defects; smears for fungal hyphae and bacteriological culture, if refractory.
Main diagnostic criteria: usually clear-cut.
Main treatments: Eliminate any underlying systemic predisposing factors. Treat intraoral candidal infection, in particular denture-related stomatitis. Treat angular stomatitis with topical antifungal such as miconazole or triamcinolone/nystatin combination, or fucidin or mupirocin if staphylococcal.

Fissured (cracked) lip

Typical orofacial symptoms and signs: chronic discomfort and, from time to time, some bleeding.
Main oral sites affected: typically in the lower lip (Figure 2.30), usually median.
Figure 2.30 Lip fissure.
Aetiopathogenesis: a fissure may develop in the lip where a patient, typically a child, is mouth-breathing. Sun, wind, cold weather and smoking are thought to predispose. A hereditary predisposition for weakness in the first branchial arch fusion may exist. Lip fissures are also common in Down syndrome and when lips swell as, for example, in cheilitis granulomatosa and orofacial granulomatosis/Crohn disease (Figure 2.31).
Figure 2.31 Fissured lip in a patient with swelling from Crohn disease.
Gender predominance: males.
Age predominance: young adult.
Extraoral possible lesions: none usually.
Main associated conditions: see aetiopathogenesis.
Differential diagnosis: see aetiopathogenesis.
Investigations: see aetiopathogenesis. If diffuse lip swelling accompanies the fissuring, biopsy is indicated.
Main diagnostic criteria: clinical. Differentiate from angular stomatitis and cheilitis glandularis (occasionally).
Main treatments: predisposing factors should be managed if possible. Bland creams or ointments (e.g. E45) may help the lesion heal spontaneously. Short-term use of low-potency topical corticosteroids with or without antifungals or antimicrobials may promote healing. If the fissure fails to heal, excision, preferably with a z-plasty, laser ablation or cryosurgery may be needed.

Mucosal purpura


• Purpura is the accumulation of blood in the mucosa, appearing usually as red or brown macules (Figure 2.32). Purpuric lesions do not blanch on pressure (cf. vascular lesions such as haemangioma, telangiectasia).
Figure 2.32 Purpura.
• Petechiae are pinpoint-sized haemorrhages from small capillaries in the skin or mucous membranes. Petechia is the term given to the individual small red or red–blue spots which are about 1–5 mm in diameter and make up the rash.
• Purpura is seen mainly in areas prone to trauma, such as at the occlusal line (Figure 2.33) or junction of hard and soft palates.
Figure 2.33 Purpura.
• Occasional small traumatic petechiae at the occlusal line are common in otherwise healthy patients. Otherwise, oral purpura is uncommon.
• Purpura is usually caused by trauma such as suction, but haemostatic disorders may also present in this manner, so a blood picture (including blood count and platelet count) and haemostatic function may be indicated.


Box 2.10   Main causes of oral purpura

Trauma or suction
Platelet defects

Causes may include:

• Trauma (including suction, forceful coughing or vomiting)
• Thrombocytopenia

image autoimmune
image drugs
image leukaemias
image viral infections:

infectious mononucleosis
• Localized oral purpura (angina bullosa haemorrhagica)
• Amyloidosis
• Mixed connective tissue disease.

Mucosal red lesions


• Mucosal red lesions are usually inflammatory in origin.
• Mucosal red lesions may also be caused by epithelial loss (as in desquamative gingivitis) or atrophy as in erythroplasia (erythroplakia) – which usually represents severe epithelial dysplasia and is potentially malignant, or redness may represent frank carcinoma or other malignant neoplasms.
• Some mucosal red lesions are due to purpura or vascular anomalies such as telangiectasia or haemangiomas (the latter are more commonly purple or blue).


Box 2.11   Main causes of oral red lesions

Any inflammatory condition

Causes may include:

Generalized redness

• Candidosis (Figure 2.34)
Figure 2.34 Red lesion: candidosis may cause a glossitis.
• Mucosal atrophy (e.g. avitaminosis B)
• Mucositis

Localized red patches

• Angiomas (Figures 2.35)
Figure 2.35 Red lesion: angioma extending from lip to gingiva.
• Avitaminosis B12
• Burns
• Candidosis (erythematous, acute atrophic and denture-related) (Figures 2.36, 2.37)
Figure 2.36 Red lesion: candidosis in the palate is common in HIV/AIDS, presenting a ‘thumb print’ appearance.
Figure 2.37 Red lesion: candidosis causing denture-related stomatitis.
• Carcinoma (Figure 2.38)
Figure 2.38 Red lesion: carcinoma.
• Contact allergy
• Crohn disease and orofacial granulomatosis (OFG)
• Deep mycoses
• Desquamative gingivitis
• Drug allergies
• Erythroplakia (Figure 2.39)
Figure 2.39 Red lesion: erythroplakia.
• Geographic tongue (erythema migrans)
• Kaposi sarcoma
• Lichen planus
• Lichenoid reactions
• Lupus erythematosus
• Median rhomboid glossitis
• Mucositis
• Plasma cell gingivitis
• Purpura
• Sarcoidosis


• Hereditary haemorrhagic telangiectasia
• Post-irradiation
• Scleroderma
Figure 2.40 Algorithm for red lesions.

Mucosal ulceration or soreness (see also mucosal erosions)


• Soreness typically indicates a break in epithelial continuity, usually caused by erosions or ulcers.
• Ulcers can have a wide range of causes.
• Single ulcers lasting more than 3 weeks are a special concern since they may represent a malignant neoplasm (Figure 2.41) or a chronic infection such as TB, syphilis or mycoses (fungal infections). Gingival ulcers may be caused by these conditions, or acute necrotizing gingivitis (Figure 2.42).
Figure 2.41 Ulceration: carcinoma presenting as an ulcerated white lesion.
Figure 2.42 Ulceration: necrotizing ulcerative gingivitis (NUG). The papillae are ulcerated.
• Other persistent ulcers may have a systemic cause, such as a skin disease like lichen planus, pemphigoid or even pemphigus.
• Recurrent ulcers may represent recurrent aphthous stomatitis (aphthae) (Figures 2.432.45) but occasionally they manifest in systemic disease and are then termed ‘aphthous-like’ ulcers (Figure 2.46).
Figure 2.43 Ulceration: recurrent aphthous stomatitis (minor aphthae).
Figure 2.44 Ulceration: recurrent aphthous stomatitis (major aphthae).
Figure 2.45 Ulceration: recurrent aphthous stomatitis (herpetiform ulcers).
Figure 2.46 Ulceration: Behçet syndrome.


Box 2.12   Main causes of oral ulceraton

Systemic disease (blood, infections, gastrointestinal, skin)
Malignant lesions
Local causes (e.g. burns)

Causes may include:

Causes are diverse and may be remembered by the mnemonic So Many Laws And Directives, which includes:

• Systemic

image blood
image infections
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Jan 12, 2015 | Posted by in Oral and Maxillofacial Pathology | Comments Off on 2: Differential diagnosis by signs and symptoms
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