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21.6 Infective Disease
reside in the trigeminal ganglion but also the facial nerve and vestibulocochlear nerve. Reactivation
of the virus in these nerves will produce the typical rash of shingles in the face (trigeminal nerve),
facial palsy and a rash around the ear (facial nerve, Ramsay– Hunt syndrome) and symptoms of
vertigo, tinnitus and hearing loss(31).
21.6.2.4 Epstein– Barr Virus (EBV / HHV- 4)
Oral hairy leukoplakia (OHL) is a condition triggered by EBV. It may present on the lateral border
of the tongue in patients with a disrupted immune system (e.g. HIV/AIDS or on immunosuppressant drugs or systemic steroids) or occasionally appears in immunocompetent patients(32).
21.6.2.5 HHV- 8 (Kaposi Sarcoma Herpesvirus/KSHV)
Kaposi sarcoma (KS) was first described in 1884 but came to prominence in the 1980s when it was
associated with HIV infection. There are three forms of non- HIV- related KS, but it is most often
seen in relation to the HIV. HHV- 8 causes KS and produces vascular tumours. KS presents on the
skin or the GI tract as pink or purple patches and can spread to lymph nodes or lungs. It can present in the oral mucosa and may be flat or become nodular. Presentation in the oral cavity is most
often related to HIV infection and is seen in 22% of patients as the first clinical sign of progression
to AIDS(33, 34).
21.6.2.6 HIV Disease
HIV disease came to prominence in the 1980s and was especially noted amongst homosexual men
in California who developed systemic disease involvement as well as oral lesions secondary to
their immunodeficiency. Some oral manifestations relate to HIV, and others to the emergence of
infections which, without immunosuppression, might lie dormant. Oral manifestations include
candidosis, aphthous ulceration, angular cheilitis, KS and periodontal disease, including necrotising gingivitis and mucosal hyperpigmentation. Without immunosuppression, viruses with oral
manifestations that would not be problematic include HSV- 1 and HSV- 2, HPV and EBV (see
above). HIV also affects salivary glands, causing reduced saliva production and salivary gland
swelling(35, 36).
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21.6.3 Bacterial Disease
Commensal organisms in the oral cavity may become pathogenic if the oral environment changes. For
example, with a dry mouth from Sjogren’s syndrome, saliva’s buffering and antimicrobial properties
are compromised, and dental caries and tooth surface loss may increase. Systemic bacterial infections
may manifest in the mouth, such as tuberculosis, where the bacterium causing disease in the lung
(Mycobacterium tuberculosis) is coughed up in mucus and infects an oral mucosal wound, inoculating
the tissue and causing a local infection. Syphilis and gonorrhoea also have oral manifestations(37).
21.6.4 Fungal Disease (Candida)
Candida, a fungus, is a commensal organism of the oral cavity. Systemic disturbances can encourage the overgrowth of candida within the normal oral flora, leading to local mucosal disease.
Disturbances such as diabetes (raised blood sugar) or the effect of systemic steroids taken to reduce
inflammation, for example, in severe asthma, chronic obstructive pulmonary disease (COPD),
rheumatoid arthritis and bullous skin disease.
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21.7 Haematological Disease
21.7.1 Neutrophil Deficiency
Neutrophil deficiency, or neutropenia, can occur in adults and children. In HIV, there may be
neutropenia, which gives rise to large, persistent oral mucosal ulceration. The ulcers will resolve
when the underlying disease is treated. In some cases of persistent neutropenia, for example, during cancer treatments or from congenital neutropenia (Kostmann syndrome), treatment with
granulocyte- colony stimulating factor (G- CSF) or granulocyte/macrophage– colony- stimulating
factor (GM- CSF) can re- establish neutrophils. In children and rarely in adults, cyclic neutropenia
can cause intermittent oral aphthous ulcers. If necessary, this also can be treated with colonystimulating factors(38, 39).
21.7.2 Malignant Disease
Leukaemia can cause infiltration of cells into tissues, including oral tissues such as mucosa and
gingiva, and in addition, it can cause suppression of haematopoietic cell lines. General signs
andsymptoms such as purpura, bleeding and lymphadenopathy can present in the head and
neck and the oral cavity with gingival enlargement, bleeding, oral ulceration and petechial
haemorrhage(40).
21.8 Endocrine Disease
21.8.1 Diabetes
In the United Kingdom, approximately 6.5% of the adult population is living with diabetes; in the
United States, it is about 10% of the population. Around 90% have Type 2 diabetes(41, 42). In
poorly controlled diabetes, there is a tendency for patients to become hyperglycaemic and dehydrated, and the altered oral environment favours the proliferation of candida species, leading to
mucosal inflammation and discomfort. Some oral medications for managing diabetes can induce
lichenoid reactions of the oral mucosa.
21.8.2 Addison’s Disease
In Addison’s disease, the failure to secrete cortisol from the adrenal cortex causes an increased
production of adrenocorticotropic hormone (ACTH) from the pituitary to try and drive cortisol
production. The excess ACTH directly causes the production of melanin from melanocytes(43).
Patchy pigmentation is seen in the vermillion, buccal mucosa, palate tongue and gingiva and may
be the first presenting sign of Addison’s disease.
21.8.3 Acromegaly
Acromegaly, the excess production of growth hormone typically from a pituitary tumour, in the
adult will drive growth wherever bony growth potential persists. In the face and jaws, this results
in forward growth of the mandible and expansion of the maxilla, resulting in a progressive
Class III skeletal pattern developing and gaps between teeth or an ill- fitting denture on an
expanding bony base(44).
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21.11 Connective Tissue Disease
21.8.4 Thyroid Disease
Both hypothyroidism and hyperthyroidism will affect the face, mouth and jaws. Common presentations of hypothyroidism include delayed tooth eruption, altered tooth shape, periodontal disease,
macroglossia and altered taste. Hyperthyroidism can cause accelerated tooth eruption in children,
loss of taste, osteoporosis in the jawbones and periodontal disease(35).
21.8.5 Parathyroid Disease
Parathyroid hormone regulates calcium metabolism, phosphorus and vitamin D, so its effects are
principally seen in bone. In hyperparathyroidism, bone density is reduced, brown tumours may
present in the oral tissues, and calcification of oral soft tissues may occur. In hypoparathyroidism,
there may be delayed dental growth and development, and calcium changes in the blood can lead
to altered sensation in the lips and tongue and facial muscle twitching(36).
21.9 Neurological Disease
21.9.1 Neurovascular Compression andMultiple Sclerosis
Nerve damage due to compression and demyelination through immune- mediated damage to
myelin can cause effects in the head and neck. The principal presentation in dentistry is trigeminal
neuralgia, where the fifth cranial nerve is involved. Decompression (typically of an impinging
vessel) can improve pain, and anticonvulsant medication can improve symptoms of classic
trigeminal neuralgia and multiple sclerosis. Compression and demyelination will produce signs
and symptoms in any cranial nerve with a distribution in the head and neck(45).
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21.10 Bone Disease
Because of the similarity between bone, cementum and dentine, diseases of bone can also manifest
in the mesenchymal- derived dental hard tissues. These diseases can be divided into diseases
of bone metabolism such as Paget’s disease, osteogenesis imperfecta (and dentinogenesis
imperfecta), osteopetrosis, osteoporosis and fibrous dysplasia, and diseases within bones such as
cysts, tumours and giant cell lesions. Biopsy and bone chemistry analyses and radiography can
suggest the likely aetiologies(46).
21.11 Connective Tissue Disease
21.11.1 Sjogren’s Syndrome
Sjogren’s syndrome is one of the connective- tissue disorders that have the most effect on the oral
tissues. Lack of saliva increases tooth decay and periodontal disease rates, affects taste and causes
difficulties with swallowing and speech. There is also an increased risk of mucosa associated
lymphoid tissue (MALT) lymphoma in the salivary glands. Both glandular and extra- glandular
manifestations can severely affect the quality of life of those with the disease. Secondary Sjogren’s
syndrome is associated with systemic connective tissue disorders such as rheumatoid arthritis,
lupus and systemic sclerosis(47).
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21.11.2 Scleroderma andSystemic Sclerosis
As noted above, scleroderma and systemic sclerosis are connective tissue disorders associated with
Sjogren’s syndrome. Sclerosis of the orofacial soft tissues causes progressive tightening, hardening
and limitation of mouth opening and, therefore, access to oral hygiene measures and for dentists and
hygienists to access the teeth and periodontal tissues. Unfortunately, because of the vital link between
sclerosis and Sjogren’s syndrome, the need for dental intervention increases simultaneously as access
to oral tissues decreases. Facial changes include smooth, shiny skin, reduced movement for facial
expression and a thin, beaked nose, all of which are immediately obvious to others(48).
21.11.3 Lupus Erythematosus (DLE and SLE)
Lupus erythematosus can be divided into discoid lupus erythematosus (DLE), which affects the
skin and mucosa and systemic lupus erythematosus (SLE), which can affect all tissues and solid
organs. The underlying disease process is autoimmune, and the inflammation damages tissues,
organs and blood vessels. DLE most commonly affects the face and scalp, presenting as scaly
plaques which become progressively scarred and in the oral mucosa as lichen- planus- like
lesions(49). A classic malar rash, or butterfly rash, often occurs with lupus. SLE presents in the
oral cavity most often as mucosal ulceration but also with hyposalivation, resulting in dental and
periodontal disease. Diagnosis is with serology and biopsy(50).
21.12 Liver Disease
Liver disease most often presents in the orofacial tissues as jaundice, with the changes in colour in
the mucosa and sclera that are typical of the disease. The dental relevance of liver disease is most
often linked to the underlying pathology and the challenges that this produces. Infective causes
may lead to challenges in cross- infection procedures, and metabolic effects may require changes in
prescribing for orofacial disease management. Reduced saliva flow and oral infective diseases are
more common in patients with chronic liver disease(51).
21.13 Renal Disease
Patients in late- stage renal failure may present with uraemic stomatitis, which can be predominantly pseudomembranous, ulcerative, haemorrhagic or hyperkeratotic(52). In patients with endstage renal disease, hyposalivation was the most common sign, and the dental effects of xerostomia
subsequently became apparent(53). Drugs used to manage hypertension resulting from kidney
disease, such as calcium channel blockers, may cause gingival hypertrophy, as might cyclosporin.
This immunosuppressant drug may be used following renal transplantation. Drug metabolism by
the kidney may influence prescribing in patients with chronic kidney disease.
21.14 Pulmonary Disease
21.14.1 Granulomatosis with Polyangiitis (GPA/Wegener’s Disease)
GPA/Wegener’s disease can cause a classic ‘strawberry gums’ appearance, which is almost pathognomic of the disease (54). Also associated with GPA are systemic vasculitis, tissue necrosis and
granulomas. Delayed diagnosis can result in severe systemic disease affecting the respiratory and
renal systems and can cause significant morbidity and mortality if left untreated(55).
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References
21.14.2 Sarcoidosis
Like GPA, sarcoidosis is a systemic granulomatous disease affecting multiple organs and tissues.
The salivary glands and cervical lymph nodes are commonly involved in the head and neck. Other
presentations include periodontal disease, mucosal ulceration, swelling and gingival nodules.
Systemic signs and symptoms include malaise, fever and weight loss. Pulmonary infiltration causes
breathing difficulty, and chest radiographs will demonstrate classic hilar lymphadenopathy(56).
Treatment involves corticosteroids, antimalarials and immunosuppressant drugs, which may
affect the orofacial tissues or dental treatments.
21.15 Cardiovascular Disease
Cardiovascular diseases are globally the leading cause of death. Risk factors for cardiovascular
disease include diet, alcohol and tobacco, which may also influence the development of oral
cancer(57). There are few direct signs of cardiovascular disease in the oral cavity, but drugs used
for management may be associated with oral manifestations. Nicorandil, used to manage angina,
can produce large, painful and slow- healing oral mucosal ulcers(58). Antihypertensive medications may reduce saliva flow and, therefore, associated dental effects of xerostomia, and statins and
other drugs may interact with medications used to manage dental disease.
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21.16 Summary
From all the above, it can be seen that there are multiple ways in which systemic disease can present in the orofacial tissues. A good knowledge of medicine and pathology will often make the
links clearer, aiding diagnosis, management and monitoring.
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22
Adverse Drug Reactions inthe Orofacial Complex
Sue- Ching Yeoh
Sydney Dental School, The University of Sydney, Camperdown, NSW, Australia
22.1 Introduction
An adverse drug reaction (ADR) is defined by the World Health Organisation as ‘a response to a
medicine which is noxious and unintended, and which occurs at doses normally used in man’(1).
ADRs are classified into six groups (Table22.1)(2).
There are a number of factors which influence the presence and severity of ADRs. These are
broadly divided into patient risk factors (such as gender, extremes of age and medical comorbidities) and drug factors (dose, duration and route of administration).
ADRs occurring in the orofacial complex are varied in their clinical appearance(3). Dentists
should be able to identify the more common orofacial drug reactions, which typically occur within
week or months of taking the drugs.
Oral manifestations of ADRs are varied and can be broadly categorised into the following
four groups:
377
1) Salivary gland involvement
2) Soft tissue involvement
3) Hard tissue involvement
4) Non- specific reactions.
22.2 Salivary Gland Involvement
22.2.1 Physiology ofSaliva Production andSecretion
Salivary secretion is controlled by the autonomic nervous system, innervated by sympathetic and
parasympathetic nerves.
Sympathetic nervous control of the production of saliva is via the superior cervical ganglion.
Stimulation results in noradrenaline release, which by acting on α- and β- adrenergic receptors,
results in reduced saliva production by the acinar cells; increased protein secretion; and reduced
blood flow to the salivary glands.
Pathological Basis of Oral and Maxillofacial Diseases, First Edition. Edited by S. R. Prabhu, Syed Ali Khurram,
Omar Kujan and Merva Soluk Tekkesin.
© 2025 John Wiley & Sons Ltd. Published 2025 by John Wiley & Sons Ltd.
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