Renal disease

In the UK, nearly 2 million patients have renal failure and a further million at least are
undiagnosed.
CHRONIC RENAL FAILURE AND DIALYSIS
The common causes are diabetes, hypertension or glomerulonephritis. Prolonged dialysis or
renal failure are now the most common causes of hyperparathyroidism. jaws may be first
affected. In severe uraemia, urea may crystallise on the skin and oral mucosa (‘urea frost’).
Approximately 70% of patients receiving dialysis can return to full-time work.
Peritoneal dialysis has no implications for dental treatment, but haemodialysis does. Patients
are heparinised before haemodialysis, and haemostasis is impaired for 6–12 hours. Dental
treatment should be delayed until the next day. These patients’ permanent venous fistulas
for the dialysis lines are susceptible to infection, and antibiotic cover may be considered for
dental surgical procedures. Drugs, including sedation, should not be given intravenously
because of the risk of damage to superficial veins, which are patients’ lifelines. A blood
pressure cuff must never be placed on the arm with the shunt. Dialysis patients also have a
greater incidence of cardiovascular and cerebrovascular disease. Patients under dialysis will
still have a uraemic oral odour and bad taste, xerostomia and sore mouth with increased
calculus
RENAL TRANSPLANTATION
Associated with the complications of prolonged immunosuppressive treatment, particularly
susceptibility to infections or lymphomas. Ciclosporin, which is widely used to help control
graft rejection, can cause persistent gingival overgrowth, and patients are often taking a
calcium channel blocker, such as nifedipine, for hypertension, enhancing the effect
Hairy leukoplakia can rarely develop in HIV-negative renal transplant patients as a
complication of immunosuppression. Complications of graft rejection, such as bone lesions
due to secondary hyperparathyroidism, may be seen
Local analgesics cause no problems, and the usual antibiotics for dental infections are safe
except in severe disease. Dose reduction according to the glomerular filtration rate is usually
sufficient precaution for most dental prescribing, but medical advice should be sought.
However, tetracyclines, itraconazole and systemic antivirals should be avoided. Children
with renal failure may have chronological enamel hypoplasia and dysplastic dentine with
delayed eruption of teeth.
Aspects of renal disease affecting dental management • Heparinisation before dialysis •
Possible hepatitis B or C carriage after chronic dialysis • Permanent venous fistulae
susceptible to infection • Increased risk of endocarditis • Secondary hyperparathyroidism •
Immunosuppressive treatment for nephrotic syndrome or transplant patients • Oral lesions
due to drugs, particularly for immunosuppression • Reduced excretion of some drugs • Oral
lesions of chronic renal failure
Oral changes in uraemia of renal failure • Mucosal pallor (anaemia) • Xerostomia • Purpura •
Mucosal ulceration • Thrush or bacterial plaques • White epithelial plaques • Brown tumours
of the jaws (secondary hyperparathyroidism)
Factors potentially affecting dental management of patients with renal disease •
Corticosteroid and other immunosuppressive treatment • Haemorrhagic tendencies •
Anaemia • Impaired drug excretion • Hypertension • Hepatitis B or C carriage • Underlying
causes (e.g. diabetes mellitus, hypertension or connective tissue disease)
Endocrine disorders and pregnancy
PITUITARY GIGANTISM AND ACROMEGALY
Overproduction of growth hormone by the anterior pituitary during skeletal growth causes
overgrowth of the skeleton and soft tissues to produce gigantism.Acromegaly arises from
excess hormone in middle age, after the epiphyses have fused. The hormone then only
increases growth of the hands and feet, membranous bones of the skull and jaws, and soft
tissues. Growth is slow, and diagnosis is often delayed. The condylar growth centre
becomes reactivated and the mandible enlarged and protrusive. Radiographically, the whole
jaw is lengthened and the angle becomes more oblique. Jaw and other bones are also made
thicker by subperiosteal bone deposition, producing frontal bossing. Teeth become spaced
or, if the patient is edentulous, dentures cease to fit the growing jaw. Hands and feet become
spade-like. Overgrowth of soft tissues causes thickening and enlargement of the facial
features, particularly the lips and nose. Tongue, lips, nose and ears enlarge, and vocal cord
thickening causes a deep voice.
Cause - adenoma of growth hormone– secreting cells in the pituitary. Expansion of this
tumour causes headaches and visual disturbances. Blindness may result from pressure on
the optic chiasma. Occasionally ectopic hormone production by a neoplasm of the pancreas
or adrenal is the cause. Diabetes results from insulin resistance caused by growth hormone.
Hypertension is common and may be associated with cardiomyopathy and dysrhythmias.
Rarely, a growth hormone–producing pituitary tumour is part of type 1 multiple endocrine
neoplasia syndrome (MEN1)
Treatment - Octreotide, a somatostatin analogue that inhibits hormone secretion or
pegvisomant, a growth hormone receptor blocker. Irradiation or resection of the pituitary
tumour may also be required. Established growth changes do not resolve. Orthognathic
surgery considered to improve the appearance with a risk of post-operative airway
obstruction because of the large tongue and narrowing of the glottis. Hypertension and
diabetes can also affect dental management. Otherwise, there is no special risk from
treatment, local analgesia or sedation.
THYROID DISEASE
Hyperthyroidism
Common in young adults, particularly women. Causes include diffuse thyroid enlargement
(goitre), a hypersecreting nodule or adenoma in the gland, and autoimmune thyroiditis
caused by stimulatory autoantibodies (Graves’ disease).
Important features of hyperthyroidism • Irritability, anxiety, insomnia, agitation • Tremor •
Sweating and high temperature • Loss of weight • Tachycardia • Diarrhoea • Cardiovascular
disease, particularly in untreated hyperthyroidism in older patients • Exophthalmos and
pretibial myxoedema caused by autoimmune inflammation in Graves’ disease
Treatment - drugs such as carbimazole, iodine131, or surgical removal of part of the gland.
All may cause hypothyroidism. Beta-blockers may be used for symptom control.
Dental management - Untreated hyperthyroid patients risks the medical emergency of
thyrotoxic crisis. Excessive cardiac excitability is only a theoretical contraindication to
lidocaine with epinephrine, and no other local anaesthetic has been shown to be safer.
Conscious sedation (nitrous oxide and oxygen) is frequently helpful.• If clinical signs are
seen but the patient is not under treatment, refer to a physician • Control of nervousness and
excitability • Thiouracil drug treatment may cause salivary gland swelling and stones • Iodine
containing agents such as radiographic contrast for sialograms or povidone iodine may
disturb thyroid function • Avoid general anaesthesia in patients with longstanding
thyrotoxicosis, particularly older patients
Hypothyroidism
Cretinism
Results from deficient thyroid activity from birth, usually in areas of iodine deficiency or as a
result of thyroid developmental anomalies.
Typical features of cretinism • Skeletal development and dental eruption greatly delayed •
Impaired mental development • Broad, rather flat face partly due to defective growth of the
skull and facial bones • Overlarge, protrusive tongue • Dull facial expression, dry thick skin •
Short stocky build and, often, umbilical hernia • Sensitivity to cold • Bradycardia and
hypotension, Short stature and intellectual impairment+.
In the untreated patient, sedatives and tranquillisers such as benzodiazepines can
precipitate myxoedemic coma and should generally be avoided. Conscious sedation with
nitrous oxide and oxygen can be given. Thyroid hormone treatment must begin early to allow
normal physical and mental development.
Adult hypothyroidism
Hypothyroidism in the UK is most frequently due to Hashimoto autoimmune thyroiditis but
can follow radioiodine, drug or surgical treatment for hyperthyroidism. In most of the world,
iodine deficiency is the main cause.
Typical features of adult hypothyroidism. Signs are often mild and easily missed. • Weight
gain • Slowed activity and thought, fatigue • Myxoedema and hoarse voice • Bradycardia •
Dry skin and hair loss • Intolerance of cold • Susceptibility to ischaemic heart disease
Dental management of hypothyroidism • Avoid sedatives including diazepam, opioid
analgesics and general anaesthetics because of the risk of myxoedemic coma • Anaemia or
ischaemic heart disease may require modification of dental treatment • Local anaesthesia
always preferable • Nitrous oxide/oxygen sedation acceptable • Iodine containing agents
such as radiographic contrast for sialograms or povidone iodine may disturb thyroid function
• Sjögren’s syndrome occasionally associated with autoimmune thyroiditis
Lingual thyroid
Failure of normal development of the thyroid gland is almost always caused by failure of the
embryonic thyroid anlage to descend into the neck. The patient’s thyroid gland lies
somewhere along the path of the thyroglossal tract but usually on the dorsum of the tongue
at the site of the foramen caecum, within the tongue or near the hyoid bone. Females are
mainly affected.
Clinically asymptomatic midline, purplish soft swelling and may cause dysphagia. Seen often
at puberty or in pregnancy, when the thyroid normally enlarges. Lingual thyroid may not be
recognised as such clinically, and biopsy may cause considerable bleeding. Nature of the
swelling determined by fine needle aspiration. Patients with lingual thyroid are often
hypothyroid.
It must not be removed before confirming that a thyroid gland is present in the neck by
ultrasound scanning, I131 or MRI scanning. If no other thyroid tissue is present, removal
would precipitate hypothyroidism and life-long thyroxine supplementation. Malignant change
rare and more frequent in males.
PARATHYROID DISEASE
Hyperparathyroidism
Usual cause - adenoma of a parathyroid gland, very occasionally a parathyroid carcinoma.
The commonest type is secondary hyperparathyroidism, a reaction to low serum calcium
levels caused by chronic renal failure or prolonged dialysis. It may also be an effect of lithium
treatment. High levels of calcium cause weakness, fatigue, constipation and kidney stones.
Typical features of hyperparathyroidism • General malaise • Peptic ulceration • Bone
resorption • Renal stones or nephrocalcinosis • Polyuria
Effects of hypoparathyroidism on calcified tissues • Retarded new bone formation and
diminished resorption are usually in equilibrium so that skeletal changes are rare • Aplasia or
hypoplasia of developing enamel*, which becomes deeply grooved • Dentine may be
incompletely mineralised but lamina dura may be thickened • Short roots to teeth
However, such florid presentations are now rare, and most cases are asymptomatic and
discovered by chance because of a high serum calcium or when patients are seen with a
renal stone. Hyperparathyroidism is the presenting sign of the uncommon disease, type 1
multiple endocrine neoplasia syndrome (see the following section). There are also other
familial forms. The hyperparathyroidism-jaw tumour syndrome is a rare autosomal dominant
disease whose features include parathyroid adenomas or carcinomas, renal cysts and fibro-
osseous jaw lesions.
Hypoparathyroidism
Most common cause - thyroidectomy, when parathyroid glands are excised with the thyroid.
Although residual parathyroid tissue undergoes compensatory hyperplasia, 20% of patients
are affected. Early-onset hypoparathyroidism is developmental in origin, or part of
autoimmune polyendocrinopathy or other syndromes. Hypocalcaemia presents as mental
changes or heightened neuromuscular excitability and tetany. These are controlled by giving
the vitamin D analogue cholecalciferol (D3) and calcium orally, with dietary adjustment to
avoid phosphorus. Recombinant parathormone (PTH residues 1-34 (teriparatide) or PTH1-
84) also available.
Tetany
Mild cases - tetany is latent but can be triggered by tapping on the skin over the facial nerve;
this causes the facial muscles to contract (Chvostek’s sign).
More severe cases - muscle cramps and tonic contractions of the muscles may progress to
generalised convulsions.
An early symptom of tetany is paraesthesia of the lip and extremities. Tetany in dental
surgery results from overbreathing due to anxiety, producing the same signs
Pseudohypoparathyroidism
Rare genetic condition caused by mutations in genes that affect the PTH receptor cell
activation pathway, including the GNAS gene associated with Albright’s syndrome. Short
stature, with a round face, hypocalcaemic, and have missing teeth, teeth with large pulps
and enamel hypoplasia.
ADRENOCORTICAL DISEASES
Adrenocortical insufficiency is rarely primary (Addison’s disease) and more frequently
secondary to corticosteroid therapy.
Adrenocortical hypofunction or Addison’s disease
Addison’s disease results from * failure of secretion of cortisol and aldosterone, usually
autoimmune with organ-specific circulating autoantibodies * Tuberculous or fungal adrenal
destruction secondary to HIV infection * polyglandular autoimmune syndromes and is then
associated with chronic mucocutaneous candidosis.
Leads to a severe disorder of electrolyte and fluid balance and serious clinical effects
Typical clinical features of Addison’s disease • Lassitude, anorexia, weakness and fatigue •
Abnormal oral and cutaneous pigmentation • Gastrointestinal disturbances, diarrhoea,
nausea, vomiting • Craving for salt (caused by lack of aldosterone) • Loss of weight • Low
blood pressure • Susceptibility to hypotensive crises • Associated with chronic
mucocutaneous candidosis in polyendocrinopathy syndrome
Pigmentation results from compensatory adrenocorticotropic hormone (ACTH) secretion as
this peptide hormone has a similar amino acid sequence to melanocyte-stimulating
hormone. Pigmentation is often an early sign and, in the mouth, is patchily distributed on
gingivae, buccal mucosa and lips. It is brown or almost black. Skin pigmentation looks
similar to suntan but with a sallow appearance due to underlying pallor. Exposed and
normally pigmented areas are most severely affected.
Addison’s disease is an exceptionally rare cause of oral pigmentation but, if there is recent
onset with general weakness and lassitude, the diagnosis should be considered. Long-term
treatment of Addison’s disease is usually by oral hydrocortisone and fludrocortisone, with
salt supplementation if necessary. The dose of steroid needs to be adjusted to provide
additional steroid support in times of stress, infection, other illness, surgery or exercise.
Failure to provide sufficient steroid, or untreated disease, may lead to Addisonian crisis.
In an Addisonian or adrenal crisis, there is rapid fall in blood pressure, circulatory collapse
(shock: pale, cold, clammy skin, sweating, rapid, shallow breathing, dizziness) and vomiting.
Associated with dehydration, headache, drowsiness or loss of consciousness. It may be
fatal, and require immediate treatment with intravenous hydrocortisone (several 100 mg) and
fluid replacement.
Adrenocortical hyperfunction
Cushing’s disease is usually due to an adrenocorticotrophic hormone-secreting pituitary
adenoma that causes adrenocortical hyperplasia. Cushing’s syndrome refers to the same
features caused by ectopic ACTH production by another neoplasm, or corticosteroid
treatment(the last being by far the commonest cause).
Important features of Cushing’s disease • Obesity of trunk and face • Bruisability and
haematomas on trauma • Hirsutism • Headaches • Hypertension • Osteoporosis, especially
of the skull • Glycosuria, hyperglycaemia and thirst
AUTOIMMUNE POLYENDOCRINE SYNDROMES
These three diseases are also known as polyglandular autoimmune disease (or APECED).
Different inheritance patterns, and several genes are responsible but all feature autoimmune
attack on multiple endocrine glands. The two more common types both have Addison’s
disease as an invariable feature, and there are several other components of significance to
dental treatment, notably chronic mucocutaneous candidosis in type 1. Candidosis is an
early and common presenting feature. Dental defects can also result from
hypoparathyroidism in the type 1 syndrome and as many as 10% of patients with Type 1
disease develop oral or oesophageal carcinoma.
DISEASES OF THE ADRENAL MEDULLA
Phaeochromocytoma
Phaeochromocytoma is a catecholamine-producing tumour of the adrenal medulla. Main
effect is potentially lethal hypertension, tachycardia and dysrhythmias. A third of cases have
a genetic predisposition.
Can be part of the multiple endocrine adenoma syndrome type IIb, when it is associated with
oral mucosal neuromas or associated with neurofibromatosis, von Hippel-Lindau or other
inherited diseases.
When an oral neuroma is found, the possibility of a phaeochromocytoma should be
considered, especially if the patient is hypertensive. Dental treatment must be delayed in any
patient with a phaeochromocytoma. A stressful event may precipitate a hypertensive crisis.
MULTIPLE ENDOCRINE NEOPLASIA SYNDROMES
Autosomal dominant disorders with prevalence of 1 in 20,000 that cause gland hyperplasia
and benign and malignant neoplasms.
MEN1  caused by mutation in the tumour suppressor gene MEN1, which encodes a
nuclear transcription factor. Parathyroid, pancreas and pituitary are affected, and
presentation is in the second and third decades. Hyperparathyroidism develops in 95%.
Enteropancreatic tumours develop in more than 40% and pituitary tumours in more than
30%. Also described are gingival papules and nodular lesions on the vermilion border.
MEN2  the mutated gene is the RET proto-oncogene, a growth factor receptor that affects
cell cycle and also the development of autonomic nerves. Medullary carcinoma of the thyroid
is present in 95%, phaeochromocytoma in 50% and hyperparathyroidism in 15% of cases.
Two forms - 2a and 2b (the latter sometimes called type 3).
Striking oral feature of MEN2b - mucosal neuromas, particularly along the lateral borders of
the tongue. These are neither neurofibromas nor schwannomas, but developmental
anomalies of tangles of enlarged nerves. Large neuromas enlarge the tongue, lips and other
sites. Small ones produce small mucosal nodules or a papillary mucosa. These are often the
first sign and can be diagnosed in infancy or childhood. Screening for MEN2 is carried out by
identifying the RET mutation. Confirmed cases will be offered total thyroidectomy in infancy
to avoid developing medullary carcinoma, which can develop in the very young.
MEN 1 • Adenomas of pituitary, adrenals, sometimes thyroid. Insulinoma, gastrinoma.
Parathyroid hyperplasia • Zollinger–Ellison syndrome and peptic ulceration
MEN 2a (Sipple syndrome) • Thyroid medullary cell carcinoma in all patients • Parathyroid
hyperplasia • Phaeochromocytoma in 33% of patients • Cutaneous neurofibromas
MEN 2b • Thyroid medullary cell carcinoma in 80%–100% of patients • Parathyroid
hyperplasia • Phaeochromocytoma in 70% of patients • Marfanoid skeletal features •
Ganglioneuromas of bowel causing distension • Mucosal neuromas orally and sometimes in
the eye
DIABETES MELLITUS
Occurs due to relative or absolute deficiency of insulin, causing persistently raised blood
glucose. UK prevalence has doubled in 20 years, and 5% of the population are affected, but
probably at least 50% of diabetics with mild or early disease pass unrecognised. By 2025 the
UK incidence will be 8%, a level already attained in the United States. World incidence is
rising as populations become urbanised, eat a more Western diet and become obese.
Type 1 diabetes (‘insulin-dependent’) - 10% of cases. Symptoms typically appear before the
age of 25, and the disease is usually severe with thirst, polyuria, hunger, loss of weight and
susceptibility to infection. Cause is failure of secretion of insulin after autoimmune
destruction of the pancreatic islets and insulin replacement is the treatment.
Type 2 (‘maturity onset’) - 90% of cases. Patients are typically older than middle age and
obese. The onset is insidious, often with deterioration of vision or pruritus or, sometimes,
thirst, polyuria and fatigue. Many cases are asymptomatic. Cause is end organ resistance to
insulin, and the disease can be controlled by dietary restriction and, if necessary, oral
hypoglycaemic drugs. The current epidemic of childhood obesity seems likely to lead to the
onset of this variety of diabetes early in life.
Dental management is difficult with ‘uncontrolled’ diabetes. Uncontrolled applies to several
diabetic states, such as the mild, unrecognised, and therefore untreated, diabetic or treated
diabetic whose disease is difficult to control (‘brittle diabetes’) or has been mismanaged. This
last group is the one most likely to have oral complications and present difficulties in dental
management.
Complications of diabetes mellitus that can affect dental management • Susceptibility to
infection, particularly candidosis, also mucormycosis • Hypoglycaemic coma • Diabetic coma
• Ischaemic heart disease • Acceleration of periodontal disease if control is poor • Dry mouth
secondary to polyuria and dehydration • Oral lichenoid reactions due to oral hypoglycaemic
drugs • Delayed healing • Sialadenosis
Dental aspects - Main oral manifestations of diabetes are usually due to the lowered
resistance to infection, particularly to fungi as a result of impaired neutrophil function. Oral
candidosis is frequent, and severe deep mycoses such as mucormycosis are a risk. Rapidly
destructive periodontal disease occurs, severity is proportional to blood glucose levels.
Severe periodontitis also seems to complicate insulin control and treatment appears to
improve diabetic markers of disease severity. Diabetics with more severe periodontitis are at
higher risk of diabetic complications such as nephropathy and ischaemic heart disease. The
relationship between diabetes and dental caries is unclear. Many patients have low caries
susceptibility, probably as a result of the sugar-free diet. However, poorly controlled
childhood patients have higher caries rates.
Type 2 diabetics with good dietary or oral hypoglycaemic drug control can be treated as a
non-diabetic patient. In type 1 diabetes, well-controlled patients are similarly very low risk.
However, hypoglycaemic coma may be precipitated by dental treatment that delays a normal
meal or unbalances food intake and insulin. This can cause an emergency in the dental
surgery. Treatment should therefore be so timed as to avoid these risks – ideally, soon after
the patient’s breakfast. Many patients now have their own glucose monitors and can check
the level immediately before treatment and when signs suggest onset of hypoglycaemia.
Diabetic (hyperglycaemic) coma is a complication of poorly controlled diabetes mellitus and
much less likely to be seen. Patients with recurrent candidosis or severe periodontitis without
cause can be relatively easily tested in a dental setting using urine dipsticks to detect
glycosuria, enabling confident referral to their medical practitioner.
Principles of dental management of diabetics • Time treatment to avoid disturbance of
routine insulin administration or meals • Use local anaesthesia for routine dentistry – the
amount of adrenaline (epinephrine) in local anaesthetic solutions has no significant effect on
the blood sugar • Sedation can be given if required • Deal with any diabetic complications •
Manage hypoglycaemic coma as described in Chapter 43 • General anaesthesia requires
special precautions
PREGNANCY
Pregnancy is a physiological process and should not deter dental treatment; this is an
important time to establish good oral health for mother and child. Changes of pregnancy
impact dental care in three main ways: hormonal influences on the oral cavity, risks to the
fetus and adjustments required for medication.
Pregnancy: oral effects and management considerations :-
Effect on the mother • Aggravated gingivitis and epulis formation • Variable effect on
recurrent aphthae • Increased intensity of pigmentation, face and sometimes oral • Risk of
hypotension when laid supine • Possible hypertension of pregnancy • Hypersensitive gag
reflex and vomiting • Possible iron or folate deficiency, especially if anaemic before
pregnancy
Risks to the fetus • X-rays hazardous, especially in first trimester • Respiratory depression
due to sedatives, including benzodiazepines • Tooth discolouration due to tetracycline •
Prilocaine may rarely cause methaemoglobinaemia • Theoretical risk of uterine contraction
caused by felypressin • Aspirin may cause neonatal haemorrhage • Theoretical risk of
depressed vitamin B12 metabolism by nitrous oxide • Teratogenic risks of thalidomide,
retinoids, azathioprine and possibly other drugs
Fetal considerations - Main risks of fetal abnormalities are from drugs and radiation; the
hazard is greatest during organogenesis in the first trimester. Few drugs are known to be
teratogenic for humans and, results only from prolonged, high dosage. For example, no
teratogenic risk from metronidazole for humans has ever been substantiated though effects
in animals have led to the avoidance of metronidazole during pregnancy
The risks from dental radiography are small, but only essential radiographs should be taken,
the minimal radiation exposure should be given and radiography delayed if possible. An
abdominal dose of radiation, particularly in the first trimester, risks congenital abnormality,
learning disorder and malignant neoplasms. Because the risk period is likely to be before the
patient will know she is pregnant, precautions must be taken for all women of child-bearing
age. In the UK this does not require routine use of lead aprons as the beam in dental
radiography will not be directed toward the abdomen. Routine collimation, fast films or digital
capture, and good technique are more important in reducing dose. Nevertheless, during
pregnancy, the patient may be offered a lead apron because the topic is so emotive, but
routine radiation protection measures are safe.
Non-steroidal anti-inflammatory drugs in high dosage may cause premature closure of the
ductus arteriosus and fetal pulmonary hypertension. Aspirin may also increase the risk of
neonatal haemorrhage and paracetamol is the only safe analgesic. Systemic corticosteroids
can cause fetal adrenosuppression. However, the only drugs known to be teratogenic are
thalidomide (used occasionally for major aphthae), etretinate (used experimentally for
leukoplakia) and possibly azathioprine (used for Behçet’s syndrome and autoimmune
diseases). Systemic antifungals and antiviral agents are considered safe, with adverse
effects limited to animal studies.
Maternal considerations
Pregnant patients should be fully evaluated as early as possible so that any treatment
necessary can be planned for the second trimester and emergency dental care avoided.
Temporary restorations and stabilisation may be required when oral health is poor. An
intensive preventive regime of oral hygiene and diet control will benefit both the mother and
future child. Prenatal fluoride supplementation provides no benefit to the child.
Chief oral effects of pregnancy are aggravation of gingivitis and possible development of a
pregnancy epulis. Initiation of a high standard of dental care and dental education at the
earliest opportunity is essential. These complications usually affect those with pre-existing
gingivitis and start around the second month. Recurrent aphthae remit during pregnancy but
may worsen due to any iron or folate deficiency. Patients in third trimester of pregnancy
become hypotensive when laid supine, when the enlarged uterus impedes venous return.
Respiratory reserve is diminished, and there is a risk of fetal hypoxia. It is easiest to treat all
late pregnant patients in a sitting position and in short appointments, as this is more
comfortable.
Neonatal respiration is further depressed by drugs such as general anaesthetics and
sedatives, especially barbiturates, diazepam and opioids, all of which cross the placenta and
are contraindicated in pregnancy. No evidence of risks from local anaesthesia, and pain is
likely to cause greater adverse consequences. Felypressin is an oxytocin analogue and
could induce uterine contractions and fetal methaemoglobinaemia. These are not considered
risks at dental doses, but lignocaine and epinephrine is generally taken to be preferable as it
is more effective. Risks from benzodiazepines such as midazolam for sedation are such that
intravenous sedation is contraindicated. Nitrous oxide sedation carries a risk of interference
with B12 and folate metabolism after very prolonged administration (weeks), but there is no
evidence that it is teratogenic and it is safe after the first trimester used with 50% oxygen.
Exposure should be limited to 30 minutes and repeated exposure avoided. The myth that
mothers lose a tooth for every pregnancy reflects poor oral health and nothing to do with
increased calcium requirements during pregnancy; this calcium is provided from bone and
diet, not teeth.
35. Nutritional deficiencies
Susceptible patients are the elderly living on a scanty diet, severe alcoholics living on a
grossly unbalanced diet and those following diets or food fads. On average, dietary intakes
of all vitamins are adequate, apart from vitamin D. Intake of some B vitamins is too low in
young and elderly females.
VITAMIN DEFICIENCIES
Vitamin A deficiency
Role in epithelial maturation and retinoids, more potent analogues, have been tried in
conditions with abnormal keratinisation such as leukoplakia. Lycopene and β-carotenes,
vitamin A precursors, have also been tried. Changes in keratinisation are reported but are
not reproducible, and whether this might reduce the risk of carcinoma is unclear. Adverse
effects are significant.
Riboflavin (B2) deficiency
Result from a malabsorption syndrome. In severe cases, there is typically angular stomatitis,
with painful red fissures at the angles of the mouth, and shiny redness of the mucous
membranes. The tongue is commonly sore. A peculiar form of glossitis in which the tongue
becomes magenta in colour and granular or pebbly in appearance, due to flattening and
mushrooming of the papillae seen. The gingivae are not affected. Resolution follows within
days when riboflavin (5 mg, three times per day) is given. Riboflavin is ineffective for the
commonly seen cases of glossitis and angular stomatitis, which are rarely due to vitamin
deficiency. Recently, riboflavin has been used to cross-link dentine collagen in an attempt to
toughen dentine for adhesion of restorations. This is because it absorbs blue light and not for
any nutritional reasons.
Nicotinamide deficiency (pellagra)
Pellagra, which affects the skin, gastrointestinal tract and nervous system, is rare in Britain
but occasionally result from malabsorption or alcoholism. Weakness, loss of appetite and
changes in mood or personality are followed by glossitis or stomatitis and dermatitis. The tip
and lateral margins of the tongue become red, swollen and, in severe cases, deeply
ulcerated. The dorsum of the tongue becomes coated with a thick, greyish fur which is often
heavily infected. The gingival margins also become red, swollen and ulcerated, and
generalised stomatitis may develop. A combination of nicotinamide and tetracycline is
sometimes used to treat oral pemphigoid, particularly in the US  no convincing mechanism
of action and no good evidence base.
Folic acid deficiency
Deficiency result from malnutrition but is more often seen in pregnancy, or as a result of
malabsorption or drug treatment (particularly with phenytoin). Women are advised to take
folic acid supplements preconceptually with the aim of reducing the risk of neural tube
defects. It also appears that multivitamin preparations containing folic acid may reduce the
risk of orofacial clefts.
Vitamin C deficiency
Scurvy, once common among crews of sailing ships, is rare. In Britain, scurvy may very
occasionally be seen among elderly people with an inadequate diet or eccentric diet or the
homeless. The main features of scurvy are dermatitis and purpura and, in advanced cases,
anaemia and delayed healing of wounds. In the young, bone growth is delayed by poor
collagen synthesis.
Grossly swollen bleeding gums. Gingival swelling due to a combination of chronic
inflammation and an exaggeration of the inflammatory congestion due to purpura. In
children, severe scurvy causes early tooth loss. The diagnosis should only be made on clear
evidence of dietary deficiency and of purpura. In these cases, treatment with vitamin C and
adequate oral hygiene relieves the gingival condition. No evidence that deficiency of vitamin
C plays any part in periodontal disease except in frank scurvy.
Vitamin D deficiency
Deficiency of vitamin D during skeletal development causes rickets. Dental hypocalcification
is a feature only of exceptionally severe rickets. In sunlight, vitamin D is synthesised in the
skin, and this is the main source, even in the UK. A few foods, notably, fish liver oils, eggs
and butter contain significant amounts. In Britain, fat spreads are fortified with vitamins A and
D, but not milk as in many other countries. As much as 15% of the UK population is
deficient, mostly the elderly and very young. Serum levels are lower in winter when as many
as 40% of children become temporarily deficient. Requirements are small except during
bone growth or pregnancy, and a small reserve is stored in fat. Rickets is now rare, but
immigrants in the North of Britain are at risk. Contributory factors are lack of sunlight, a high-
carbohydrate diet and possibly also the use of whole meal flour (as in chupattis) containing
factors that impair calcium absorption. There is no basis for the idea that dental caries is due
to poor calcification of the teeth. Hypervitaminosis D causes hypercalcaemia and renal
calcinosis. Mild osteoporosis has been considered to predispose to periodontitis.
Effects of specific vitamin deficiencies

Deficiency Systemic effects Oral effects

Vitamin A Night-blindness None
xerophthalmia
Thiamine B1 Neuritis and cardiac failureNone
Riboflavin (B2) Dermatitis Angular stomatitis and
glossitis
Nicotinamide Dermatitis, central nervous Glossitis, stomatitis and
system disease, diarrhoea gingivitis
Vitamin B12 Pernicious anaemia Glossitis, aphthae
Folic acid Macrocytic anaemia Glossitis, aphthae
Vitamin C Scurvy (purpura, delayed Gingival swelling and
wound healing, bone lesions bleeding
in children)
Vitamin D Rickets Hypocalcification of teeth
(severe rickets only)
34. Gastrointestinal and liver disease
GASTRO-OESOPHAGEAL REFLUX AND GASTRIC REGURGITATION
Gastro-oesophageal reflux and consequent oesophagitis - common cause of the symptoms
of dyspepsia and ‘heart burn’. Smoking, excessive alcohol consumption, obesity, frequent
stooping and overlarge meals are frequent precipitating factors. If persistent, the
oesophageal lining may undergo metaplasia to a more resistant gastric-type mucosa
(Barrett’s oesophagus). Only severe reflux alone can cause dental erosion. Inhibition of acid
secretion by protein pump inhibitors, such as omeprazole, is highly effective in controlling it.
By contrast, chronic vomiting or regurgitation of gastric acid contents, due to such causes as
hypertrophic pyloric stenosis or in bulimia, can lead to marked dental erosion, which can be
worse on the palatal and occlusal aspects of the anterior teeth.
COELIAC DISEASE
Common and important cause of malabsorption affecting 1% of the population. Cause is
hypersensitivity to gluten in wheat and other cereal products. Almost all patients have the
predisposing human leukocyte antigen (HLA) DQ2. Specific degradation products of gluten
trigger ileal mucosal inflammation, with loss of villi causing failure of absorption.
Asymptomatic, and it may not be recognised until adult life as a result of its complications.
Malabsorption, stunting of growth, fatty diarrhoea and abdominal pain or discomfort are
typical consequences. The malabsorption can lead to vitamin and mineral deficiencies
resulting in anaemia or bleeding tendencies.
Dental aspects - Anaemia can have a variety of oral effects such as glossitis or recurrent
aphthae. As many as 5% of patients with coeliac disease may have recurrent aphthae, even
in the absence of anaemia. Enamel hypoplasia is common in coeliac disease, seen as spotty
hypoplastic mottling, localised opacities, chronological banding, pitting or discolouration.
These probably result from malabsorption and are not specific to the disease. Usually only
permanent teeth are affected. Hypoplasia in a child of short stature and with bowel
symptoms should raise suspicion of coeliac disease, recognising that many cases are
diagnosed late.
CROHN’S DISEASE
Crohn’s disease is an inflammatory bowel disease of unknown aetiology. It shares many
features with the autoinflammatory diseases, and associated with mutations in the gene
NOD2 that controls inflammatory responses to bacteria. Mutations cause failure of the
formation of the mucin and antimicrobial barrier lining the bowel and may also inhibit
degradation of bacteria. Changes in bowel flora are probably also important.
Granulomatous inflammation affects the ileocaecal region, causing thickening and
ulceration. Symptoms vary with the severity of the disease, but effects can include
abdominal pain, variable constipation or diarrhoea and, sometimes, obstruction and
malabsorption. Repeated bowel resections may ultimately be needed. Many other sites can
be affected including any part of the bowel, joints and skin. Treatment controls symptoms but
is not curative. Dietary adjustment, corticosteroids, antibiotics, sulfasalazine or mesalazine,
immunosuppressants and tumour necrosis factor (TNF)-alpha blockers (e.g. infliximab) are
used.
Most patients have no oral signs, although aphthous ulcers and candidosis may be
associated with anaemia. When the disease process itself affects the mouth, the signs and
symptoms are the same as those in orofacial granulomatosis. Non-caseating granulomas
resembling those in the intestine develop in the oral mucosa. The common sites of
involvement are lips and buccal mucosa. These show prominent oedema with folds tethered
to the underlying deeper tissues, producing the characteristic cobblestone mucosa
appearance. Linear ulcers often run along the buccal sulci, particularly the lower sulci, and
have hyperplastic folds of inflamed mucosa along their margins. The gingiva show an
erythematous nodular gingivitis with hyperplastic tags.
Typical orofacial features of Crohn’s disease • Diffuse soft or tense swelling of the lips, or
mucosal thickening • Cobblestone thickening of the buccal mucosa, with fissuring and
hyperplastic folds • Gingivae may be erythematous and swollen • Sometimes, painful
mucosal ulcers, linear in sulci or resembling aphthae • Mucosal tags in sulcuses • Glossitis
due to iron, folate or vitamin B12 deficiency can result from malabsorption • Orofacial
granulomatosis shares many features
Granulomas are typically small, loose and contain few multinucleate giant cells and are often
sited deeply in underlying muscle. They may be few in number, and a biopsy needs to
extend unusually deeply to increase the chance of finding them because only by identifying
granulomas can the diagnosis be made. The granulomas are associated with vascular
dilatation and tissue swelling in early disease. Later, there is dense fibrosis that fixes the
tissues in their distorted shape. Occasionally oral lesions precede gastrointestinal symptoms
by a long period. Oral disease is much more likely to progress to bowel disease in children
than when diagnosed in an adult. Oral lesions may lessen in severity with treatment of
systemic disease. Aggressive treatment is merited in the early stages to prevent fibrosis and
permanent disfigurement. The same drugs as are used for bowel disease are required,
together with steroid injections of swollen mucosa.
OROFACIAL GRANULOMATOSIS
Oral mucosal granulomatous inflammation without an identifiable cause. The clinical features
are very similar to oral lesions of Crohn’s disease, but this is probably a distinct disease. The
chances of eventually developing Crohn’s disease are higher if orofacial granulomatosis is
diagnosed in childhood.
Orofacial granulomatosis presents mainly in young adults, and lip and buccal mucosa are
the main sites involved, with marked oedema and a cobblestone appearance. Linear sulcus
ulcers and gingival lesions are less frequent than in Crohn’s disease. Diagnosis requires
biopsy and, as in Crohn’s disease, a deep biopsy is required to give the best chance of
finding granulomas.
The cause of orofacial granulomatosis is related to food allergy. The patients often have
subclinical bowel disease, a higher than average risk of allergy to a range of common
allergens and react to common food additives such as cinnamon, benzoates and phenolic
compounds. Both type 1 and type 4 hypersensitivity mechanisms are implicated. Treatment
is initially by exclusion diet, and nearly two-thirds of patients respond. Intralesional steroid
injections, immunosuppressants such as tacrolimus or ciclosporin, methotrexate or tumour
necros is factor (TNF)-alpha inhibitors (infliximab) may be used depending on severity.
MALABSORPTION SYNDROMES
Malabsorption syndromes can cause haematological deficiencies that can contribute to
development or exacerbation of recurrent aphthae, glossitis, candidosis or other symptoms.
Important causes of malabsorption syndrome • Coeliac disease and other allergies • Crohn’s
disease • Resection of stomach or ileum • Pancreatic insufficiency • Liver disease (failure of
bile secretion into the gut) • Some parasitic and other chronic gut infections
ULCERATIVE COLITIS
Ulcerative colitis is an inflammatory disease of the large intestine causing ulceration and
fibrosis. Patients are typically between 15 and 50 years. The main effect is intractable
diarrhoea with blood and mucus in the stools. Abdominal pain, fever, anorexia and weight
loss are seen in severe cases.
Oral aspects - Anaemia can have its usual effects on the oral mucosa. No direct oral
involvement, but the oral condition of pyostomatitis vegetans is closely associated. This is a
rare disease, with diffuse mucosal oedema and erythema on which there are slightly raised
multiple tiny pustules just below the surface. Histologically, the epithelium contains clusters
of neutrophils and eosinophils. The lesions often resolve with treatment of the bowel disease
or with steroids, but occasionally they are the presenting sign of unsuspected bowel disease.
INTESTINAL POLYPOSIS SYNDROMES
Gardner’s syndrome with polyposis of the colon, multiple osteomas of the jaws and a high
malignant potential in the colon
Peutz-Jeghers syndrome of intestinal polyposis with skin pigmentation
ANTIBIOTIC-ASSOCIATED COLITIS
Mild diarrhoea following prolonged antibiotic treatment follows disturbance of the bowel flora
and is often self-limiting.
Pseudomembranous colitis is more severe, with passage of blood and mucus in the stools
and sometimes fragments of necrotic bowel mucosa (pseudomembrane). It is typically a
complication of prolonged antibiotic therapy, particularly with clindamycin or lincomycin and
due to proliferation of Clostridium difficile resistant to these antibiotics. Pseudomembranous
colitis is treated with metronidazole but can be fatal in the elderly and debilitated. Antibiotics
prescribed for dental reasons must be used for the shortest courses that are effective and
selected according to guidelines or culture and sensitivity and not repeated unnecessarily to
avoid such adverse effects.
LIVER DISEASE
Common types of liver disease are infections (particularly viral hepatitis), obstructive
jaundice, cirrhosis (often due to alcohol) and tumours.
Important aspects of liver disease relevant to dentistry • Haemorrhagic tendencies • Impaired
drug metabolism • Transmission of viral hepatitis • Drug-dependent patients are frequently
viral hepatitis carriers • Cutaneous manifestations (purpura, telangiectasia, finger clubbing) •
Sialadenosis • Sjögren’s syndrome (in primary biliary cirrhosis)
Impaired drug metabolism
Most drugs are metabolised in the liver, and no drugs should be given to patients with liver
disease without first consulting the British National Formulary or drug datasheet. Drugs of
dental relevance metabolised by the liver include local anaesthetics, aspirin, diazepam and
intravenous sedatives, penicillins and metronidazole.
Important causes of liver failure • Idiopathic cirrhosis • Alcoholic cirrhosis • Viral hepatitis
(particularly C), Cirrhosis is frequently the result of alcoholism but often of unknown cause.
VIRAL HEPATITIS
The main types of hepatitis, are B, C and D. Hepatitis B is the chief risk to dental personnel,
but hepatitis C can also be transmitted during dentistry. The hepatitis B virus can also carry
within it the delta agent that can cause a particularly virulent combined infection (hepatitis D).
Hepatitis A
Hepatitis A is the common form of infectious hepatitis. Acquired from contaminated food or
water during a holiday abroad in a hot developing country. Incubation period is 2–6 weeks,
jaundice is usually mild and spontaneous recovery takes 3 months or so. Long-term
complications are extremely rare. A vaccine is available.
Hepatitis E
Transmission by the faecal–oral route, but the reservoir of infection is in animals. Infection is
endemic in hot developing countries, particularly India, but the risk to travellers abroad is
small. Spontaneous recovery is usual. A vaccine has recently become available.
Hepatitis B
Hepatitis B is usually spread vertically at birth or horizontally in families in endemic areas.
Where prevalence is low, as in developed countries, transmission is by sexual contact or
through infected blood. Before effective vaccination, this was the greatest infective hazard to
dental staff and there are still risks from blood transfusions and medical procedures in parts
of the world.
Special hazards to dental staff from hepatitis B • The virus is widespread in Southeast Asia
and Africa • The majority of cases are in those from high-risk areas outside the UK • A
chronic infective carrier state is common • Minute traces of body fluids can transmit infection
• The virus survives well outside the body for short periods • The virus is relatively resistant
to disinfection • Hepatitis B infection can cause serious complications
Possible results of hepatitis B infection • Complete resolution • Asymptomatic carrier state •
Acute hepatitis (rarely fatal) • Chronic active hepatitis • Cirrhosis • Liver failure • Liver cancer
Clinical aspects - Incubation period is at least 2–6 months. The virus replicates in
hepatocytes, and the immune response to the virus eventually clears the infection, damaging
the liver in the process. Majority of infections are subclinical (anicteric), but 5%–10% of
patients, particularly those who have had no overt illness, become persistent carriers and
can transmit the infection. A minority develop acute hepatitis with loss of appetite, muscle
pains, fever, jaundice and often a swollen, painful liver. The illness is often severe and
debilitating but usually followed by complete recovery and long-lasting immunity. Overall
mortality from clinical infection is probably approximately 1%. Occasionally, it has been as
high as 30%, probably as a result of co-infection by the delta agent. Biochemical markers of
infection are raised serum levels of liver enzymes, bilirubin and often of alkaline
phosphatase. However, confirmation of the diagnosis is by serology
Serological markers of hepatitis B
The hepatitis B virus (HBV) is a DNA virus termed the Dane particle. The Dane particle
consists of a central core and an outer shell. The core contains DNA, an enzyme (DNA
polymerase – DNA-P) and the hepatitis B core antigen (HBcAg). The protein shell contains
the hepatitis B surface antigen (HBsAg). The e antigen is related to the HBcAg but is only
expressed by some strains and is only produced during viral replication by alternative
transcription. Immune responses to these antigens can be used to track the progression of
disease, recovery and infectivity.
The carrier state and complications
Most patients with acute hepatitis B recover completely within a few weeks. Approximately
5%–10% fail to clear the virus within 6–9 months and develop chronic infection and become
chronic carriers. Chronic carriage of HBsAg alone indicates a low risk of severe liver
damage. Persistent carriage of both HBsAg and HBeAg is associated with chronic active
hepatitis and infectivity. These patients have biochemical evidence of liver damage. They
are chronically ill and at special risk from cirrhosis and, possibly, carcinoma of the liver as a
result of continued viral replication and damage mediated by the immune response. Chronic
active hepatitis with persistent malaise, and sometimes mild jaundice, is particularly likely to
develop in the very young, the old and the immunosuppressed.
Risks to dental staff
The carriage rate of hepatitis B virus in the general population of Britain is 0.3%. The rate in
British dentists used to be double that in the general population, though this should fall now
that dentists are vaccinated. There are also high risk groups. In endemic areas in Asia and
Africa, carriage rates may be 20% and dental staff there are potentially at high risk.
Transmission of hepatitis B
Blood and blood products can transmit infection in as little as 0.000 000 1 mL fluid,
particularly when containing the e antigen. Many cases have followed needle-stick injuries,
injections and blood transfusions. Saliva can also contain hepatitis B antigens and,
experimentally, can transmit the virus. Saliva is frequently also contaminated with blood and,
when splashed on to the conjunctiva, might transmit infection to a dentist. Hepatitis B can
also be transmitted sexually, and carriage rates are high in sex workers and those with HIV
infection. The degree of infectivity is indicated by the serological markers. Infective carriers
can only be suspected if they have a history of jaundice or are in a high-risk group.
Nevertheless, it must be emphasised that only 1 in 4 carriers gives a positive medical
history. Many infectious patients, as in the case of HIV carriers, will therefore be treated
unknowingly.
Patients with higher risk of being hepatitis B carriers - In the UK vaccination is now offered
to: • Intravenous drug users and their partners • Men who have sex with men • Those with
frequent changes of sexual partners • Babies, family and partners of those infected • Anyone
with chronic liver or renal disease • Those who need regular blood transfusions • Male and
female sex workers • Travellers to endemic areas • Prison staff and prisoners • Healthcare
staff, including dentists • Families adopting children from endemic areas And these are also
at risk: • Patients and staff of institutions for the handicapped • Immunosuppressed or
immunodeficient patients • Patients who have received unscreened blood or blood products
• Patients who have had acupuncture or tattooing, especially in tropical countries
Prevention and management of hepatitis B
It is essential for dentists to have active immunisation. It is effective, safe and protects
against both hepatitis B and delta infection. The vaccine is the HBsAg engineered in yeast
and thus contains no complete virus. Three injections should be given at intervals into the
deltoid muscle (the vaccine is less effective injected into fatty tissue), but adequate
protection may not develop until after 6 months. Side effects are mild and rare, but a few
(particularly the obese) do not produce adequate antibody levels after a normal course of
vaccination and may need it to be repeated. It is technically possible to measure the
resulting antibody levels, but this is no longer considered necessary, either to measure
effectiveness or the need for a booster vaccination. Immunity does not depend on the
circulating antibody level, rather on the cell-mediated response and memory B lymphocytes
primed to respond when needed. Although booster doses are no longer recommended in the
UK, they are in other countries. The effectiveness of the current vaccines exceeds 95% but
is not complete.
Hepatitis D: the delta agent
The delta agent is a defective RNA virus that can only infect and replicate in the presence of
HBsAg, which it uses to bind to hepatocyte receptors. Delta infection is, therefore, only
transmitted with hepatitis B or to a person already infected by it. It is endemic in the Middle
East, Africa and parts of South America, but in the UK and developed countries it is usually
spread by intravenous drug users, by blood or blood products. Only 100 patients per year
test positive for hepatitis D in the UK, and approximately 2% of patients in the UK with
hepatitis B carry the delta agent. Delta infection causes acute hepatitis, and this rarely
resolves but causes progressive liver disease with a high mortality rate. Carriage rates are in
decline because immunisation against hepatitis B also protects against the delta agent.
Hepatitis C
The hepatitis C virus (HCV) is now more important than the B virus in dentistry because no
vaccination is available. It is also a more severe infection and more frequently fatal. After
infection, only approximately 15% of patients have signs or symptoms of hepatitis. Few
patients, perhaps 20%, clear the infection despite their immune response. This is because
the virus has an extremely high rate of genetic variability (even higher than HIV virus) and
each patient becomes infected with many newly generated genetic variants. Most patients
become chronically infected without realising it. Almost all transmission is via blood, not
transfusion products (which are tested in the UK), but primarily through needle sharing by
drug users or tattooing. Unfortunately, blood is not screened in most developing countries,
and the highest incidences are in China, Africa and parts of South America. Only
approximately 150,000 patients are chronically infected in the United Kingdom, but 2% of the
population in the United States and 3% worldwide are infected. Many HIV-positive patients
are also positive for hepatitis C. Once infected, 85% of patients progress to chronic hepatitis,
potentially causing cirrhosis and liver failure. In some high-incidence countries, particularly in
Italy, an association between hepatitis C infection and lichen planus is reported. This has not
been confirmed in Britain or the United States, and a plausible pathological link between the
two diseases does not yet exist, although infection is associated with other autoimmune
diseases.
Management
HCV is detected serologically by anti-viral antibodies, and polymerase chain reaction (PCR)
reaction for viral RNA is used to monitor treatment. Liver damage can be assessed by
circulating liver enzymes and confirmed by biopsy. Treatment is improving, and success
depends on the strain of virus. Interferon and various hepatitis C specific antiviral drugs such
as ledipasvir can prevent chronic hepatitis in over three-quarters of patients. However,
hepatitis C remains the commonest cause requiring a liver transplant, though even this is not
guaranteed to remove the infection as the virus can also replicate in lymphocytes. Those
that do not respond to treatment have a high mortality from liver failure, liver carcinoma and
a range of unusual extrahepatic complications including encephalopathy, myocarditis or the
complications of cirrhosis such as oesophageal varices. Hepatocellular carcinoma will
develop in approximately 2% of patients after 30 years. This complication continues to
appear in those who contracted the disease before screening tests for blood and blood
products were available. Universal infection control is more than adequate to prevent
transmission, and sharps injury is the main risk to dentists.
Control of transmission of viral hepatitis
Although hepatitis B vaccination and improved infection control have much reduced
occupational transmission, the risk remains. There is as yet no vaccine against hepatitis C.
Hepatitis B vaccination is not completely effective, immunity may fade with age and it is less
effective when given to older individuals. Immunisation is not a substitute for good infection
control. Gloves, masks and eye shields provide only partial protection and must be used
correctly. Many infected patients will be treated unknowingly, and hepatitis B can be
transmitted by saliva. In the event of a sharps injury, follow local guidelines. Knowing the
patient’s medical history may be important in assessing the risk. The average UK dentist
gives themselves 2–3 sharps injuries a year, and nurses are at higher risk while clearing
away and cleaning instruments
Hepatitis B virus is more resistant than HCV, but sterilisation and disinfection measures.
Restrictions on dentists who are infected by any blood-borne virus change from time to time.
In the UK, advice is available from the UK Advisory Panel for Healthcare Workers Infected
with Bloodborne Viruses (UKAP) and working restrictions from the General Dental Council
UK, both of which are available on their websites. Almost all dentistry constitutes ‘exposure
prone procedures’, and any potential infection risk to a patient will probably require
restriction of practice. Note that it is the infectivity of the dentist that is key, not simple
serological positivity
Standard precautions against transmission of viral hepatitis • Take a good medical history,
following a sharps injury you may need details from it • Treat all patients as infectious
(‘universal precautions’) • Wear gloves for all clinical dental work and cover exposed skin
and abrasions • Take special care to avoid sharps injuries • Use safety syringes or needle
retraction devices • Wear goggles for eye protection • Consider use or rubber dam for more
procedures • Zone work areas, disinfect them and follow good working practice with zoning •
Follow hand hygiene protocols • Use disposable instruments and autoclave all others •
Clean and prepare instruments for sterilisation without risking injury • Handle saliva
contaminated impressions and patient samples as though infected • Clean saliva and blood
contaminated spillages correctly and quickly • Be immunised against hepatitis B • Be aware
of guidelines for dealing with possible exposure and follow them • Be aware of legal
responsibilities under the Health and Safety at Work Act 1974 and the Control of Substances
Hazardous to Health Regulations 1999 (COSHH). • Take precautions with waste disposal
Sterilisation and disinfection for hepatitis B and C Sterilisation • Autoclaving at 134°C for 3
minutes or • Hot air at 160°C for 1 hour (effective but automatic control necessary; not used
in UK) Disinfectants • Sodium hypochlorite, 1% of freshly diluted stock solution (0.1% with
detergent for surface disinfection) (hepatitis C virus is also susceptible to solvent detergents)