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Chronic liver disease affects hundreds of millions of people worldwide, and its prevalence continues to rise with the epidemic of metabolic liver disease. The liver is central to haemostasis, drug metabolism and immune competence, and its failure therefore alters the risk profile of almost every ...

Chronic liver disease affects hundreds of millions of people worldwide, and its prevalence continues to rise with the epidemic of metabolic liver disease. The liver is central to haemostasis, drug metabolism and immune competence, and its failure therefore alters the risk profile of almost every dental procedure. Patients with compensated disease usually tolerate routine dentistry without modification, while those with cirrhosis or a transplant require careful planning and coordination with the medical team.
Global Burden of Disease analyses published in The Lancet in 2020 estimated that liver disease accounted for approximately two million deaths annually, roughly half of which were attributable to cirrhosis. Viral hepatitis remains a major contributor, and the World Health Organization has estimated that approximately 296 million people are living with chronic hepatitis B and 58 million with chronic hepatitis C.
Metabolic dysfunction-associated steatotic liver disease is now the most rapidly growing cause, driven by obesity and type 2 diabetes.
The liver synthesises most clotting factors, produces albumin and bile, and metabolises the majority of drugs used in dentistry. It is also responsible for converting ammonia to urea, and its failure produces the encephalopathy and coagulopathy that dominate the perioperative risk profile.
Protein synthesis is impaired early in cirrhosis, and hypoalbuminaemia affects drug binding and therefore the free fraction of active drug.
Jaundice of the sclera and soft palate is a visible marker of advanced disease, and xerostomia is reported by a large proportion of patients with cirrhosis. A study in the Journal of Oral Pathology and Medicine in 2011 found that reduced salivary flow was present in over 60 per cent of patients with decompensated liver disease.
Lichen planus-like lesions have been repeatedly associated with hepatitis C, and a meta-analysis in the Journal of Oral Pathology and Medicine in 2015 reported a pooled odds ratio of approximately 2.5 for the association. Oral examination in a patient with hepatitis C should therefore include careful mucosal assessment.
Gingival bleeding, petechiae, delayed healing and increased caries have all been reported, and a study in the Journal of Clinical Periodontology in 2013 found that patients with cirrhosis had significantly greater periodontal attachment loss than controls.
The most recent liver function tests should be reviewed before treatment, including bilirubin, albumin, alanine aminotransferase and alkaline aminotransferase, together with the model for end-stage liver disease score where available. A study in the Journal of the American Dental Association in 2009 recommended deferring elective treatment when bilirubin was markedly elevated or when the patient had been hospitalised for hepatic decompensation.
Thrombocytopenia from splenic sequestration is common in cirrhosis and is present in a majority of patients with portal hypertension. Prolongation of the international normalised ratio reflects impaired synthesis of clotting factors, and a study in the Journal of Hepatology in 2016 reported that values above 3.5 indicated a substantially increased risk of post-operative bleeding.
Patients should be screened for the international normalised ratio, platelet count and liver function before extraction or periodontal surgery. Local haemostatic measures, including sutures, oxidised cellulose, tranexamic acid mouthrinse and atraumatic technique, should be prepared in advance.
Standard precautions should be applied to every patient, since a substantial proportion of patients with viral hepatitis are unaware of their status. A study in the Journal of Hepatology in 2018 noted that universal vaccination of dental personnel against hepatitis B has reduced occupational transmission to a negligible level.
Eligibility for hepatitis B vaccination should be confirmed for all clinical staff, and post-exposure protocols should be displayed in the surgery.
Paracetamol is the analgesic of choice but the daily dose should be limited in cirrhosis, and a report in the American Journal of Gastroenterology in 2015 recommended a maximum of 2 grams per day in patients with compensated disease. Non-steroidal anti-inflammatory drugs are contraindicated because they increase the risk of variceal bleeding, renal impairment and fluid retention.
Antibiotics that undergo hepatic metabolism, including metronidazole and erythromycin, may require dose reduction, and a study in the British Journal of Clinical Pharmacology in 2014 demonstrated prolonged half-lives for metronidazole in patients with cirrhosis. Consultation with the prescriber or pharmacist is advisable where the choice is uncertain.
Lidocaine is metabolised hepatically, and its half-life is prolonged in liver disease, so the total dose should be reduced. A study in the Journal of Oral Rehabilitation in 2010 recommended limiting the dose to approximately half the usual maximum in patients with severe hepatic impairment.
Articaine is also metabolised by plasma esterases and by the liver, which limits its advantage in this group. Adrenaline-containing solutions should be used cautiously in patients with severe disease and oesophageal varices, but they are generally safe in compensated disease.
Decompensated cirrhosis carries risks of variceal bleeding, encephalopathy and spontaneous bacterial peritonitis, and elective treatment should be deferred until the patient is medically stable. A study in the Journal of Clinical Gastroenterology in 2012 reported that invasive dental treatment during decompensation was associated with a significant increase in hospital admission.
Patients with a liver transplant require immunosuppressive therapy, and ciclosporin is associated with gingival overgrowth in a substantial proportion of patients. A study in the Journal of Periodontology in 2009 reported gingival enlargement in approximately one third of patients taking ciclosporin, and meticulous plaque control reduced its severity.
Immunosuppression increases the risk of infection and of mucosal malignancy, and any suspicious lesion should be referred promptly.
Patients with alcohol-related disease frequently have malnutrition, impaired wound healing and a high prevalence of tobacco and alcohol use. Brief intervention and referral for cessation support should be offered as part of routine care.
Preventive care reduces the need for invasive procedures and should be prioritised in every patient with liver disease. Twice-daily brushing with a soft powered brush such as the BrushO allows effective plaque removal with minimal trauma to gingival tissue that may bleed easily, and it is helpful for patients with tremor or fatigue that compromise manual dexterity.
Regular recall intervals, fluoride application and dietary counselling further reduce the risk of caries and of periodontal deterioration.
Liver disease alters haemostasis, drug handling and immune function, and each of these changes has direct dental implications. Compensated disease usually requires no modification, while cirrhosis and transplantation demand coordinated planning, dose adjustment and meticulous haemostasis. Preventive care delivered consistently is the most valuable intervention a dental team can provide for these medically complex patients.
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