Asthma & COPD (chronic respiratory disease)

Oral health effects

• Oral thrush from inhaled steroids (oropharyngeal candidiasis)

  Fungal overgrowth, typically Candida albicans, in the mouth/oropharynx is a well-documented adverse effect of inhaled corticosteroid (ICS) therapy used for both asthma and COPD.

  Mechanism: ICS particles deposit on oral/oropharyngeal mucosa during inhalation and cause local immunosuppression, allowing Candida overgrowth; risk rises with higher ICS dose and poor inhaler technique.

  Clinical management: Rinse mouth with water and spit after each ICS dose, use a spacer device, ensure good denture/oral hygiene, and treat candidiasis if it develops.

• Xerostomia (dry mouth)

  Reduced salivary flow occurs both as a disease-related change in saliva composition and as a side effect of beta2-agonist and anticholinergic bronchodilators/ICS.

  Mechanism: Asthma alters stimulated salivary components; beta2-agonists and anticholinergic bronchodilators further reduce salivary flow.

  Clinical management: Frequent water sipping, saliva substitutes, topical fluoride, and rinsing after inhaler use.

• Increased dental caries and erosion risk

  More severe asthma/COPD is associated with greater risk of dental caries and erosion, linked to reduced salivary flow, acidic dry-powder inhaler residue, and behavioral factors.

  Clinical management: Fluoride varnish/rinses, dietary counseling, and more frequent recall for at-risk patients.

• Gingival inflammation and periodontal disease

  Asthma itself, independent of medication, is associated with a higher risk of gingival inflammation, and more severe disease correlates with greater periodontal disease risk.

  Clinical management: Reinforce oral hygiene instruction and periodontal maintenance as part of routine asthma/COPD care.

• NSAID/aspirin hypersensitivity (aspirin-exacerbated respiratory disease)

  A subset of asthma patients, often with nasal polyps/chronic rhinosinusitis, develop acute bronchospasm, rhinorrhea, and wheezing within 30 minutes to 3 hours of taking aspirin or other COX-1-inhibiting NSAIDs.

  Mechanism: COX-1 inhibition shifts arachidonic acid metabolism toward overproduction of cysteinyl leukotrienes, triggering respiratory reactions.

  Clinical management: Avoid COX-1-inhibiting NSAIDs (ibuprofen, naproxen, diclofenac, ketorolac) for dental pain in these patients; acetaminophen under 1,000 mg or selective COX-2 inhibitors are safer alternatives. Take a thorough respiratory/allergy history before prescribing analgesics.