Chronic Low-Dose Doxycycline as a Treatment for Periodontal Disease in Primates
Abstract
Periodontal disease has been documented in many non-human primate species and is often a progressive condition leading to gingival retraction and tooth loss. Alveolar bone and periodontal tissues are composed of 60–90% collagen, and destruction of this collagen causes periodontal ligament and bone loss. Oral bacteria damage the gingival tissues, but it is the host immune response that triggers a cascade of inflammation involving collagenases, inflammatory products and osteoclasts resulting in collagen loss. Dentists use doxycycline at sub-antimicrobial doses in human patients to modify host immune response, resulting in less inflammation and less bone and periodontal ligament destruction.1 This low-dose doxycycline administration has also been used successfully in great apes, old world monkeys, and prosimians to treat periodontal disease. After dental cleaning and systemic antibiotics as indicated, doxycycline 0.3 mg/kg is given orally twice daily in a pulsatile regimen of 3 months on, 3 months off medication. Doxycycline suspension (10 mg/ml, various flavors and manufacturers) or capsules can be used. Some primates have stayed on the pulsatile regimen chronically without negative systemic effects. A male orangutan has now been treated for 4 years in this manner. Periodontal disease in other primates has resolved, allowing for discontinuation of doxycycline. Ideally, low-dose doxycycline should be initiated prior to gingival retraction and root exposure. Sequential pictures of the gingiva and measurements of periodontal pocket depth will aid in monitoring disease progression. In numerous human studies, low-dose doxycycline has not induced bacterial resistance.2
Literature Cited
1. Golub, L.M., M.E. Ryan and R.C. Williams. 1998. Modulation of the host response in the treatment of periodontitis. Dentistry Today. 17: 102–109.
2. Thomas, J., C. Walker, and M. Bradshaw. 2000. Long-term use of subantimicrobial dose doxycycline does not lead to antimicrobial susceptibility. J. Periodontol. 71:1472–1483.