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Implications of bisphosphonate calcium ion depletion interfering with desmosome epithelial seal in osseointegrated implants and pressure ulcers.
Journal article

Implications of bisphosphonate calcium ion depletion interfering with desmosome epithelial seal in osseointegrated implants and pressure ulcers.

  • Touyz LZG Department of Periodontics, Faculty of Dentistry, McGill University, Montreal, QC H3A 0C7, Canada. Electronic address: Louis.Touyz@mcgill.ca.
  • Afrashtehfar KI Division of Oral Health and Society, Faculty of Dentistry, McGill University, Montreal, QC H3A 1G1, Canada; Department for Reconstructive Dentistry & Gerodontology, School of Dental Medicine, Faculty of Medicine, University of Bern, Berne 3010, Switzerland.
  • 2017-09-17
Published in:
  • Medical hypotheses. - 2017
BRONJ
Bisphosphonates
Calcium
Dental implants
Epithelial attachment
Hemidesmosomes
Osseointegration
Osteonecrosis
Osteoporosis
Pressure ulcer
Titanium
Wound healing
Bisphosphonate-Associated Osteonecrosis of the Jaw
Bone Density Conservation Agents
Calcium
Desmosomes
Diphosphonates
Epithelium
Female
Humans
Male
Models, Biological
Osseointegration
Osteoporosis
Pressure Ulcer
English Osteoporosis (OP) is a global bone disease prevalent in aging in humans, especially in older women. Bisphosphonates (BPs) are commonly used as therapy for OP as it influences hard and soft tissues calcium metabolism. Mucosal and dermal ulceration with exposure of underlying bone arises from incomplete epithelial recovery due to reduced desmosome formation deriving from lack of available calcium. Pathological situations such as bisphosphonate-related osteonecrosis of the jaw have been described. This hypothesis states other situations which demand intact functional desmosomes such as healing skin over chronic pressure points leading to pressure ulcers (as well-known as bedsores, pressure sores, pressure injuries, decubitus ulcers), and hemidesmosomes such as epithelial seals in contact with titanium surfaces will have a higher prevalence of breakdown among patients being treated with BPs. This may be proven through the diminished modulation of calcium ions due to BPs, and its effect on the formation of intercellular gap junctions.
Language
  • English
Open access status
closed
Identifiers
Persistent URL
https://roar.hep-bejune.ch/global/documents/178430
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