TY - JOUR
T1 - Osteogenesis imperfecta
T2 - Potential therapeutic approaches
AU - Members of the Brittle Bone Disease Consortium
AU - Rousseau, Maxime
AU - Retrouvey, Jean Marc
AU - Bober, Michael
AU - Esposito, Paul
AU - Eyre, David R.
AU - Gomez, Danielle
AU - Harris, Gerald
AU - Hart, Tracy
AU - Jain, Mahim
AU - Krisher, Jeffrey
AU - Nagamani, Sandesh C.S.
AU - Orwoll, Eric S.
AU - Raggio, Cathleen L.
AU - Rush, Eric
AU - Smith, Peter
AU - Tosi, Laura
N1 - Funding Information:
This work was supported by the Brittle Bone Disorder Consortium (BBDC 7701). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Publisher Copyright:
© 2018 Rousseau et al.
PY - 2018
Y1 - 2018
N2 - Osteogenesis imperfecta (OI) is a genetic disorder that is usually caused by disturbed production of collagen type I. Depending on its severity in the patient, this disorder may create difficulties and challenges for the dental practitioner. The goal of this article is to provide guidelines based on scientific evidence found in the current literature for practitioners who are or will be involved in the care of these patients. A prudent approach is recommended, as individuals affected by OI present with specific dentoalveolar problems that may prove very difficult to address. Recommended treatments for damaged/decayed teeth in the primary dentition are full-coverage restorations, including stainless steel crowns or zirconia crowns. Full-coverage restorations are also recommended in the permanent dentition. Intracoronal restorations should be avoided, as they promote structural tooth loss. Simple extractions can also be performed, but not immediately before or after intravenous bisphosphonate infusions. Clear aligners are a promising option for orthodontic treatment. In severe OI types, such as III or IV, orthognathic surgery is discouraged, despite the significant skeletal dysplasia present. Given the great variations in the severity of OI and the limited quantity of information available, the best treatment option relies heavily on the practitioner's preliminary examination and judgment. A multidisciplinary team approach is encouraged and favored in more severe cases, in order to optimize diagnosis and treatment.
AB - Osteogenesis imperfecta (OI) is a genetic disorder that is usually caused by disturbed production of collagen type I. Depending on its severity in the patient, this disorder may create difficulties and challenges for the dental practitioner. The goal of this article is to provide guidelines based on scientific evidence found in the current literature for practitioners who are or will be involved in the care of these patients. A prudent approach is recommended, as individuals affected by OI present with specific dentoalveolar problems that may prove very difficult to address. Recommended treatments for damaged/decayed teeth in the primary dentition are full-coverage restorations, including stainless steel crowns or zirconia crowns. Full-coverage restorations are also recommended in the permanent dentition. Intracoronal restorations should be avoided, as they promote structural tooth loss. Simple extractions can also be performed, but not immediately before or after intravenous bisphosphonate infusions. Clear aligners are a promising option for orthodontic treatment. In severe OI types, such as III or IV, orthognathic surgery is discouraged, despite the significant skeletal dysplasia present. Given the great variations in the severity of OI and the limited quantity of information available, the best treatment option relies heavily on the practitioner's preliminary examination and judgment. A multidisciplinary team approach is encouraged and favored in more severe cases, in order to optimize diagnosis and treatment.
KW - Bisphosphonates
KW - Crowns
KW - Dentinogenesis imperfecta
KW - Genetics
KW - Orthodontic
KW - Orthodontics
KW - Osteogenesis imperfecta
KW - Osteonecrosis of the jaw
KW - Rare bone disease
KW - Surgery
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U2 - 10.7717/peerj.5464
DO - 10.7717/peerj.5464
M3 - Article
AN - SCOPUS:85051823552
SN - 2167-8359
VL - 2018
JO - PeerJ
JF - PeerJ
IS - 8
M1 - e5464
ER -