title: Osseointegration of titanium, titanium alloy and zirconia dental implants: current knowledge and open questions.
abstract: Bone healing around dental implants follows the pattern and sequence of intramembraneous osteogenesis with formation of woven bone first of all followed later by formation of parallel-fibered and lamellar bone. Bone apposition onto the implant surface starts earlier in trabecular bone than in compact bone. While the first new bone may be found on the implant surface around 1 week after installation, bone remodeling starts at between 6 and 12 weeks and continues throughout life. Bone remodeling also involves the bone-implant interface, thus transiently exposing portions of the implant surface. Surface modifications creating micro-rough implant surfaces accelerate the osseointegration process of titanium implants, as demonstrated in numerous animal experiments. Sandblasting followed by acid-etching may currently be regarded as the gold standard technique to create micro-rough surfaces. Chemical surface modifications, resulting in higher hydrophilicity, further increase the speed of osseointegration of titanium and titanium-zirconium implants in both animals and humans. Surface modifications of zirconia and alumina-toughened zirconia implants also have an influence on the speed of osseointegration, and some implant types reach high bone-to-implant contact values in animals. Although often discussed independently of each other, surface characteristics, such as topography and chemistry, are virtually inseparable. Contemporary, well-documented implant systems with micro-rough implant surfaces, placed by properly trained and experienced clinicians, demonstrate high long-term survival rates. Nevertheless, implant failures do occur. A low percentage of implants are diagnosed with peri-implantitis after 10 years in function. In addition, a low number of implants seem to be lost for primarily reasons other than biofilm-induced infection. Patient factors, such as medications interfering with the immune system and bone cells, may be an element contributing to continuous bone loss and should therefore be monitored and studied in greater detail.
authors.forename: Dieter D
authors.initials: DD
authors.lastname: Bosshardt
authors.forename: Vivianne
authors.initials: V
authors.lastname: Chappuis
authors.forename: Daniel
authors.initials: D
authors.lastname: Buser
mesh_terms: D016301:Alveolar Bone Loss / Q000209:etiology; D000818:Animals; D016723:Bone Remodeling / Q000502:physiology; D000069343:Bone-Implant Interface; D003722:Dental Alloys / Q000737:chemistry*; D003758:Dental Implantation, Endosseous; D015921:Dental Implants; D017267:Dental Prosthesis Design; D006801:Humans; D016348:Osseointegration / Q000502:physiology*; D057873:Peri-Implantitis / Q000209:etiology; D012307:Risk Factors; D013499:Surface Properties; D014025:Titanium / Q000737:chemistry*; D014945:Wound Healing / Q000502:physiology; D015040:Zirconium / Q000737:chemistry*
chemical_list: D003722:Dental Alloys; D015921:Dental Implants; D015040:Zirconium; D014025:Titanium; C028541:zirconium oxide