Perioimplantitis

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We welcome all the patients, whether referred by themselves or by our dental colleagues, to prevent and treat their dental implant biological or biomechanical failures.

26/12/2020

Nico Kamosi

Aetiology of dental Implant biomechanical failures.

Implants biomechanical failures include a great deal of arbitrariness and encompasses a large variety of clinical situations, ranging from symptomatic mobile implants to implants showing more than 0.2mm of peri-implant bone loss after the first year of loading (Adell et al, 1986), or bleeding on probing (BOP) from deep pockets (Mombelli & Lang 1998). Clinical failures can be divided into biological failures, mechanical failures, iatrogenic failure, and inadequate patient adaptation due to psychological, aesthetic and phonetic mal-adaptations (Esposito et al. 1998).

The risk of implant failures in the edentulous maxillary cases has been reported to be in excess of mandibular cases by 3 times (Esposito et al. 1998). The inferior quantity and quality of maxillary bone have been associated to the higher failure rate (Adell et al. 1990) and the predictability of implant treatment for partially dentate subjects is better with a failure rate of about half of that for totally edentulous subjects.

Biological failures may be failures to establish osseointegration (early/primary failures) or failures to maintain the achieved osseointegration (late/secondary failures).
Mechanical failures include the failures of the components e.g. fixture fractures, coating, connecting screws and prosthesis.
Iatrogenic failures may be caused by malpositioning of implants, rendering the restoration of implant impossible due to functional, technical and aesthetical complication or may be caused by the violation of the anatomical structure, leading to explantation (Esposito et al. 1998).
Excessive surgical trauma and premature loading (iatrogenic factors) together with impaired healing ability, infection and insufficient bone volume and quality (host-related factors) are believed to be responsible for the early (47%) implant failures, while insufficient jaw volume and bone quality compromising biomechanical capability coupled with overloading (90%), and progressive chronic marginal infection presenting as peri-implantitis (10%) are shown to have the predominant role in the late (53%) implant failures (Esposito et al. 1998).

Biological factors contributing to implant failures can be divided into endogenous (systemic and local) and exogenous (operator-related & biomaterial-related) factors.

Endogenous local factors include bone quality, quantity and anatomical location, bone grafting, para functions & biomechanical loading, local immune response, presence of "adequate" attached keratinized soft tissue, and irradiation therapy (Esposito et al. 1998).
Despite changes in mineral composition, collagen and BMP content coupled with delayed fracture healing resulted from ageing, clinical investigations seem to reject the assumption of the adverse role of age in the implant success (Jemt 1993).

Although there are some clinical situations where the presence of the attached keratinized gingivae may reduce bacterial and possible traumatic induced inflammation, clinical evidence-based data fail to demonstrate a consistent association between the presence of "adequate" attached keratinized mucosa and implant failures (WWP 1996 Berglundh et al. 2018).

Endogenous systemic factors include genetics, the medical status of the patient, and smoking.
At present, there exists inadequate information on the importance of genetic factors on implant survival.
The following adverse nutritional status, general diseases and disorders have been suggested to influence the outcome of the implant treatment: bone metabolic disease (e.g. osteoporosis, osteomalacia, hyperparathyroidism & Paget's disease); rheumatic diseases (e.g. rheumatoid arthritis, Sjogren's disease, systemic lupus erythematosus); hormonal disease (e.g. diabetes, Cushing's syndrome, hyperparathyroidism); lichen Planus, PMN anomalies, delayed hypersensitivity & immunological disorders; and malabsorption syndrome. Patients with Sjogren's syndrome (a chronic autoimmune inflammatory connective tissue disease) suffering from severe xerostomia may be ideal candidates for a fixed implant-supported prosthesis (WWP 1996). The consensus of the proceeding of the world workshop in periodontics (WWP 1996) concluded that compromised medical status of the patient has a negative influence on implant survival.

25/12/2020

Nico Kamosi

Consensus for the strategies involved in the treatment of peri-implantitis are determined by:

Lesion-related factors
- Severity and extent of the peri-implantitis lesion which determines the indication for non-surgical versus surgical approach for successful debridement of the infected implant surface
- Implant location, position, architecture and dimension of the peri-implantitis lesion
- Implant proximity to the adjacent teeth or implants
- The strategic value of the implant within the prosthetic construction
- Number of the adjacent implants & the strategic value of the implant within the arch

Patient-related factors
- The total equilibrium between the cost/time/risk-benefit parameters
- Hygienist access during professional supportive peri-implant treatment or care
- Patient compliance, preference and expectation
- Presence of confounding systemic and local health risk factor
- Patient capability to achieve an efficient self-performed plaque removal

Operator-related factors
- The aim of Survival vs. Success
- The risk assessment for the possible recurrent infection, further bone loss despite the use of systemic antimicrobials adjunctive to surgical debridement.
- Modification of the design and of the prosthetic supra-structure
- Modification of the dimension of the prosthetic supra-structure. (e.g. emergence profile overhang, convexity, interproximal space)
- Explantation & GBR in a view to the provision of the different prosthetic option or future implant
- Osseous re-contouring & APF respective implant surface modification

06/05/2019

“Cell-to-Cell Communication”

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London
W1B1QN

Opening Hours

Monday 8:15am - 5:30pm
Tuesday 8:15am - 5:30pm
Wednesday 8:15am - 5:30pm
Thursday 8:15am - 5:30pm
Friday 8:15am - 5:30pm
Saturday 10:15am - 5pm

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