periimplantitis.pptx. .

Periimplantitis

1. PERI-IMPLANTITIS ~ Zoya Shaikh 3 rd year B.D.S

2. Dental implant and implant failures Dental implant (also known as an endosseous implant or fixture) is a prosthesis that interfaces with the bone of the jaw or skull to support a dental prosthesis such as a crown, bridge, denture, or facial prosthesis or to act as an orthodontic anchor. Implant failure causes : Early - Overheating, contamination and trauma during surgery, poor bone quantity and/or quality, lack of primary stability, and incorrect immediate load indication Late - Periimplantitis , occlusal trauma, and overloading A dental implant is considered to be a failure if it is lost, mobile, or shows peri-implant bone loss of greater than 1.0 mm in the first year

3. Differences between... Peri -implant mucosa Direct bone-to-implant contact Subepithelially more collagen fibers and less fibroblasts/vessels Parallel collagen fibers in relation to implant surface Physiological periodontium Anchoring system of root cementum, alveolar bone and desmodontic fibers Subepithelially more fibroblasts and vessels Dentogingival , dentoperiostal , circular and transseptal fiber orientation

4. Desmosomes and hemidesmosomes of epithelium and junctional epithelium (biological width) are linked with the contact surface

5. Etiology Multi factorial, poly-microbial anaerobic infection Microbial biofilm: Prevotella intermedia, Prevotella nigrescens , Streptococcus constellatus , Aggregatibacter actinomycetemcomitans , Porphyromonas gingivalis , Treponema denticola  and  Tannerella forsythia Staphylococcus aureus  appears to play a predominant role for the development of a peri- implantitis ,  according to the results of  Salvi et al This bacterium shows a high affinity to titanium .   Smoking  History of periodontitis. Lack of compliance and limited oral hygiene (including missing checkups ). Systemic diseases (e.g. maladjusted diabetes mellitus, cardiovascular disease, immunosuppression) and drug therapies, which inhibit bone modulations Iatrogenic causes (FBR) Soft tissue defects or poor-quality soft tissue at the area of implantation (e.g. lack of keratinized gingiva). History of one or more failures of implants In a study by  Ver   vaeke et al.  maxillary implants were at a significantly higher risk for peri-implant bone loss compared to mandibular implants

6. Pathogenesis Formation of salivary pellicle consisting of salivary proteins and peptides
Initiation of bacterial colonization
The high-molecular-weight mucins , salivary α-amylase, and proline -rich glycoproteins.(salivary pellicles on titanium ) nonmotile coccoid cells and gram negative spirochetes
mediates microorganisms’ adhesion. 
Cement and titanium particles take part in the breakdown of the established equilibrium. 
As a response to this triggering factor,(FBR) complement and macrophages become activated and upregulate osteoclastic activities leading to marginal bone loss.  Peri-implant bony lesions usually follow a typical crater shape rather than the atypical periodontal bone loss. 

7. Peri -implant mucositis and peri-implantitis Peri implant mucositis : An inflammatory lesion of the peri -implant mucosa in the absence of continuing marginal bone loss beyond biological remodelling. It can be reversed through treatment Peri implantitis : An irreversible, destructive Inflammatory process affecting the soft and hard tissues around Osseo integrated implants, leads to the formation of a peri-implant pocket, decreased Osseo integration and marginal bone loss with purulence.

8. Features and diagnosis Bleeding and suppuration on probing
Swelling and hyperplasia of the peri-implant tissues
Pain, if present, is usually associated with an acute infection . Increased probing depth (PD) compared to the initial or baseline examination A bad taste in the mouth.
Loosening of the implant.

9. Biomarkers in peri-implant crevicular fluid (PICF)[ proinflammatory cytokines (IL-1 β, TNF α, MMP-8) ] and GCF  (MMP-8, MMP-9, Osteoprotegerin , C-reactive Protein and IL-1 β) show promising results in regard to their diagnostic and prognostic value. Since RANKL and OPG are key factors regulating bone metabolism, it is likely they are involved in alveolar bone destruction in PI Metabolomic analysis, mass spectrometry and nuclear magnetic resonance spectroscopy show promise. In the absence of initial radiographs and probing depths, radiographic evidence of bone loss of ≥3 mm and/or probing depths ≥6 mm in conjunction with profuse bleeding fits the definition for PI. Radiographically a typical crater shape rather than the atypical periodontal bone loss is seen cervically . Apical portion is still osseointegrated

10. Treatment

11. References Shafers textbook of o ral pathology https://onlinelibrary.wiley.com/doi/10.1111/j.1600-0757.1998.tb00124.x https://pmc.ncbi.nlm.nih.gov/articles/PMC3612185/ https://pmc.ncbi.nlm.nih.gov/articles/PMC7536094/ https://head-face-med.biomedcentral.com/articles/10.1186/1746-160X-10-34 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7536094/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612185/ The end