PERI- IMPLANTITS

 

INTRODUCTION

 

Dental implants have become a critical necessity for replacement of lost natural teeth in modern times. Although implants are considered to be a predictable treatment option, peri‑implant diseases do occur, posing significant challenges for both – the clinician and patient.Implant success is only defined as a short‑term effect that is, whether the implant has osseointegrated or not and whether it is able to support a restoration following its placement. There are no proper guidelines that define implant success or maintenance over a long‑term, except for implant survival. In the last decades increasing evidence raised on the presence of peri-implant inflammations representing one of the most frequent complications affecting both the surrounding soft and hard tissues which can lead to the loss of the implant.

 

The term “peri‑implantitis” was introduced to describe an inflammatory process caused by microorganisms affecting the supporting tissues around an osseointegrated implant in function, resulting in a loss of alveolar bone.Peri‑implant diseases include peri‑implant mucositis and peri‑implantitis.

Peri‑implant mucositis is similar to gingivitis and is defined by the presence of an erythematous peri‑implant mucosa, bleeding on probing and a pocket with a probing depth of < 4 mm.  Peri‑implantitis is synonymous to periodontitis and is defined by the presence of bleeding on suppuration, a pocket with a probing depth of > 4 mm, and a saucer‑shaped bone loss which can be observed on a radiograph or up on opening a flap.

 

ETIOLOGY OF PERI‑IMPLANTITIS

The presence of bacterial biofilms has been noted in numerous experimental and clinical examinations as the primary etiological factor for the development and progression of peri‑implant infections.

Additional risk factors include:

• Smoking

• Interleukin‑1 (IL‑1) genotype polymorphism

• History of periodontitis

• Lack of compliance

• Systemic diseases ‑ diabetes mellitus , immunosuppression, cardiovascular diseases

• Iatrogenic causes

• Lack of keratinized gingiva

• Previous history of failed implants.

 

MICROBIOLOGICAL AND IMMUNOLOGICAL FACTORS

 

The peri‑implant infections have the microbiota very similar to that found in the periodontal disease. Subgingival biofilms in peri‑implantitis have been found to exhibit greater bacterial diversity with the presence of Porphyromonas gingivalis, Prevotella intermedia, Prevotella nigrescens, and Aggregatibacter actinomycetemcomitans. Apart from these, other species such as Staphylococcus aureus, enteric bacilli, and Candida albicans have also been detected. These microorganisms secrete higher levels of both lactoferrin and elastase which result in site‑specific inflammatory changes in the soft tissues surrounding oral implants, and it may lead to their progressive destruction (peri‑implantitis) and ultimately to implant failure. The apical extension of the inflammatory cell infiltrate in peri‑implantitis lesions is more prominent and in most cases located further apical of the pocket epithelium and comprised a greater proportion of neutrophils and macrophages when compared with periodontitis lesions. Lymphocytes and plasma cells are pronounced in both types of lesions. Fibroblasts in peri‑implantitis lesions exhibit a discrete cytokine profile that contribute to matrix breakdown.These features of peri‑implantitis imply a more acute inflammatory response when compared with periodontitis.

 

Reducing the inflammatory response may be an effective way to prevent the tissue destruction caused by the peri‑implant disease. It has been recognized that during the inflammatory process, inflammatory mediators such as prostaglandin E2 and other arachidonic acid metabolites are responsible for bone resorption and periodontal disease. There are development of topical administration forms such as gels, toothpastes, and rinses which contains nonsteroidal anti‑inflammatory drugs (NSAIDs) that can be useful to manage failing implants.

 

 

 

DIAGNOSIS OF PERI‑IMPLANTITS

Diagnostic procedures used with implants need to be sensitive so that early signs and symptoms of infection can be detected and intervention initiated before substantial bone loss occurs.  The parameters to be assessed include:

• Peri‑implant probing‑A rigid plastic probe is ideal for probing. The soft tissue cuff around an implant in a model has been shown to be about 3–3.5 mm and the connective tissue attachment of 1–1.5 mm.

• BOP: It has been shown that it is not a reliable predictor for progression of periodontal disease, instead its absence is a much better predictor for stability.

• Mobility: Implant mobility is an indication of lack of osseointegration, but it is of no use in diagnosing early implant disease, rather it shows the final stages of de‑integration. Periotest or RFA can be used to assess the stability of an implant.

• Radiography: Bone loss is a definite indicator for peri‑implantitis. The distance from implant shoulder to the alveolar bone crest is a reliable parameter providing the radiographs are properly standardized.

 

CLASSIFICATION OF PERI-IMPLANTITIS (Forum and Rosen, 2012)

 

1.      Early : PD ≥ 4mm ( bleeding and / or suppuration on probing ) ; bone loss < 25% of the implant length

2.      Moderate : PD ≥ 6mm (bleeding and / or suppuration on probing ) ; bone loss  25% to 50%  of the implant length

3.      Advanced : PD ≥ 8mm (bleeding and / or suppuration on probing ) ; bone loss > 50%  of the implant length

 

PREVENTIVE MEASURES

Prevention of peri-implantitis should start at treatment planning itself. An elective supportive implant therapy program must be planned prior to treatment that constitutes meticulous oral hygiene practices, careful peri-implant examination, reducing  any associated risk factors and periodic removal of microbial deposits from the implants. A patient centered recall program of

supportive implant therapy must be followed with a minimum of 3-6 months recall interval, can help return the mucosa to a  healthy state and continue to maintain its health to prevent the development of peri-implantitis. During recall when probing, plastic, graphite, nylon instruments should be used instead of metal with minimal probing force to prevent damage to the peri-implant soft tissue cuff and implant surface. Loss of the titanium oxide layer present on the implant surface leads to surface roughness and corrosion that acts as a site for plaque accumulation.

To prevent or minimize plaque accumulation around the implant site novel techniques of controlled localized delivery of antibiotics and systemic antibiotics are being researched

 Chitosan gold nanoparticles (Ch-GNPs) a gene delivery material can be used to carry anti-inflammatory peroxisome proliferator activated receptor gamma molecules (PPARγ cDNA) into the required areas of the implant surfaces, thus aiding to inhibit inflammation and promote osteoblast function. Titanium implant surface with zinc oxidehydroxyapatite nanoparticles or an erythritol  chlorhexidine combination or engineered chimeric peptides or a multilayer coating with AMPCol or disinfecting the surface  with titanium brush and photodynamic therapy, is used to prevent the formation of a biofilm.

Newer oral hygiene aids are being introduced to maintain optimal periodontal health. Water irrigation units are found to be beneficial in implant maintenance.  Plastic ultrasonic scalers and curettes must be used to remove hard deposits on the implant surface. Air polish systems using hydroxylapatite/tricalcium phosphate as a medium is least abrasive and found to remove plaque without altering the surface of the implant.

 CONCLUSION

Implant treatment is often the choice for the replacement of missing or failing teeth. High success rates have been reported, and the recent observations of an increased rate of peri-implant disease must be addressed. The peri‑implant disease is biofilm based and relies on the host inflammatory response for its manifestation. The inflammatory response in peri‑implant disease is acute leading to a wide area of tissue destruction within a short period of time. Proper understanding of the biology of healing is fundamental to safe practice of implant dentistry. Implant maintenance with regular periodic recalls is critical for preventing peri‑implant disease and for ensuring the long‑term success of implant‑supported restorations.

 

                                                                                                            Dr. Anjusha Sharda