Dr. Darko Veljanovski, Oral Surgeon
When dental implants came into our lives as dentists and patients, it seemed that they were the perfect solution for every and any case. An opinion of “ you do not need to take care of your own teeth, you will have implants placed when you lose them, or even: take out your healthy teeth and replace them with implants” was adopted. It seemed that implants are a panacea. It seemed they could last forever and cause no problems. But nowadays we know the truth is different. We are aware that implants are a viable treatment solution for many clinical cases, with a high survival rate more than 95 percent. However, survival rate is not a synonym for success rate. Osseointegration, the primary biologic goal of implants is not considered as the one and only parameter of success anymore. Bone and soft tissues condition along with aesthetics come into first place when it comes down to implant success ratings. Problems associated with implants do occur in clinical practice.
One of the main problems of the modern implant dentistry are the periimplant diseases: periimplant mucositis and periimplantitis.
Peri-implant mucositis defines the presence of inflammation in the soft tissue surrounding a dental implant without signs of any loss of supporting bone. Periimplantitis is a destructive inflammatory process affecting both soft and hard tissues around dental implants.
Periimplantitis is often referred to as a “ time bomb” since its clinical onset is quiet, appears within a time frame of years after implant placement and often has not distinctive symptoms. Moreover, the increasing number of implants placed worldwide every year makes it inevitable for us to be seeing more and more implant-associated problems. Are we (dentists and patients) really sitting on a “time bomb”?
I find this term very interesting so I took the liberty of naming this article after one of the Stanley Kubrick’s famous movies “Dr.Strangelove or….”
From a clinical standpoint, periimplant mucositis is characterized with bleeding on probing and/or suppuration, probing depth values of 4mm or more, without radiographic signs of bone loss apart from periimplant bone remodeling. It is completely reversible if treated effectively. Periimplantitis, on the other hand, presents with clinically and radiographically evident progressive circumferential periimplant bone loss.
Etiology and pathogenesis
Periimplant diseases are a result of two components: periimplant tissues, which have specific anatomy and presence of bacterial biofilms( Zitzmann, Berglundh, 2008). Let us take a closer look at both.
Bacterial biofilms are layers of bacteria present in the oral cavity that populate periimplant tissues and are similar to those around teeth. Apart from osseointegration upon implant placement, “ bacterial integration” as a phenomenon occurs. Bacteria love titanium and they form biofilms around implants. The oral cavity has millions of of bacteria.
What bacteria will be present in bacterial biofilms depends on four factors:
1.Remaining teeth and their periodontal status
2.Sulcus anatomy around implants
4.Fitting of components
Bacterial biofilms around implants with periimplant disease have approximately 60 times larger counts of bacteria, less cocci, more gram negative and anaerobic bacteria compared to healthy periimplant biofilms. They are very similar to bacterial biofilms found in chronic periodontitis.
B.Anatomy of periimplant tissues
Periimplant tissues have several specifics compared to natural teeth.
1.Biological width that forms around implants with its horizontal and vertical component consists of junctional epithelium and connective tissue and measures around 2mm, same as in teeth. Its function is protective. Another important parameter is dentogingival complex, which adds the measure of gingival sulcus to the biological width and can be objectively measured with a perio probe. Its measures are always bigger around implants because of the orientation of the longitudinal periimplant collagen fibers.
2. Collagen fibers. The difference is that collagen fibers from the surrounding connective tissue do not attach to implants. The dentogingival and alveologingival attached fibers are absent around implants and the fibers run parallel to implant surface which make their sulcus deeper and more vulnerable.
3. Connective tissue around implants has more collagen fibers (85 % vs. 60%), less fibroblasts (1-2% vs. 5 – 10%) than in teeth and is similar to scar tissue.
4.Implants have no periodontal ligament. Osseointegration is a direct structural and functional link of implants and bone. Buser et al. (2015) have pioneer in vivo animal studies in developing periodontal ligaments around implants.
5. Less blood supply. Compared to teeth, the blood supply from periodontal ligament lacks, there is only blood supply from supraperiosteal vessels.
6. Implants are not teeth Periimplant diseases are a result of the response of periimplant structures to bacterial biofilms. This result has a prevalence of 50% for periimplant mucositis and 12-43% for periimplantitis. Regarding the pathogenesis of periimplant diseases, these are important issues to consider.
1.Is the response of periodontal and periimplant tissues to bacterial biofilms the same? No, since periimplant tissues are less effective against bacterial infiltration than periodontal tissues.
2.Do periimplant mucositis lesions differ from peridontal gingivitis lesions?
No, there are no fundamental differences in terms of clinical features and pathogenesis (Lang et al. 2011).
3. Do periimplantitis lesions differ from peridontitis lesions? Yes, they have significant histopathological differences although they are clinically similar (Berglundh et al. 2011).
Periimplantitis research has several limitations:
1. The studies are mostly on animals due to ethical reasons
2. The data on humans is poor and limited to perimplantitis therapy
3. It is controversial if periimplantitis is a true disease or periimplant reaction
The risk factors for developing periimplantitis are divided into 4 groups based on the evidence about their association with periimplantitis: (Heitz-Meyfield, 2008)
1. Risk factors with clear evidence of association:
-Poor oral hygiene: patients with poor oral hygiene have 14.3 times higher risk for periimplantitis (dose dependant relation: more biofilm, higher risk)
2. Risk factors with limited evidence of association:
-Diabetes ( poor metabolic control, prevalence of 64.6% for periimplant mucositis and 8.9 % for periimplantitis – in only few studies)
-Alcohol consumption (only one study to support the link between intake of average 10 g of alcohol per day together with poor oral hygiene and periimplantitis
3. Risk factors with limited and controversial evidence of association:
-Genetic traits (interleukins relation research)
-Implant surface ( rough surface more prone to periimplantitis than smooth and moderate surfaces)
4. Other factors with no evidence:
-Patient related factors: diseases affecting neutrophils, osteoporosis
-Environmental and acquired factors: stress, radiotherapy, chemotherapy, and bisphosphonate therapy
-Clinical and microbiological factors: lack of keratinized tissue, prosthesisrelated factors (hygiene, implant position)
-Detection of specific bacteria
The recommendations from the 6th European Workshop for Periodontology suggest “further research to validate the most plausible putative risks for periodontitis:
1.History of treated and/or current periodontitis
3.Smoking and other subject – related factors
4.Local factors such as malpositioning of implants (within the basal bone, interimplant, implant-tooth), lack of cleansibility of the reconstruction, excess cement and implant surface characteristics
The treatment goals of periimplant mucositis are:
1.Disruption of bacterial biofilms
2.Reduction of pathogenic bacteria
3.Favour conditions for health-compatible biofilms
They can be achieved with mechanical and chemical debridement.
Mechanical non-surgical therapy enhanced with antimicrobial rinses is an effective treatment modality for periimplant mucositis.
Periimplantitis therapy can be divided into nonsurgical and surgical.
Nonsurgical therapy includes:
Surgical therapy includes:
1.Access surgery for mechanical and chemiical debridement
2.Resective surgery (apically positioned flap with or without implantoplasty)
3.Regenerative surgery (different approaches)
( Claffey et al, 2008)
Surgical treatment of periimplantitis and its scientific viability has several limitations:
1.Limited number of studies
2.Low quality studies: no control, no randomization
3.Heterogeneity: non comparable studies
5.Animal studies with periimplant ligatures
6.Different implants, different surfaces
This brings us to one word: prevention.
Today, the reference treatment for periimplantitis is to prevent its onset. Long term success of implant therapy is based on prevention of periimplant diseases.
But, is prevention easier in dental implants with an adequate width of keratinized tissue?
To answer this question, we have to be aware that:
1.Periimplant tissues are less effective in fighting against bacterial biofilms.
2.Limited (less than 2mm or absent keratinized tissue) may be associated with poorer biofilm control and inflamation
3.Sites with limited or absent keratinized tissue may be more prone to mucosal soft tissue recessions and/ or attachment loss
4.Additional evidence is expected from studies about soft tissue augmentation around implants
What is the conclusion?
Dental implants frequently suffer from periimplant diseases and no predictable treatments of periimplantitis are available. Therefore, the best strategy today is prevention. Prevention is possible only with good planning. So if we, the dentists, plan well – we can sleep well. This is the only way to ““stop worrying and love the bomb”.