Dental implant therapy has developed over the past half century to have documented successful outcomes in most patients who receive treatment. The long-term survival of dental implants depends upon a variety of factors including patient, surgeon, restorative dentist, and materials-related factors. The impact of patient-associated factors may impact significantly on the success of dental implants including diabetes mellitus, medications, smoking, parafunctional habits, oral hygiene, head and neck radiation, and the use of bisphosphonates, antiangiogenic, and antiresorptive medications.
Key points
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Patient-related factors may impact upon long-term success of dental implants.
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Medical history must be reviewed to identify potential systemic disease or medications that may affect dental implant success.
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Diabetes mellitus, smoking, radiation, medications, parafunctional habits, oral hygiene, and bisphosphonates may affect dental implant osseointegration.
Introduction
Contemporary dental implant therapy continues to experience major advancements, due to improvements in digital dentistry technology, surgical planning, techniques and protocols, as well as dental implant designs. As a result, the placement of dental implants and prosthetic reconstructions are highly predictable and safe procedures with a mean success rate of approximately 90% at 10 years, with even higher success rates in younger patient populations. Initial short-term implant success depends upon many factors including sufficient hard and soft tissues, adequate prosthetic restorative dimensions, and primary implant stability that allow for improved chances for successful osseointegration. However, long-term outcomes are dependent upon many interrelated biologic and mechanical variables, which include fibrous integration or lack of osseointegration, peri-implantitis, and prosthetic complications such as screw fracture or loosening, prosthetic failure, and implant fracture.
There have been many attempts to simplify and classify implant success criteria since the introduction of implants by Brånemark. Today, one of the most widely used definitions of optimal success was outlined by the International Congress of Oral Implantologists Pisa Consensus Conference in 2008 citing there should be (1) no pain or tenderness upon function, (2) no mobility, (3) less than 2 mm radiographic bone loss from initial surgery, and (4) no history of exudates ( Box 1 ). Additionally, as the primary function of the dental implant is to act as support for prosthetic devices, success criteria also must include evaluation of the implants ability to support a functional prosthesis in the Long-term, with long-term success defined as greater than 7 years. In contrast to successful implant osseointegration, the term implant survival simply means that the implant is still present in the mouth. Also, long-term success should include that the implant is restored prosthetically and functional with speech and mastication. There are a variety of patient-related and systemic factors that may impact upon dental implant survival.
- I.
Success (optimum health)
- a.
No pain or tenderness upon function
- b.
0 mobility
- c.
Less than 2 mm radiographic bone loss from initial surgery
- d.
No exudates history
- a.
- II.
Satisfactory survival
- a.
No pain in function
- b.
0 mobility
- c.
2 to 4 mm radiographic bone loss
- d.
No exudates history
- a.
- III.
Compromised survival
- a.
May have sensitivity on function
- b.
No mobility
- c.
Radiographic bone loss greater than 4 mm (<1/2 of implant body)
- d.
Probing depth greater than 7 mm
- e.
May have exudates history
- a.
- IV.
Failure (absolute or clinical failure)
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Any of the following:
- a.
Pain on function
- b.
Mobility
- c.
Radiographic bone loss greater than 1/2 length of the implant
- d.
Uncontrolled exudate
- e.
No longer in mouth
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Systemic factors related to implant survival
Diabetes Mellitus
Diabetes mellitus is a chronic metabolic disorder causing hyperglycemia, which can lead to microangiopathy and macroangiopathy, decreased immune response, delayed wound healing, and increased periodontitis. Chronic diabetes can lead to a pro-inflammatory state, which dysregulates the coupling of osteoblasts (decreased proliferation) and osteoclasts (increased cell recruitment), and increased receptor activator of nuclear factor kappa beta (RANK) ligand, increased cytokines (IL-1B, IL-6, IL-8, tumor necrosis factor [TNF]-alpha), and prostaglandins (PGE2), all resulting in a cumulative effect of decreased bone formation and increased bone resorption, ultimately resulting in bone loss. These factors all can directly and indirectly impair wound healing and maintenance of healthy bone. Diabetes is not a contraindication to implant placement; however, tight glycemic control is necessary with periodic hemoglobin A1c (HbA1c) monitoring. If there is evidence of patient noncompliance and uncontrolled hyperglycemia, the disease process can greatly impact upon dental implant success. The incidence of diabetes continues to rise, so this patient situation is becoming more commonly encountered, with an estimated 537 million adults affected worldwide in 2021, and there will be an estimated 643 million adult cases of diabetes by 2030. Thus, the relationship between diabetes and implant longevity needs to be well understood by clinicians who place dental implants.
In general, the overall survival of mandibular implants in patients with diabetes has been comparable to healthy patients, with most failures seen within the first year. However, there is a significant increase in the failure rate of maxillary implants in diabetics, where there is poorer bone quality (types III, IV) at baseline. Implants placed in type I diabetics were shown to have a higher risk of implant failure than in type II diabetics. Furthermore, a correlation has been found between increased HbA1c levels and greater marginal bone loss around dental implants. Diabetics have been found to take twice as long to reach initial osteointegration, but implant stability at 1 year is not negatively affected even by poorly controlled diabetes (assessed by HbA1c levels). Overall, the literature about implant survival and diabetes is quite heterogeneous, with many opposing conclusions being drawn. Some studies show a higher implant failure rate in diabetics, while some studies show no effect of well-controlled diabetes on implant survival, and others who show an increased HbA1c (>8.1) are correlated with increased peri-implant bone loss and bleeding on probing. Current consensus can conclude that diabetes can negatively affect long-term survival for diabetics, especially in the maxilla or poorer quality bone sites, and with uncontrolled hyperglycemia (HbA1c), and clinicians should factor in the possibility of poor wound healing and long-term increased marginal bone loss when planning dental implant cases in patients with diabetes.
Medications
Patients take a wide array of medications for many diseases, and in general, the effects of each individual medication on dental implant success are unknown. However, some medications have been evaluated thoroughly and it has been determined that some medications may have negative effects on implant survival.
Selective serotonin reuptake inhibitors (SSRIs) are the most prescribed antidepressant and also have been associated with increased risk of implant failure in multiple recent studies. , Osteoblasts, osteoclasts, and osteocytes all possess serotonin transporters and receptors, which can be targeted by SSRIs, and then impede osteoblast activity, resulting in disrupted bone remodeling and osteoblast differentiation. Implant failures with SSRI are more commonly early failures.
Proton pump inhibitors (PPIs) are one of the most used medications worldwide, used to prevent and treat acid-related conditions of the gastrointestinal system. Prolonged use results in chronic acid suppression in the stomach, which in turn reduces the absorption of vitamins and nutrients, namely B12, iron, calcium, and magnesium. Decreased calcium absorption from PPIs has been linked with increased bone fractures throughout the body and increased risk of dental implant failure (6.8% for PPI users, and 3.2% for nonusers). ,
Vitamin D supplementation has been shown to be beneficial for implant survival, and multiple studies have shown positive results by supplementing vitamin D in postsurgical implant patients to increase implant survival. Vitamin D stimulates osteoclastic activity and causes osteoblasts to produce extracellular matrix proteins, and there is an increased intestinal absorption of calcium. Additionally, low vitamin D levels are correlated with increased infection rates. Osteoporosis has been found not to confer a significant increase in risk for implant failure in multiple studies and meta-analyses, but these patients do demonstrate a significantly increase in marginal bone loss. The literature recommends vitamin D supplementation for patients whose serum levels are not within normal range.
Non-steroidal anti-inflammatory drug (NSAIDs) effects on implant survival are controversial in the literature, with conflicting outcomes, where some studies show more failures and poorer bone healing in the NSAID group, , while others show no difference. There is a lack of human studies on this topic to draw conclusions definitively one way or another; therefore, use of NSAIDs in the perioperative period is controversial. Clinicians should realize that NSAIDs can potentially indirectly inhibit prostaglandins, specifically cyclooxygenase-2 (COX-2), which helps induce new bone formation and is upregulated after bone fractures. Therefore, current recommendations are to avoid NSAIDs post-implant placement, if possible.
Systemic corticosteroids, hormonal replacement therapies, and oral contraceptives are all frequently prescribed medications. Steroids have been linked to reduced bone formation and increased bone resorption throughout the body. Studies have shown direct links between implant failure and use of these medications, regardless of the presence of systemic diseases or if the patient is a smoker or diabetic. Zou and colleagues showed the implant failure rate to be 5 times higher in women taking any steroid medications compared to controls. Steroids have been shown to increase bone resorption that induces inflammatory mediators in the periodontium. This mechanism causes a progression of periodontal disease, affecting both bone breakdown and progression of caries, plaque, and calculus. Even short-term steroid use can cause a significant decrease in type-I procollagen N-terminal propeptide and osteocalcin, both which are markers for bone formation. Additionally, these patients experience an increase in RANK ligand, and decrease in osteoprotegerin that opposes RANK ligand, resulting in increased osteoclast activity and more bone resorption. Dental implant failures in the acute phase are more common with steroid use; however, studies suggest that once osteointegration has occurred, the implant will be less affected by steroid use, and the long-term prognosis is favorable.
Patient-related factors
Smoking
Smoking is a well-known risk factor for long-term implant failure, as well as its negative effects on oral and systemic health, with delayed wound healing, in general. It affects both survival and success of implants, especially in areas of poor-quality bone. Studies have also been able to show a correlation between heavier smoking and a worse overall implant survival. In the acute phase, smokers experience delayed wound healing in part from the vasoconstriction caused by nicotine that decreases blood flow required for tissue healing, especially in sites of limited perfusion like the gingiva. Nicotine, carbon monoxide, and hydrogen cyanide all alter wound healing by decreasing the proliferation of fibroblasts and other reparative cells. Nicotine also increases blood viscosity by increased platelet adhesion. Smoking also upregulates multiple pro-inflammatory cytokines, namely IL-1 and TNF alpha, which cause destruction of surrounding bone. Inhaled smoke also has deleterious effects on the secretory immune function, which can adversely affect maxillary sinus health. Long-term effects linked to poor implant success are decreased osteoblast activity, which causes delayed bone healing and reduces overall bone mineral density. Smokers also have increased peri-implantitis and mucositis, are more resistant to treatments, and have worse clinical outcomes after therapy.
Studies agree that implant failure rates are statistically higher in smokers, with failure risks estimated to be 140% times higher than in nonsmokers, and maxillary implants have worse outcomes than mandibular implants. There is also evidence of a dose effect of smoking where more than 10 cigarettes per day, or greater than 10 pack-year smoking history significantly increases the risk of implant failure. The risk of implant failure and bone loss is further increased in smokers with a history of periodontitis. However, smoking is not a contraindication for dental implants, but smokers should be advised of the risks of continuing to smoke before or after their surgery. The current consensus paper on the effect of smoking and dental implant therapy suggests advising patients to stop smoking completely or consider a nicotine holiday 8 weeks before and after implant placement; but if this is not possible, they should be warned of the increased risk of implant failure and postoperative complications.
Parafunctional Habits (Bruxing/Clenching)
The definition of bruxism has changed overtime and is now defined by an international consensus as a wide range of muscle activities characterized by clenching and grinding of dentition or by bracing or thrusting the mandible. In addition, bruxism can be further classified as sleep bruxism and awake bruxism. The prevalence of awake bruxism is reported to occur in approximately 31% of adults and sleep bruxism is reported to occur in approximately 12% of adults. Occlusal parafunctional habits, such as bruxism, clenching, grinding, and others (eg, gum chewing, nail biting), can lead to various oral complications including temporomandibular joint disorders, headaches, orofacial pain, generalized occlusal wear, fractures, screw loosening, and abutment or implant fracture ( Fig. 1 ). ,
Since parafunctional habits are relatively common, implant placement in patients with such habits might not be avoidable. In addition, an increase in parafunctional habits has been reported, especially in patients who had implants restored with fixed complete dentures. Bruxism has been associated with increased loading of the implants and restorations that can lead to crestal bone loss and ultimately, when not managed properly, to implant failure. Therefore, it is important to understand the correlation between increased occlusal loading in parafunctional habits and decreased implant success.
An osseointegrated implant is essentially ankylosed to the alveolar bone without the support of a periodontal ligament (PDL). Therefore, the lack of proprioceptive protection from the PDL and the potential formation of a fulcrum at the crestal bone position due to ankylosis increase the chances of peri-implant bone loss on application of excessive occlusal forces. This major difference between the natural dentition and dental implants causes a difference in the biomechanical reaction to occlusal load. The natural dentition is surrounded with a PDL that triggers a central nervous system response to the muscles of mastication when excessive or non-axial forces are delivered to a tooth. Implants do not have this protective capability. In addition, the lack of PDL support reduces the capability of detecting excessive loads on implants. A study by Hammerle and colleagues demonstrated that implants had an 8 fold higher threshold for tactile perception when compared to the natural dentition. Forces delivered to the natural dentition tend to be distributed equally; however, in implants, these forces tend to concentrate at the marginal bone level. Therefore, implants have a higher potential to be overloaded leading to peri-implant bone loss, implant failure, and/or prosthetic failure. Large cantilevers, parafunctional habits, and inappropriate occlusal schemes including premature contacts are some of the leading causes of the implant overloading. When the equilibrium of bone deposition and resorption is disrupted by occlusal overload, fatigue-related microfractures may be observed at the bone-implant junction. This micromovement can lead to fibrous integration of the implant and lack of osseointegration.
Systematic reviews have shown an increased risk of implant loading in bruxers, thus increasing the risk of implant failure, prosthetic complications, and even implant fracture. Chrcanovic and colleagues concluded that 5 factors that contribute to the incidence of implant fracture include (1) the grade of titanium, (2) implant diameter, (3) implant length, (4) prosthetic cantilevers, and (5) bruxism.
Three-dimensional finite analysis of the stress generated at the abutment-implant level and the implant-bone level on functional and parafunctional axial and oblique loading demonstrated an increased stress with parafunctional forces, specially at the implant-bone level. The use of an occlusal device demonstrated reduction in stresses at the implant abutment level and a reduction in the mean stress at the implant-bone level for long implants placed at the crestal bone level. Randaelli and colleagues demonstrated in their 3 dimensional finite analysis that placement of implants 2 mm subcrestally reduced stresses at the implant abutment level and the crestal bone.
Since there is an increased risk of complications with implants in bruxers, treatment planning and management of implants in these patients should be carefully considered. The occlusion should be monitored, and the use of occlusal therapy should be reinforced to help reduce the occlusal load on the implants and prosthetics.
Oral Hygiene
Peri-implant adverse tissue reactions to high plaque index have been documented extensively in both animal and human studies. High bacterial load has been shown to affect the peri-implant tissue health and to significantly increase the risk of crestal bone loss. Therefore, proper oral hygiene and maintenance of a low plaque index are crucial for the long-term success of dental implants.
The biologic complications that can affect implant osseointegration can be grouped into 2 clinical presentations: peri-implant mucositis and peri-implantitis. The major difference between the 2 entities is the presence of bone loss in peri-implantitis. Poor oral hygiene is associated with peri-implant mucositis, defined by tissue inflammation specifically redness and edema, and peri-implantitis, associated with progressive bone loss around the implants. When the pattern of progression from peri-implant mucositis to peri-implantitis was observed in a group of 80 patients over 5 years by Costa and colleagues , the incidence of peri-implantitis in patients with regular recall was less than those without regular implant hygiene and maintenance. Peri-implant mucositis is considered a precursor for peri-implantitis; thus, prevention and treatment of peri-implant mucositis are necessary in order to prevent the progression to peri-implantitis. Schwarz and colleagues found strong evidence to indicate an increased risk of peri-implant bone loss in patients with history of chronic periodontitis, poor plaque control, and irregular hygiene and maintenance after implant therapy.
A tailored dental implant maintenance program for patient with peri-implant mucositis or peri-implantitis should be based on their risk assessment and not the standard 6 month recall regimen. The additional use of topical agents has been proven to help improve peri-implant mucositis and to reduce the risk of bone loss. When evaluating outcomes of routine recall with the use of topical agents and oral hygiene, it was found by Ramberg and colleagues that the use of dentifrices with .3% triclosan helps significantly improve periodontal health and microbial outcomes in patient with peri-implant mucositis. In addition, De Sienna and colleagues found the combination of professional maintenance and either 2% chlorhexidine solution or 1% topical gel chlorhexidine application can successfully manage peri-implant mucositis. Other studies have also shown that regular hygiene maintenance, with or without chlorhexidine application, helped to reduce microbial load and improve gingival and periodontal tissue health around dental implants.
Acquired factors related to implant survival
Radiation to the Jaws
The demographics of head and neck cancer have been shifting dramatically over the late 20 years. The patient population affected has become significantly younger, in large part due to the rise in human papillomavirus-related cancers. Many of these patients are treated with primary radiotherapy and chemotherapy with a relatively high survival rate. This has led to an increased population of patients presenting to dental offices with a history of radiotherapy to the jaws, at the same time that there has a large increase in the use of dental implants by dentists and dental specialists.
The effects of radiation on hard and soft tissues can be summarized by the “3 H’s”: hypocellularity, hypovascularity, and hypoxia. The use of dental implants in this radiated patient population is very attractive since some of the most well-known radiation side effects such as xerostomia and compromised mucosal tissues make traditional dentures more difficult to fabricate and more difficult for patients to wear.
Most studies show relatively high rates of implant survivals in patients with head and neck radiation, but all note the potentially devastating complication of osteoradionecrosis (ORN) with increased doses of tumoricidal radiation ( Fig. 2 ). A recent meta-analysis by Schiegnitz in 2022 reported a mean overall survival rate of 87.8% that was a statistically significant higher rate of failure over non-irritated bone ( P >.00001, odds ratio [OR] 1.97, confidence interval [CI] [1.63,2.37]). Other studies also show that dental implant placement into grafted irradiated bone was even more likely to fail than implant placement into native irradiated bone ( P <.0001, OR 2.26, CI [1.50, 3.40]).
