Periodontics: Implant Complications and Maintenance Issues

By Jim Yuan Lai, DMD, MSc(Perio), FRCD(C) and Francine Albert, DMD, MSc(Prosth), FRCD(C)

The high predictability and long-term success of implant therapy has been well documented (Adell 1981, Albrektsson 1986). Complications do arise, as it may be the case after any Prosthodontic or Surgical procedure. In recent years, a number of authors have specifically looked at implant related complications and maintenance requirements.

Once osseointegration is established, complications can be divided into biological and mechanical ones. The literature has reported biological complications which may include adverse soft tissue reactions, sensory disturbances, progressive marginal bone loss and loss of integration. Mechanical complications may include fractures or loosening of components in the system. Thorough understanding of the etiology and the frequency of these complications is lacking due to the failure of establishing standardized methods of data collection.

Regular recall examination for patients with dental implants may minimize or prevent such complications. They generally include an evaluation of patient satisfaction, oral hygiene compliance, occlusal harmony, implant and prosthesis stability, overall soft and hard peri-implant tissue health and radiographic follow-up (Jovanovic, 2002). The purpose of this paper is to review the main complications related to implant therapy with the purpose of bringing attention to general biological and mechanical factors related to implant success.


Soft tissue reactions

To monitor and maintain the health of the peri-implant tissue, one must first have an understanding of the anatomy and diseases that exist around teeth and implants.

The supra-crestal soft tissue attachment around a tooth is comprised of epithelial and connective tissue attachment. Hemidesmosomes connect the Junctional Epithelium to the tooth surface and apical to the epithelial layer, the gingival fibers perpendicularly insert into the cemented layer (Fig. 1).

Around the root of a tooth, the periodontal ligament is a fibrous connective tissue structure, with neural and vascular components, that joins the cementum to the alveolar bone. Collagen fiber bundles originate from the mineralized surfaces (Sharpey’s fibers) and join up with adjacent fibers to produce a meshwork of interconnected fibers oriented between bone and cementum. The thickness of the periodontal ligament varies from 100m to 400m with a mean around 200m.

On the other hand, for dental implants, due to the absence of a cementum layer, a soft tissue attachment does not truly exist. It is mainly a peri-implant soft tissue seal. The junctional epithelium attaches to the implant surface via hemidesmosomes, but the gingival fibers do not insert into the implant. Instead, these collagen fiber bundles originate from the bone surfaces and run mainly parallel to the implant surface (Berglundh 1991, Listgarten 1992; Fig. 2). Instead of a periodontal ligament, there is intimate contact of bone with implant titanium surface at the light microscopic level. Consequently, the space between the implant and bone is less than 10m.

The pathogenesis of inflammatory periodontal diseases (gingivitis and periodontitis) around teeth is well documented. In gingivitis, the presence of bacterial plaque induces pathological changes resulting in gingival inflammation without any clinical attachment loss. Gingivitis is a reversible disease with the elimination of etiologic factors. Periodontitis is inflammation of the gingiva and the adjacent attachment apparatus. It is characterized by loss of periodontal ligament, disruption of the attachment to cementum, and resorption of the alveolar bone. Although many factors (eg. environmental, genetic and systemic) contribute to the pathogenesis of periodontitis, it is widely accepted that the presence of bacterial pathogens is required for initiation and progression of the disease.

Many studies have investigated if similar diseases exist around implants. Peri-implant mucositis has been defined as reversible inflammation of soft tissue surrounding implants in function and peri-implantitis as an inflammatory reaction with loss of supporting bone in the tissues surrounding a functioning implant (Albrektsson and Isidor 1994).

In comparison of gingivitis and peri-implant mucositis, studies have demonstrated a similar response on the effect of bacterial plaque to the peri-implant mucosa as in the gingiva around natural dentition (Berglundh 1992, Ericsson 1992). Pontoriero (1994) allowed plaque to accumulate around implants and teeth for 3 weeks and found a correlation between plaque accumulation and peri-implant mucositis (or gingivitis) and a similar response of the soft tissues around teeth and implants when exposed to plaque (Fig. 3).

On the other hand, the evidence is not clear as to whether peri-implantitis is similar to periodontitis. Studies have shown that the pathogens involved in peri-implantitis and ligature-induced experimental models are the same species involved in periodontitis. However, these studies do not demonstrate that colonization of these periodontal pathogens actually initiate disease. It is uncertain if the presence of these pathogens is the cause or the result of implant instability. (Ellen, 1998) Clinically, patients with refractory periodontitis that received implants had a high success rate and did not exhibit any signs of peri-implantitis (Nevins, 1995). Furthermore, there is no cementum layer where contamination by the pathogens and their toxins can occur and implants are not prone to subgingival calculus formation (Ellen, 1998).

Because there is no interlocking or penetration of the deposit with the implant surface and the absence of cementum, the calculus is readily removed from implants. Light lateral pressure is only required. Gauze, flosses, yarns or tapes used in a “shoe-shine rag” fashion can be used to remove deposits. However, stainless steel or carbon steel instruments and ultrasonic or sonic devices with metal tips are to be avoided since they will create roughen surfaces on implants, which will favour plaque accumulation and calculus formation (Thomson-Neal, 1989, Meschenmoser, 1996). Instead, instruments that are fabricated with materials that are softer than the implant material should be used. These instruments are either plastic instruments or may contain graphite fillers (Figs. 4 & 5).

Because of the difference in anatomy and disease around implants, the traditional clinical periodontal parameters of probing depth and attachment level do not necessary correlate with active or imminent peri-implant bone loss (Koka, 1998). The tip of a periodontal probe displaces the junctional epithelium as well as the connective tissue in a lateral direction (Ericsson and Lindhe, 1993, Fig. 6).

Measurement of probing depths and attachment levels around teeth determines attachment loss, but since a true connective tissue attachment is not present in implants, these measurements do not have relevance in monitoring disease activity around implants.

Soft tissue hyperplasia is a common complication in the implant patient population. Likely causes are chronic irritation, poor oral hygiene and gaps between components caused by loose abutment screws or framework (Tolman & Laney, 1992). The question of whether attached mucosa at the peri-implant cuff is required for healthy function has been discussed by various authors. It seems that its role is of less importance than was previously believed. Furthermore, there is no correlation between soft tissue changes and the maintenance of osseointegration (Zarb & Schmitt, 1996). Soft tissue complications can usually be resolved conservatively. Removal of a fixed prosthesis at a recall appointment may be necessary to provide access for adequate treatment (Fig. 7).

Sensory Disturbances

Sensory disturbances are potential complications following implant surgery. The available data suggests that this phenomenon is fairly uncommon and seems transient in the majority of implant patients. In a study by Walt
on, approximately 24% of subjects reported altered sensation in the short-term after implant surgery in the anterior mandible with only about 1% experiencing sensation changes 1 year after implant surgery (Walton, 2000). A broader search reveals extreme variation in the reported prevalence of neurosensory disturbances (0% to 100%). The prevalence may depend on several factors: the site of implant placement, the type of surgical procedures adopted, the design of the studies, the sensitivity of the testing methods, the choice of the outcome measures, and the terminology used to describe sensory disturbances. Their potentially profound impact on the quality of life of patients and the possibility that they may persist suggests a need for prospective studies, using validated testing protocols and outcome measures (Dao & Mellor, 1998).

Progressive Bone Loss and Loss of Integration

The incidence of implant loss due to failure to osseointegrate or to loss of integration after loading has been well-documented. Early implant loss is assumed to be caused by the failure of the implant surface to integrate whereas late implant loss is associated with many potential causes of failure. Late losses are usually detected radiographically or through mobility testing with or without concurrent symptoms at a recall visit (Fig. 8). Causes of late implant failure that have been suggested in the literature include poor quality of bone, misfit of prosthesis, occlusion, non-axial loading and others (Taylor, 1998). Anecdotal evidence has attributed late failures to biomechanical overload. The loading limit of individual implants is unknown however, overload may cause microfractures at the bone-implant interface which may exceed the reparative capacity of the bone. Sequelae that may occur are continuing marginal bone resorption, loss of integration and implant fracture (Rangert, 1995).

Studies reporting on the average marginal bone loss during the first year range from 0.4 to 1.6mm. While the mean loss that occurred per year in subsequent years was 0.1mm. (Goodacre et al., 1999). Slight marginal bone loss after implant placement has been reported as a common phenomenon. According to the success criteria proposed by Zarb and Albrektsson, the mean vertical bone loss around implants should not exceed 0.2 mm annually after the first year of service (Zarb & Albrektsson, 1998). Consequently, it has been advised that extra precautions should be taken to lessen improper loading especially in the first year of function. Moreover, forces should be axially directed to the implants so that they will be well distributed along the threads and be resisted by compression stress in the bone. Individual standardized periapical radiographs can be made at recall examinations to monitor the progression of bone loss. Only when the bone loss is excessive and progressive should it be considered a complication (Quirynen, 1992).


Mechanical complications may arise as a result of occlusal loading. The frequency of component fracture varies widely between articles reviewed. The fatigue of implant components is considered a sequela of biomechanical overload. In its most catastrophic form, overload results in the fatigue fracture of the fixture. Other complications involve screw loosening, screw fractures, cement failure, framework fracture, veneer material wear and/or fracture as well as overdenture mechanical retention problems.

Biomechanical Overload

Several animal studies have attempted to demonstrate the effect of the magnitude and direction of occlusal forces on supporting implants and bone (Miyata et al., 1998, Isidor, 1996). To date, the evidence is contradictory and needs to be researched further. Moreover, the occlusal scheme for restorations supported by implants has not been examined scientifically. In single tooth applications, it has been suggested that keeping the restoration slightly out of occlusion or narrowing the occlusal table would transmit less force to an underlying implant. However, it has been shown that the forces of occlusion with food particles between the teeth are substantially higher than forces generated in an empty mouth clench (Richter, 1995, 1998). Therefore, it is not likely that a slight lack of occlusal contact would be of any protective value (Taylor & Agar, 2002).

Implant fracture

Implant fracture rates have been reported in numerous studies and they range from 0% to 16% (Taylor, 1998). The occurrence of implant fracture has been associated with overload-induced bone loss. Cupping of bone prior to the identification of implant fracture has also been reported. When reviewing records of patients with fractured implants, Rangert (1995) indicated that 59% of those implants that ultimately fractured had had previous mechanical complications such as screw loosening or fractures.

Therefore, it is important to address mechanical problems promptly. Prosthodontic intervention may include revisiting the prosthesis design and occlusion as well as considering the placement of additional implants. Maximizing the implant support for a prosthesis may reduce the flexure fatigue of the metallic components involved. It has been suggested that implant fixed partial dentures be supported by three implants placed in a tripod alignment to minimize stress and torque distribution (Rangert, 1995). The placement of two implants to replace a single molar has been also advocated. This practice would provide more surface area for osseointegration and could spread the occlusal loading forces over a wider area, reducing the potential bending forces that would otherwise exist in a single-implant molar restoration (Balshi, 1997).

Prosthesis Misfit

Few studies have specifically examined the effects of misfit of implant restorations on osseointegration. Many authors have stated that passive seating of a prosthesis is a prerequisite for maintaining successful integration. To date, authors who have explored this area have been unable to demonstrate negative outcomes of misfit on the bone/ implant interface (Jemt, 1996). It remains to be determined whether any amount of misfit is damaging to the bone/implant interface. However, it is likely that prosthesis misfit is a cause of component loosening and fracture.

Screw Loosening

Screw loosening is a difficult problem to discern from the literature. Most studies combine screw loosenings and fractures in their results. In a literature review by Goodacre et al. abutment screw loosening ranged from 2% to 45 % of the abutments. The highest rate was found with single crowns followed by overdentures. While as prosthetic screw loosening ranged from 1% to 38% (Goodacre, 1999). The etiology of the screw loosening is most likely multifactorial. Factors that have been attributed to screw loosening are: occlusion, prosthesis fit as well as screw design and composition (Cooper & Moriarty, 1997).

Over the years, manufacturers have modified components in order to mitigate the problem of screw loosening. To overcome problems with joint instability, the abutment screw has evolved in shape and composition. The transition to gold-alloy screws has allowed a more effective tightening to higher preloads due to its lower coefficient of friction than titanium (Binon, 2000). In an effort to further reduce frictional resistance, dry lubricant coatings have been applied to abutment screws. The reported data indicate an effective increase in attainable preload. However, the effectiveness of this technology on screw joint stability has yet to be fully documented with independent research and in clinical trials.

Screw loosenings are usually detected at recall examinations with mobility testing and/or radiographic examination (Fig. 9). They can be an inconvenience to the patient and the practitioner but more importantly, some authors believe that they are signs of impending failure of other components. It remains unclear exactly what clinical parameters promote the screw loosening encountered by many investigators. However, routine retightening at recall examinations is recommended.

Screw fractures

ture of prosthetic and abutment screws are commonly reported. Initially, it was thought that since the prosthetic screw was smaller and weaker than the abutment screw that it would fracture before other components. In spite of this, many studies report that the abutment screw fractures as often if not more often than the prosthetic screw. A mechanical hypothesis has been elaborated to explain this phenomenon.

The implant abutment interface coincides with the level at which osseous support terminates and at the level of maximum bone stiffness. This increased rigidity magnifies the strain localized to the crestal area around the implant neck. The abutment screw may be subjected to much greater force and may be more susceptible to fatigue failure even though it is a more massive structure (Taylor, 1998). Patients and practitioners should be aware that screw fracture is not a rare complication of implant therapy.

Complications Related to Cementation

Cementation of implant restorations may seem appealing for compensating prosthetic misfit. However a major drawback to this procedure is the loss of retrievability. Some practitioners have advocated the use of temporary cements to overcome this problem but with limited success. Accidental de-cementations are a frustrating problem for the patient and the dentist. Moreover, in the long term, implant supported restorations may need adjustment or revision and a temporary cement may not always allow for predictable retrievability. The ability to unscrew a prosthesis facilitates its maintenance at recall appointments. Other retentive devices such as lateral set screws or lingual composite plugs are more recent aesthetic and retrievable options.

Framework/Prosthesis Fracture

Metal framework fracture has been attributed to inadequate metal thickness, poor solder joints, excessive cantilever length, alloys with inadequate strength, patient’s parafunctional habits and improper framework design. (Goodacre, 1999, Tolman & Laney, 1992). As seen in Figure 10, the alloy used for the framework was found to be too weak for the applied load. Further research is required to determine the best design and material to resist loading over extended periods of time.

Acrylic resin fractures for implant overdentures are usually caused by inadequate space. The use of metal reinforced overdenture bases may minimize this complication (Schwartz, 1996). With fixed partial dentures, acrylic resins and composites tend to fracture more than porcelain veneering material (Gunne, 1994). Since studies have not been able to identify a superior veneering material, porcelain has been used more frequently in recent years for esthetic reasons (Goodacre et al., 1999).

High overdenture complication rates have been reported in association with clips and attachments. These components tend to loosen and fracture over time and require regular replacement.


The practitioner who treats patients with dental implants should be familiar with the potential complications and maintenance needs of such restorations. Although these complications have been documented, a standardized method of data collection would further enhance our understanding of the etiology and the frequency of these complications. Regardless, regular maintenance and addressing these complications promptly may prolong the longevity of implant restorations.


Sincere thanks to Dr. Izchak Barzilay and the Implant Prosthodontic Unit, Faculty of Dentistry, University of Toronto for their pictorial support.OH

Dr. Jim Yuan Lai is Assistant Professor and Director of Undergraduate Periodontics at the Faculty of Dentistry, University of Toronto and maintains a private practice in Toronto.

Dr. Francine Albert is Assistant Professor of Prosthodontics at the Faculty of Dentistry, University of Toronto and maintains a private practice in Toronto.

Oral Health welcomes this original article.


1.Adell R, Lekhom U, Rockler B. A 15-year study of osseointegrated implants in the treatment of the edentulous jaw. Int J Oral Surg 1981;10:387.

2.Albrektsson T, Zarb G, Worthington P. The long-term efficacy of currently used dental implants. A review and prognosis criteria for success. Int J Oral Maxillofac Implants 1986;1:11

3.Albrektsson T, Isidor F. Consensus report of session IV. In: Lang NP, Karring T (eds). Proceedings of the First European Workshop on Periodontology. London: Quintessence, 1994;365-369

4.Balshi TJ, Wolfinger GJ. Two-implant-supported single molar replacement: interdental space requirements and comparison to alternative options. Int J Periodontics Restorative Dent 1997 Oct;17(5):426-35

5.Berglundh T, Lindh J, Ericsson I, Marinello CP, Liljenberg B, Thomsen P. The soft tissue barrier at implants and teeth. Clin Oral Implants Res 1991;2:81-90.

6.Berglundh T, Lindhe J, Marinello CP, Ericsson I, Liljenberg B. Soft tissue reactions to de novo plaque formation at implants and teeth: An experimental study in the dog. Clin Oral Implants Res 1992;2:1-8

7.Binon PP. Implants and components: entering the new millennium. Int J Oral Maxillofac Implants. 2000 Jan-Feb;15(1):76-94.

8.Cooper L, Moriarty J. Prosthodontic and periodontal considerations for implant-supported dental restorations. Current Opinion in Peridontology 1997, 4: 119-126.

9.Dao TT, Mellor A. Sensory disturbances associated with implant surgery. Int J Prosthodont 1998 Sep-Oct;11(5):462-9

10.Ellen RP. Microbial Colonization of the peri-implant environment and its relevance to long term success of osseointegrated implants. Int J Prosthodont 1998;11:433-441

11.Ericsson I, Berglundh T, Marinello CP, Liljenberg B, Lindhe J. Long-standing plaque and gingivitis at implants and teeth in the dog. Clin Oral Implants Res 1992;3:99-103

12.Ericsson I, Lindhe J. Probing at implants and teeth: An experimental study in the dog. J Clin Periodontol 1993;20:623-627

13.Goodacre CJ, Kan JY, Rungcharassaeng K. Clinical complications of osseointegrated implants. J Prosthet Dent 1999 May;81(5):537-52

14.Gunne J, Jemt T, Linden B. Implant treatment in partially edentulous patients: a report on prostheses after 3 years. Int J Prosthodont 1994; 7: 143-8.

15.Isidor F. Loss of osseointegration caused by occlusal load of oral implants. A clnical and radiographis ctudy in monkeys. Clin. Oral Implants Res 1996; 7: 143-52.

16.Jemt T. Fixed implant-supported prosthesis in the edentulous maxilla. A five year follow-up report. Clin Oral Impl Res 1994;5:142

17.Jemt T., Book K. Prosthesis misfit and marginal bone loss in edentulous implant patients. Int J Oral Maxillofac Implants 1996; 11: 620-2.

18.Jovanovic S. Clinical aspects of dental implants. In: Newman M, Takei H, Carranza FA (eds). Carranza’a Clinical Periodontology 9th edition. Toronto: WB Saunders Co, 2002;889-896.

19.Koka, S. The implant-mucosal interface and its role in the long-term success of endosseous oral implants: a review of the literature. Int J Prosthodont 1998;11:421-432

20.Listgarten MA, Buser D, Steinemann SG, Donath K, Lang NP, Weber HP. Light and transmission electron microscopy of the intact interfaces between nonsubmerged titanium-coated epoxy resin implants and bone or gingiva. J Dent Res 1992;71:364-371.

21.Meschenmoser A. Effects of various hygiene procedures on the surface characteristics of titanium abutments. J Periodontol 1996;67:229

22.Miyata T, Kobayashi Y, Araki H et al. The influence of controlled occlusal overload on per-implant tissue: a histologic study in monkeys. Int J Oral Maxillofac Implants 1998; 13: 677-83.

23.Nevins M, Langer B. The successful use of osseointegrated implants for the treatment of the recalcitrant periodontal patient. J Periodontol 1995;66:150-157

24.Pontoriero P. Experimentally induced peri-implant mucosistis: a clinical study in humans. Clin Oral Implants Res 1994;5:254

25.Quirynen M, Naert I, can Steenberghe D. Fixture design and overload influence marginal bone loss and fixture success in the Branemark system. Clin Oral Implatns Res 1992; 3: 104-11.

26.Rangert B, Krogh PH, Langer B, Van Roekel N. Bending overload and implant
fracture: a retrospective clinical analysis. Int J Oral Maxillofac Implants 1995; 10: 326-34.

27.Richter EJ. In vivo vertical forces on implants. Int J Oral Maxillofac Implants 1995; 10: 99-108.

28.Richter EJ. In vivo horizontal bending moments on implants. Int J Oral Maxillofac Implants 1998; 13: 232-244.

29.Schwartz IS, Morrow RM. Overdentures. Principles and procedures. Dent Clin North Am 1996; 40: 169-194.

30.Thomson-Neal D, Evans G, Meffert R. Effects of various prophylactic vs treatment on titanium, sapphire, and hydroxylapatitie-coated implants: an SEM study. Int J Perio Rest Dent 1989;9:301

31.Taylor T, Prosthodontic problems and limitations associated with osseointegration. Journal of Prosthetic Dentistry, 1998, 79 (1), 74-78

32.Taylor T, Agar J. Twenty years of progress in implant prosthodontics. Journal of prosthetic dentistry, 2002, 88 (1), 89-95.

33.Tolman DE, Laney WR. Tissue integrated prosthesis complications. Int J Oral Maxillofac Implants 1992 Winter;7(4):477-84

34.Walton JN. Altered sensation associated with implants in the anterior mandible: a prospective study. J Prosthet Dent 2000 Apr;83(4):443-9

35.GA, Albrektsson T. Consensus Report: Towards optimized treatment outcomes for dental implants. Int J Prosthodont 1998;11:389

36.Zarb GA, Schmitt A. The edentulous predicament. II: The longitudinal effectiveness of implant-supported overdentures. J Am Dent Assoc. 1996 Jan; 127(1):66-72.