Periodontics: Implant Complications and Maintenance Issues

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Periodontics: Implant Complications and Maintenance Issues
July 2003
By Jim Yuan Lai, DMD, MSc(Perio), FRCD(C) and Francine Albert, DMD, MSc(Prosth), FRCD(C)
Oral Health Journal
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.
I - BIOLOGICAL COMPLICATIONS:
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 100¨µm to 400¨µm with a mean around 200¨µm.
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 10¨µm.
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 Walton, 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 bo