15

Reparative Surgery and Complication Management

When surgery is performed, complications are always imminent:

Those who operate little have many complications.

Those who operate a lot have few complications.

Only those who do not operate at all have no complications.

— F. Härle

15.1 Reparative Surgery and Implant Replacement

The number of patients is increasing who already had their teeth replaced with implants (ie, third teeth) and have acquired ridge defects after implant loss and present for restoration with fourth teeth (Fig 15-1). One cannot repair defects after implant loss with the same success rate as with initial surgery.¹ There are visible reasons for this, such as soft tissue scarring after the initial surgery with consequent deterioration of the blood supply. However, there are also non-visible reasons, eg, the long half-life of proteins such as the proinflammatory cytokines in the tissue. Even long periods of time after inflammation subsides, residues of the proinflammatory cytokine environment are present in the tissue.

In a recently published study of second- and third-time removals of failed implant restorations, the following revealing statistics emerged. The first-implant group of a cohort of more than 5,000 patients had 95.4% implant survival. Second implant placements had 77.4% implant survival, third implant placements had 72.7% implant survival, and fourth implant placements had 50% implant survival.² Another study of more than 10,000 patients came to a similar conclusion, with 94% survival of first implants and 73% survival of second implants.³ It can be seen that the chances of success of the repeat procedure are lower than for the initial procedure, and these continue to decrease with further repeat procedures. This is different from the technology and consumer world, where a like-new condition can be achieved through repair and replacement parts. Clinicians must disengage patients and payers from the idea of technical repair of a consumer good in the case of implant loss; otherwise, expectations will be too high (Fig 15-2).

Three main conclusions can be drawn from these results. Firstly, defensive incision patterns (midcrestal and sulcus incision), full-layer subperiosteal flap formation, and generally a conservative as opposed to a more invasive therapeutic approach should be used during the initial implant placement. The goal is to not complicate a potential second procedure with significant scarring. Some humility on the part of the surgeon is required here, to recognize that he or she may not be the last to perform surgery at this site in the patient’s life.

Fig 15-1 Fourth teeth: repair after implant loss. a. Panoramic radiograph of 76-year-old patient with complete loss of the maxillary alveolar process after 26 years of wearing an implant-supported maxillary total denture. After implant removal, remnants of former IMZ implants (Friatec) are still visible apically in the maxillary left central incisor and canine sites; see also the mandibular left lateral incisor site. b. The lateral cephalometric radiograph shows that only the palatal plate remains of the maxilla; during inspection, a spatula can be placed flat on the palatal plate from anterior. c. Intraoperative image of a LeFort interpositional bone graft. After sinus elevation and downfracture, a frame of strip-shaped autogenous iliac crest grafts has already been built up here. Osteosynthesis plates support the interposition gap. d. The voids between the bone strips are filled with a 25%/75% mixture of autogenous chips and bone substitute (Bio-Oss, Geistlich). This material makes up the main volume of the grafts. e. The bone grafts are covered by collagen membranes in the suture area (Bio-Gide, Geistlich). f. Because the maxilla was physically displaced inferiorly by downfracture and because the mucosa on the maxilla was not detached, there is relatively little need for mobilization of the soft tissue. This aspect also makes the surgery more tolerable than an onlay bone graft.

Fig 15-1 Fourth teeth: repair after implant loss. g. Panoramic radiograph after augmentation. h. The lateral cephalometric image shows significant vertical and volume gain compared to Fig 15-1b. i. Four months after augmentation, the osteosynthesis material is removed. Here, the position screws have already been loosened. The retaining screws of the osteosynthesis plates show that no major surface resorption has occurred except for a slight rounding of the bone edges. j. The already vascularized bone of the iliac crest grafts allows correct implant osteotomies. However, the bone is still quite soft at this stage (like type IV bone, according to Lekholm and Zarb classification). k. Inserted dental implants. The implant in the maxillary left first premolar site was lost subsequently as an early loss, confirming that second implants placed in the same site have a worse prognosis than the initial implants. l. Prosthetic restoration by bar-supported overdenture (Dr J. Tetsch, Münster).

Fig 15-1 Fourth teeth: repair after implant loss. m. The overdenture allowed chewing function for another 10 years, at which time the patient suffered a severe stroke from which he did not recover. n. Good esthetics of the fourth teeth.

Fig 15-2 Reparative surgery after implant removal. a. Clinical view of a 27-year-old female patient 5 years after immediate implants were placed at a different dental practice for severe tooth trauma. There has been extensive bone and soft tissue loss in the esthetic area labial to the maxillary central incisors. b. Removal of the old implants, which were too large and malpositioned in relation to the ridge width. c. Pronounced soft tissue defect after implant removal. d. The vascularized palatal connective tissue flap (axial pattern flap) with contained central vessel from the nasopalatine artery in the incisive foramen (adapted from Sclar⁴). e. Soft tissue coverage by vascularized connective tissue flaps on both sides. f. A removable pontic-type provisional is placed in the soft tissues to form the subsequent emergence profile. g. A few days later, the connective tissue of the vascularized flaps already shows a fibrin coating and granulation tissue, both of which are an activity of the flap and require substance and cell transport that would not be present in a free transplant. h. Panoramic view after implant placement with bone grafting (autogenous external oblique ridge block graft). i. Placement of the new prosthetic restoration (Dr H. Schröder, Kassel); some soft tissue deficits still exist. j. The maxillary mirror image shows that thanks to the augmentation, the implants could be placed vertically despite the anatomical obliquity of the maxillary alveolar process, allowing the screw channels to emerge palatally and enabling a screw-retained restoration. Scars from removal of the connective tissue flaps are visible on both sides of the palate.

Fig 15-2 Reparative surgery after implant removal. k. Panoramic radiograph after prosthetic restoration. l. Follow-up examination 5 years later with spontaneous improvement of the soft tissue deficit, see Fig 15-2i. As a consequence of implant removal and second implant placement, a visible soft tissue scar will remain for life. m. The panoramic radiograph after 5 years shows no marginal bone resorption on the new implants, and therefore stable conditions can be expected for the further life of the young patient.

Second, if a biologic implant complication such as peri-implantitis has occurred, then it follows from the above figures to prioritize retention of the initial implant over removal and replacement.

Third, reparative surgery can no longer be mapped with the SAC (straightforward, advanced, complex) classification due to the reduced chances of success. Here, in many cases, a degree of difficulty beyond C is present, and these problems require experienced teams.

15.2 Augmentative Treatment of Peri-implantitis

From the worsened prognosis of secondary implant placement, it follows that surgical therapy of periimplantitis is usually justified while the implant is still stable. Another prerequisite for surgical periimplantitis therapy is that a conservative therapy attempt was not sufficient to eliminate bleeding on probing and suppuration of the pockets.⁵ Therapyresistant peri-implantitis requires relatively rapid surgical intervention in about a month’s time, because peri-implant infections can progress rapidly and lead to implant loss.

Attempting to maintain infected implants, as opposed to removal or waiting inactively until they are lost, is supported by the relatively good success rates of peri-implantitis treatment. A meta-analysis yielded implant survival rates of 81.73% to 100% at 3 years, 74.09% to 100% after 4 years, 76.03% to 100% after 5 years, and 69.63% to 98.72% after 7 years.⁶

Surgical peri-implantitis treatment aims to permanently remove the biofilm on the implant surface.7 Pocket elimination is necessary for this, because the gingival pocket protects the biofilm and allows it to escape the patient’s oral hygiene. The patient cannot get into the pocket with normal oral hygiene measures. Therapy of peri-implantitis starts with nonsurgical pretreatment a few weeks before the surgical procedure, eg, supragingival professional cleaning, glycine powder air abrasion (Air-Flow Perio, EMS) and pocket rinsing with chlorhexidine solution. This is firstly to test a nonsurgical pretreatment and secondly to reduce the inflammation to create better conditions for surgical treatment.

The surgical intervention has the purpose of exposing the biofilm and making it accessible (Fig 15-3). The surgical difficulty of peri-implantitis therapy is to clean and clearly expose all implant surfaces so that the blasting devices and brushes can engage the implant threads at a 90-degree angle, even from the lingual direction in the floor of the mouth. This requires a great deal of surgical skill and patient cooperation. The surgical procedure consists of the steps of degranulation, decontamination, and regeneration. Degranulation is important to remove titanium particles⁸ and toxic granulocytes from the wound and to resect the pocket epithelium. Decontamination ensures the macroscopic removal of concretions (with an air scaler), the microscopic cleaning of the metal implant threads (with a titanium brush), and complete removal of the toxin molecules by glycine powder air abrasion and chemical rinsing, for example, with chlorhexidine solution. The goal of the treatment of peri-implantitis is the permanent elimination of the biofilm. For the prevention of re-infection, pocket elimination or reduction is the goal. This goal could be achieved after completion of the first therapeutic steps by apical displacement of the mucoperiosteal flap, but this then leads to recession with exposed titanium and is at best suitable in non-visible areas. The more tissue-sparing approach is to raise the pocket floor by filling the bone defect with a bone substitute filler. Here no clear material recommendation can be given. Bone substitute material with and without membranes, with the aim of fibrous regeneration, is recommended. Even if only integrated in scars, it limits the apical growth of the junctional epithelium. A metaanalysis yielded an average of 3.5-mm reduction in probing depth by these measures.⁹ An implantoplasty did not yield any advantage over glycine powder irradiation.¹⁰ The goal of the subsequent maintenance phase is to prevent re-infection through patient cooperation and periodontal supportive treatment.

Fig 15-3 Peri-implantitis treatment: degranulation, decontamination, and regeneration. a. Severe peri-implantitis at the maxillary first premolar and right lateral incisor sites almost without externally visible symptoms, but with probing depths >10 mm. b. Panoramic image shows severe osteolysis at the maxillary right lateral incisor and first premolar sites near the apex and at the left first premolar periapically. c. After conservative anti-infective pretreatment for 4 weeks, the flap was opened via a sulcus incision with visualization of the granulation tissue. The left first premolar implant was removed. d. The granulation tissue was carefully excised from the palatal and buccal aspects with a scalpel and sent for pathohistologic evaluation.

Fig 15-3 Peri-implantitis treatment: degranulation, decontamination, and regeneration. e. Careful exposure of all contaminated metal surfaces under good visibility. f. Removal of visible concretions by ultrasonic scaler and hand instruments. g. Visualization of palatal implant surfaces via palatal flaps. h. Cleaning of the titanium surfaces with rotating titanium brushes (HANS Korea). i. Fine decontamination by glycine powder blasting (Air-Flow). j. Deposition of bone substitute material (BoneCeramic, Straumann).

Fig 15-3 Peri-implantitis treatment: degranulation, decontamination, and regeneration. k. The material has a certain stability and shapeability in the defect due to adhesion and sharpness. l. The material is introduced in excess, although a bone regeneration can only be expected in the vertical defect components. m. Wound closure by interdental sutures according to Lindhe. n. Panoramic radiograph postoperatively with defect filling in excess. o. The follow-up photograph 2 months postoperatively shows recession compared to Fig 15-3a of about 3 mm at the right second premolar to lateral incisor sites. The probing depth at the right lateral incisor and first premolar sites is 8 mm without bleeding on probing.

15.3 Infectious Complications of Augmentations

Complications of augmentation procedures are mostly infectious in nature (Fig 15-4). The most obvious factor for early dental implant¹¹ and augmentation loss is infection due to primary and secondary wound contamination by endogenous bacteria. The patient must be informed preoperatively about the possibility of infection and its possible subsequent treatments; otherwise the patient will have unrealistic expectations that must be corrected. Impaired wound healing can cause considerable economic and psychologic damage due to exposure of implants and augmentation materials with consecutive loss, which is often accompanied by a loss of confidence in the physician:

• Wound dehiscence with exposed augmentation material
• Membrane exposure
• Purulent or fistulous lesion
• Osteosynthesis material loosening
• Implant loss
• Graft loss
• Sinusitis after sinus floor augmentations
• Abscesses with and without tendency to spread
• Osteomyelitis

Intraoral surgery belongs to the class of cleancontaminated procedures, because it always takes place in a non-sterile environment. In this infectious class, according to general experience, wound infections can statistically be expected to be about 5% in minor procedures and 20% to 50% in major procedures with transplants.¹² Infections occurred in 1% to 30% of oral surgical procedures such as third molar removal, depending on the study and counting method.¹³ Implantology procedures are no exception to this rule. Most infectious complications of augmentation operations in healthy patients remain localized because drainage is ensured quite quickly via the wound dehiscence. Such local infections should also only be treated with local disinfection. It is important to recognize deep cervical abscesses and infections with a tendency to spread and to treat them surgically in a maxillofacial surgery clinic within a short time frame.

Fig 15-4 Late extrusion of a sequestrum after block grafting. a. A 31-year-old patient had a jaw fracture in the mandibular left canine site 14 years previously with tooth loss and subsequent implant restoration, which was later removed. As a consequence, there is a bone defect in the canine region. b. Two-stage augmentation with autogenous bone block graft from the external oblique ridge. c. Use of Bio-Gide collagen membrane. d. Autogenous chips for contour filling. e. Use of membrane sections and more bone chips for recession coverage on the neighboring lateral incisor. f. Staged implant placement was performed 4 months later. Panoramic radiograph taken another 3 months later, after crown restoration of the new implant. g. Six years postoperatively, the patient presented again because of complaints in the area of the implant; the findings were a slight bleeding on probing at a probing depth of 5 mm. Initially, conservative treatment was attempted. h. After surgical opening for exploration of the canine region, a small loose bone sequestrum was found to be the cause of infection, originating from a bone block that was not completely vascularized. i. After debridement and decontamination of the implant surface, marginal bone loss was found on the implant. This was treated with bone substitute material. j. Result after treatment of the complication.

15.4 Preoperative Measures to Prevent Wound Dehiscence in Augmentation Sites

Primary and secondary wound contamination

Contamination of a wound in the mouth can occur primarily due to bacterial presence (see chapters 2 and 5). Such primary infections occur quite quickly postoperatively, after 1 to 4 days, and are very acutely accompanied by pain and swelling. However, contamination of the wound may also occur secondarily by ingrowth of a biofilm on the augmentation materials. Such infections announce themselves slowly only about a week postoperatively by wound dehiscence and are not so foudroyant in course.

Intraoral infection prophylaxis

The aim of intraoral infection prophylaxis and antisepsis is to reduce the infection dose of the wound. The goal of oral antisepsis is not a sterile surgical field, but to reduce the bacterial load of the surgical wound as much as possible. Bactericidal antibiotics should directly inactivate invading bacteria before they can establish and multiply. The step-by-step concept of general infection prophylaxis is listed in chapter 5 (section 5.6 Anti-infective Patient Preparation).

Antibiotic administration against primary wound contamination

Extensive and prolonged or even preoperative antibiotics with reserve antibiotics are not the right way to control surgical wound infections^14,15 because they promote the selection of resistant germs. Single-shot antibiotics should be administered no earlier than 60 minutes before surgery and repeated if surgery lasts longer than 4 hours.¹⁶ The dose of penicillins must be sufficiently high to be bactericidal. Intravenous administration of 3 g ampicillin-sulbactam achieved infection prevention rates equal to long-term antibiotics for 5 days in a prospective oral surgery study.¹⁷ When administered orally during implant surgery, 3 g of amoxicillin 1 hour preoperatively was most effective, according to a network meta-analysis.¹⁸ In a retrospective study of third molar extraction, oral and intravenous drug applications had equivalent effects.¹⁹ This may be explained by the fact that bactericidal antibiotics such as penicillin, once sufficiently effective, kill all bacteria inside the tissue and inside the autogenous grafts. Then the tightly sutured wound is initially sterile inside. New bacterial colonization takes place only secondarily through the suture gaps and stitch channels, and this takes several days. In many cases, antibiotics in the first days after a tightly sutured wound are therefore overtreatment that only promotes side effects (dysbiosis in the intestine) and selection of resistant germs.

Perioral skin antisepsis and intraoperative wound irrigation with chlorhexidine

There is no reason why preoperative perioral disinfection with chlorhexidine should not be performed prior to augmentation surgery, since the patient also rinses intraorally with it anyway. In skin antisepsis, chlorhexidine was superior to povidone-iodine.²⁰

15.5 Intraoperative Measures to Prevent Wound Dehiscence in Augmentation Sites

Ten-point plan for the prevention of wound dehiscence

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