Avascular necrosis (AVN) is a disease caused by the temporary or permanent loss of blood supply to the bones.1,2 It is also known as osteonecrosis, aseptic (bone) necrosis, or ischemic bone necrosis.1,2 To date, many theories have been presented regarding the causative factors of AVN. Hypertension, excessive steroid use, and various genetic factors, as well as vascular pathologies such as vascular compression and vasculitis, that disturb the dynamic interaction between bone and vasculature, are thought to be potential causes of AVN.2–5
Avascular necrosis of the jaw (ONJ) is a significant complication involving painful areas of exposed bone and nonhealing in the mouth.6 Since 2003, bisphosphonates (BPs) have been commonly accepted as the biggest risk factor of ONJ.7–9 Bisphosphonates reduce the rate of bone remodeling, which may decrease the removal of micro-damaged regions of bone.6 Furthermore, even in patients who do not take BPs, AVN of the jaws can occur in bony areas that were exposed after invasive dental procedures, such as tooth extraction and implant surgery.2,6 This condition is observed more commonly in the mandible, which is thought to have less blood flow than the maxilla.2,6 The AVN-associated complications are not common in systemically healthy individuals and are more often observed after oral surgery or implant placement in patients with certain risks.10
Unfortunately, an efficient treatment protocol has not been determined for AVN of the jaw.6,9 Currently, surgical debridement, coverage of exposed bone with mucosal flaps, and antimicrobial applications are among the possible treatment options.9,11 In addition, various studies have reported that hyperbaric oxygen treatment (HBOT), either applied alone or with surgical techniques, is also successful in early-stage AVN.12 Hyperbaric oxygen treatment involves the intermittent inhalation of 100% oxygen at a pressure less than 1.5 atmosphere absolute.13 An optimal environment for repair processes is provided by HBOT as the additional oxygen carried to ischemic sites by circulation raises the oxygen tension in the tissues.12 Hyperbaric oxygen therapy positively affects peri-implant bone healing, which increases the osseointegration of titanium implants.14–16
Implant-supported overdenture prostheses are much preferred over conventional complete dentures as a treatment option in patients with total edentulism. In such cases, when there is severe bone resorption, implant placement may be more difficult.
When implants are placed, significant complications can occur after surgery, albeit rarely.17 In this report, we present a case of early-stage AVN in a patient who underwent mandibular implant placement; the area of bony exposure was caused by a labial flap rupture associated with masticatory activity in the surgical area. We also present the clinical results of its treatment with peri-implant plastic surgery and HBOT, followed by prosthetic rehabilitation.
Description of the Case
A 50-year-old female patient was referred to the periodontology clinic for the placement of dental implants. Her medical history revealed no systemic diseases except for hypertension. She was not taking any hormone replacement therapy despite menopause; she was taking antihypertensive drugs and antidepressants. She was a nonsmoker. Intraoral examination revealed severe bone resorption in both the maxilla and mandible. Radiologic investigation showed that the maxillary sinuses were suspended over the posterior maxilla with no alveolar bone height, while only 1–2 mm of bone height existed over the inferior alveolar canal in the posterior mandible (Figure 1a and b). Clinicians from both the periodontology and prosthetics departments decided to insert 2 dental implants into the anterior mandibular area. The patient was informed in detail about the procedure and possible complications after surgery before providing informed consent. While the patient was under sedation, dental implants were placed into the mandibular canine area, and a mucoperiosteal flap was sutured using 3.0 silk filament (Figure 2a through c). She was given postoperative instructions. One week later at the follow-up visit for suture removal, it was noted that most of the sutures were detached and that the flap in the labial area did not attach to the bone, resulting in an area of exposure (Figure 3a). The exposed bone displayed early-stage AVN. In addition, secondary epithelialization in the inner part of the labial flab started to form. The decision was made to intervene immediately at the same visit to prevent further progression of the necrosis. In the context of AVN treatment, surgical operations and HBOT were done.
The surgical procedure was carried out in 2 steps.
Clearance of the necrotizing area. The inner surface of the labial flap in the surgical field was deepithelized under local anesthesia. Next, necrotic fields without blood flow in the exposed bone were scraped with a surgical chisel, and holes were opened in the bone with steel round milling cutters. At least a few bleeding points were generated in this manner (Figure 3b).
Peri-implant plastic surgery. After vascularization of the necrotizing area, a free gingival graft (FGG) was applied to help cover the exposed bone surface, eliminate masticatory activity, and increase the width of the attached gingiva within the context of the peri-implant plastic surgery. The FGG obtained from the hard palate was placed in the receptive site, after which 5.0 sutures were used for closure (Figure 3c). The patient then received HBOT on the fifth day following surgical intervention (Figure 4a).
Hyperbaric oxygen therapy
The patient was treated with three 30-minute sessions of HBOT under 2.4 ATA pressure in a multiperson pressure room over 5 days. A total of 15 sessions were provided. No complications related to HBOT were observed (Figure 4b–d). Two weeks after the completion of HBOT, the implant area was corrected with Er,Cr:YSGG laser (Figure 4e).
Prosthetic restorations were performed in the second month following the FGG procedure (Figure 4f, Figure 5). Implant-supported overdenture prostheses were constructed to address the patient's functional, psychological, esthetic, and phonation problems. The patient was followed up to 1 year for any possible complications related to the prosthetic rehabilitation. However, no complications were observed during this period.
While AVN of the jaws is commonly observed in patients taking BPs, the condition is rare in systemically healthy persons, even after invasive procedures such as implant surgery.2,6,10 In fact, surgical complications during implant placement are not uncommon.10 According to a retrospective study by McDermott et al, operative complications made up a mere 1% of overall complications, whereas inflammatory and prosthetic complications were 10.2% and 2.7%, respectively.17 Misch and Wang10 divided complications into 4 categories: treatment plan related, anatomy related, procedure related, and others. In this report, we presented a patient in whom an implant was placed into the mandibular basal bone (ie, due to decreased vertical bone height resulting from severe bone resorption) who subsequently developed AVN. After combined treatments, the patient showed improvement, and prosthetic rehabilitation was eventually performed.
Although many theories have been suggested regarding AVN, hypotheses associated with bone metabolism physiology may be especially helpful in clarifying its pathophysiology, which is still not completely understood. In particular, the initiating role of vasculature in osteogenesis and the effects of vascular pathology on osteosynthesis remain to be explained.12 In addition to these theories, individual factors may also play important roles in AVN. In the present case, activity of the mentalis muscle was high, thereby causing stress in the anterior mandible and resulting in a shallow vestibule related to severe bone resorption. In light of this unfavorable condition, possible complications were preoperatively discussed with the patient. However, because the patient could not postoperatively protect the surgical area, the sutures were detached, the labial mucoperiosteal flap was separated from the vestibule, and the bone was ultimately exposed. Likewise, in cases involving a shallow vestibule, increasing the depth of the area with an FGG before surgery may be an effective treatment approach within the context of peri-implant surgery. Nonetheless, considering that some surgical complications related to tissue necrosis may occur due to the systemic and psychological characteristics of the patient, we decided to place the FGG, as needed, after implant placement. Indeed, this type of graft is suggested for use both before and after implant placement in peri-implant plastic surgery.18 Moreover, mandibular vertical bone height might not be enough in certain cases in which only the mandibular basal bone is available. In other cases, the mentalis or buccal muscles may be reattached to the area, rendering an FGG ineffective in increasing the depth in the vestibule. For such reasons, we did not consider deepening the vestibule before implant placement. Although the patient was warned after the operation, AVN developed related to bone exposition in the surgical area due to the intense mental muscle activity and lack of patient compliance.
Avascular necrosis may be observed in different stages. Early stages are asymptomatic, and no pain is expected.6 As our case was also in an early stage, no pain or infection was detected. While the necrotic region in mandibular AVN was being cleaned, bleeding points were produced with a round bur to maintain recirculation in the bone. In addition, the labial flap region was deepithelized again, which was aimed at inducing bone vascularization from the vessels in the labial flap. In some cases, necrotic bone resection may be required, with the margins providing some residual marrow, bleeding points, and bone in normal color, because smaller margins might result in the continuation or extension of the exposed bone.9,11 Moreover, an FGG was applied to the region so as to avoid additional AVN complications. The FGG was placed into the region to maintain necrotic bone coverage and to eliminate mucogingival stress. Furthermore, after this procedure, HBOT was performed to prevent necrosis formation in the FGG and to help alleviate bone necrosis. The patient was followed regularly over 2 months for complete epithelialization of the soft tissues and presence of bone vitality. Hyperbaric oxygen treatment may have efficacy not only in the bone but also in the soft tissue. Increased oxygen in tissues may induce various physiologic changes. High amounts of oxygen induce antihypoxic, antiedemic, and antibacterial effects.12,19,20 Our patient regained her health in both the soft and hard tissues, and no bone resorption or other problems were encountered in the implant region.
In summary, we presented a significant complication related to both the soft and hard tissue that developed after implant surgery. The treatment of mandibular AVN involved a combination of peri-implant plastic surgery and HBOT. The success of the implant may depend on the balance between the soft and hard tissues. Peri-implant plastic surgery and interdisciplinary approaches to address complications may increase overall clinical outcomes and help to prevent additional complications.