Introduction

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.25 

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.79  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.1416 

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.

Figure 1.

Radiographic evaluation of the case. (a) Dental computerized tomography (severe bone loss in the basal bone in the anterior and posterior regions). (b) Panoramic radiography after implant surgery.

Figure 1.

Radiographic evaluation of the case. (a) Dental computerized tomography (severe bone loss in the basal bone in the anterior and posterior regions). (b) Panoramic radiography after implant surgery.

Figure 2.

Intraoral clinical images. (a) Before implant surgery. (b) During the surgery. (c) After the surgery.

Figure 2.

Intraoral clinical images. (a) Before implant surgery. (b) During the surgery. (c) After the surgery.

Figure 3.

Avascular necrosis (AVN) findings and surgical treatment steps. (a) One week after the operation, AVN formation was observed due to bone exposition after the lack of attachment of a labial flap during implant surgery. (b) Bleeding points formed to treat AVN in the bones in the surgical area. (c) Free gingival graft procedure to maintain the coverage of bone in the area of AVN.

Figure 3.

Avascular necrosis (AVN) findings and surgical treatment steps. (a) One week after the operation, AVN formation was observed due to bone exposition after the lack of attachment of a labial flap during implant surgery. (b) Bleeding points formed to treat AVN in the bones in the surgical area. (c) Free gingival graft procedure to maintain the coverage of bone in the area of AVN.

Surgical procedure

The surgical procedure was carried out in 2 steps.

  1. 1.

    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).

  2. 2.

    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).

Figure 4.

Improvement after free gingival graft (FGG) and hyperbaric oxygen treatment (HBOT). (a) Five days after FGG (HBOT was started). (b) Ten days after FGG. (c) Three weeks after FGG. (d) Four weeks after FGG (end of HBOT). (e) Six weeks after FGG and application of gingivoplasty with laser. (f) Two months after FGG.

Figure 4.

Improvement after free gingival graft (FGG) and hyperbaric oxygen treatment (HBOT). (a) Five days after FGG (HBOT was started). (b) Ten days after FGG. (c) Three weeks after FGG. (d) Four weeks after FGG (end of HBOT). (e) Six weeks after FGG and application of gingivoplasty with laser. (f) Two months after FGG.

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 rehabilitation

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.

Figure 5.

Prosthetic rehabilitation after completion of hyperbaric oxygen treatment 2 months after free gingival graft.

Figure 5.

Prosthetic rehabilitation after completion of hyperbaric oxygen treatment 2 months after free gingival graft.

Discussion

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.

Abbreviations

     
  • AVN

    avascular necrosis

  •  
  • BP

    bisphosphonate

  •  
  • FGG

    free gingival graft

  •  
  • HBOT

    hyperbaric oxygen treatment

  •  
  • ONJ

    avascular necrosis of the jaw

References

References
1
DiGiovanni
CW
,
Patel
A
,
Calfee
R
,
Nickisch
F
.
Osteonecrosis in the foot
.
J Am Acad Orthop Surg
.
2007
;
15
:
208
217
.
2
Lafforgue
P
.
Pathophysiology and natural history of avascular necrosis of bone
.
Joint Bone Spine
.
2006
;
73
:
500
507
.
3
Laroche
M
.
Intraosseous circulation from physiology to disease
.
Joint Bone Spine
.
2002
;
69
:
262
269
.
4
Dannemann
C
,
Grätz
KW
,
Riener
MO
,
Zwahlen
RA
.
Jaw osteonecrosis related to bisphosphonate therapy: a severe secondary disorder
.
Bone
.
2007
;
40
:
828
834
.
5
Dietrich
EM
,
Antoniades
K
.
Bone-vasculature interactions in the mandible: is bone an angiogenic tissue?
Med Hypotheses
.
2012
;
79
:
582
584
.
6
Sambrook
P
,
Olver
I
,
Goss
A
.
Bisphosphonates and osteonecrosis of the jaw
.
Aust Fam Physician
.
2006
;
35
:
801
803
.
7
Marx
RE
.
Pamidronate (Aredia) and zoledronate (Zometa) induced avascular necrosis of the jaws: a growing epidemic
.
J Oral Maxillofac Surg
.
2003
;
61
:
1115
1117
.
8
Wang
J
,
Goodger
NM
,
Pogrel
MA
.
Osteonecrosis of the jaws associated with cancer chemotherapy
.
J Oral Maxillofac Surg
.
2003
;
61
:
1104
1107
.
9
Shirota
T
,
Nakamura
A
,
Matsui
Y
,
Hatori
M
,
Nakamura
M
,
Shintani
S
.
Bisphosphonate-related osteonecrosis of the jaw around dental implants in the maxilla: report of a case
.
Clin Oral Implants Res
.
2009
;
20
:
1402
1408
.
10
Misch
K
,
Wang
HL
.
Implant surgery complications: etiology and treatment
.
Implant Dent
.
2008
;
17
:
159
168
.
11
Marx
RE
.
Reconstruction of defects caused by bisphosphonate-induced osteonecrosis of the jaws
.
J Oral Maxillofac Surg
.
2009
;
67
(
5 suppl
):
107
119
.
12
Bejar
J
,
Peled
E
,
Boss
JH
.
Vasculature deprivation: induced osteonecrosis of the rat femoral head as a model for therapeutic trials
.
Theor Biol Med Model
.
2005
;
2
:
24
.
13
Mayer
R
,
Hamilton-Farrell
MR
,
van der Kleij
AJ
,
et al
.
Hyperbaric oxygen and radiotherapy
.
Strahlenther Onkol
.
2005
;
181
:
113
123
.
14
Oliveira
PA
,
Oliveira
AM
,
Pablos
AB
,
et al
.
Influence of hyperbaric oxygen therapy on peri-implant bone healing in rats with alloxan-induced diabetes
.
J Clin Periodontol
.
2012
;
39
:
879
886
.
15
Goiato
MC
,
Santos
DM
,
Danelon
M
,
et al
.
Hyperbaric oxygen: therapy for patients with maxillofacial implants?
J Craniofac Surg
.
2009
;
20
:
1519
1522
.
16
Chen
X
,
Matsui
Y
,
Ohno
K
,
Michi
K
.
Histomorfometric evaluation of hyperbaric oxygen treatment on healing around hydroxyapatite implants in irradiated rat bone
.
Int J Oral Maxillofac Implants
.
1999
;
14
:
61
68
.
17
McDermott
N
,
Chuang
S
,
Dodson
T
,
et al
.
Complications of dental implants: identification, frequency, and associated risk factors
.
Int J Oral Maxillofac Implants
.
2003
;
18
:
848
855
.
18
Kazor
CE
,
Al-Shammari
K
,
Sarment
DP
,
Misch
CE
,
Wang
HL
.
Implant plastic surgery: a review and rationale
.
J Oral Implantol
.
2004
;
30
:
240
254
.
19
Ditri
L
,
Montanari
M
,
Melamed
Y
,
Reis
D
.
Femoral head necrosis
.
In
:
Mathieu
M
,
ed
.
Handbook on Hyperbaric Medicine
.
Dordrecht, the Netherlands
:
Springer;
2006
:
546
552
.
20
Hammarlund
C
.
The physiologic effects of hyperbaric oxygenation
.
In
:
Kindwall
EP
,
Whelan
HT
,
eds
.
Hyperbaric Medicine Practice. 2nd rev ed
.
North Palm Beach, Fla
:
Best Publishing Company;
2002
:
37
68
.