Energy-Dispersive X-ray Spectroscopic Investigation of Failed Dental Implants Associated with Odontogenic Maxillary Sinusitis
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https://www.researchgate.net/publication/350981291_Energy-Dispersive_X-ray_Spectroscopic_Investigation_of_Failed_Dental_Implants_Associated_with_Odontogenic_Maxillary_Sinusitis?origin=publication_list
Truc Thi Hoang Nguyen, Mi Young Eo, Buyanbileg Sodnom-Ish, Hoon Myoung * and Soung Min Kim *
https:// doi.org/10.3390/app11083684
Published: 19 April 2021
Department of Oral and Maxillofacial Surgery, Dental Research Institute, School of Dentistry, Seoul National University, 101 Daehak-ro, Jongno-gu, Seoul 03080, Korea; hoangtruc.bb@snu.ac.kr (T.T.H.N.);
miyoungeo@snu.ac.kr (M.Y.E.); buyan@snu.ac.kr (B.S.-I.) * Correspondence: myoungh@snu.ac.kr (H.M.); smin5@snu.ac.kr or smin_kim@msn.com (S.M.K.); Tel.: +82-2-2072-3059 (H.M.); +82-2-2072-0213 (S.M.K.); Fax: +82-2-766-4948 (H.M. & S.M.K.)
Abstract:
The failed dental implant associated with maxillary sinusitis is a multifactorial phenomenon and should be investigated thoroughly.
The inflammatory process induced by accumulated biofilm and wear debris may increase mucous secretion and mucous thickening, which finally may lead to severe complications such as maxillary sinusitis.
The inflammatory cytokines might compromise the long-term osseointegration of the related implant.
In this study, implants retrieved from three patients who experienced implant failure relating to maxillary sinusitis were investigated using scanning electron microscopy (SEM) and energy-dispersive X-ray spectroscopy. SEM analysis of the implant apical region revealed a less-compact bone structure, indicating the high bone turnover due to an inflammatory process.
The ratio of calcium (Ca) and phosphorus (P) was negligible in all specimens. Detection of fluorine (F), sodium (Na), silicon (Si), gold (Au), aluminum (Al), and magnesium (Mg) confirmed the contamination.
The selected cases presented different biological aspects that might play the central role in the failed dental implants associated with maxillary sinusitis: the contamination of potentially toxic elements, microorganism infection, and long perforation of implant apex into the sinus.
Each of the above phenomena needs to be confirmed with further clinical study with a larger number of failed implants and accompanying tissue samples.
Keywords: dental implant; maxillary sinusitis; maxillary sinus floor augmentation; scanning electron microscopy (SEM); energy dispersive X-ray spectroscopy (EDS)
Figure. Preoperative radiographic examination of case 1. The panoramic radiograph shows generalized alveolar bone loss and calculi deposition; furcation involvement of the #36, #37, #46, and #47 teeth; and a round retention pseudocyst surrounding the #16i and #17i implants (marked with arrows) (A). Upon CT examination, the #16i implant fixture had a missing abutment and, together with the #17i implant in the right maxillary sinus (marked with arrows), mucosal thickening and retention pseudocyst were observed in the right maxillary sinus in the axial view (B). Intraoperative view of #16i implant removal (C). The #16i implant was removed using forceps and trephine burr (D).
Figure. Preoperative radiographic examination of case 2. The panoramic radiograph shows generalized alveolar bone loss and calculi deposition, apical involvement of the #36 tooth; furcation involvement of the #37 tooth; peri-implant bone loss around the #15, #24, #25, and #26 teeth; and left maxillary sinus opacification (marked with arrows) (A). CT imaging showed bone fracture and sequestrum formation in the right and left sides of the maxilla and left mandible. Cortex destruction, sequestrum, calculated marrow attachment, and adjacent bone sclerosis were observed in the areas of #11 to #17, #24 to #27 (marked with arrows), and #36 and #37 teeth, and the upper and lower cortices were overserved, thus lost in the area of maxillary bone destruction in the axial view (B). Intraoperative view of the partial maxillectomy (#25i, #26i, and #27i alveolotomy) surgical procedure. Necrotic bony exposure was observed on the buccal side of the left maxilla (C). The extracted #25i, #26i, and #27i implants with necrotic bone attachment (D).
Figure. Preoperative radiographic examination of case 3. The panoramic radiograph shows an impacted #18 tooth, submerged #36 and #46 teeth, and a displaced #16i implant protruding into the right maxillary sinus (marked with arrows) (A). The CT imaging shows a retention pseudocyst in the right maxillary sinus and slight mucosal thickening of both maxillary sinuses. The apical portion of the protruded #16i implant is visible from the axial view (marked with arrows) (B). Intraoperative view of the #16i implant cutting. After careful removal of the inflamed cystic lesions for the sinus, the apical portion of the #16i implant was cut using a high-speed fissure burr (C). The 5-mm apical portion of the #16 implant (D).
Figure. SEM photograph showing the whole implant specimens with the marking of SEM-EDS examined points. In the implant fixture from case 1, the high magnification micrograph and EDS analysis were performed at three points: one in the thread surface to show the fixture morphology (0101-T), one on the attached bone in the upper region (0102-U), and one on the attached bone in the apical region (0103-A), to compare the bone structure and chemical composition at these two regions (A). In implant fixture and attached bone mass from case 2, two points in the apical area of the implant, one on the integrated bone in the middle of the fixture (0204-M), and one on the fixture surface in the apical region (0205-A) were chosen to examine the BRONJ-affected and fungal-infected bone and implant morphology (B). In the implant apex from case 3, the exposed surface of the fixture thread was chosen to be analyzed by EDS (C).
OBS:
Note the table where it is possible to say that the implant composed of titanium and zirconium interacted and migrated to the bone, being found both in the upper and apical regions of the bone.
The value of zirconium (9.19%) that migrated to bone was much higher than that of titanium (0.64%).
Another important finding is the aluminum that was seen in the apical region of the analyzed bone.
Figure. SEM micrograph at 500 and 10,000 magnification, EDS elemental distribution map and a spectrum of representative points pertaining to the three failed implants. In case 1, the SEM micrograph of the exposed implant surface revealed the pattern of sandblasting and acid etching surface (0101-T, white asterisk). Bone tissue attached at the implant upper part (0102-U, white asterisk) was found to have a more compact structure than bone in the apical region, per both SEM micrograph analysis and EDS composition results (0103-A, blue arrowhead). A Ti particle was also detected and is displayed on the distribution map (0103-A, distribution map, arrow). The Ca/P ratio of bone in 0102-U is higher than that in 0103-A (4.1 vs. 2.6). Noticeably, a significant level of zirconium (Zr) (9.19%) was detected in 0102-U, together with trace signals of Ti, Na, and Si. In case 2, The integrated bone on the implant surface showed a pattern of sclerosing bone with rare signs of bone lacunae (0204-M). In the apical region of the implant, massive infiltration of fungal hyphae was seen (0205-A, arrows). EDS analysis was performed at the implant surface and also revealed a significantly high percentage of Au (15.68%), along with two other major components, which were Ti and O. Si. In case 3, the implant surface was covered in organic membrane tissue, which can be observed on the low magnification (0306-A, black asterisks), blood cells (0306-A, blue arrowheads), and fibrin (0306-A, blue asterisks). Ti, O, and C were major compositions of this region, with a high percentage of Ti (71.06%).
Conclusions
The selected three cases in this study presented different biological aspects that might play the central role in the failed dental implants associated with OMS.
In case 1, the detection of elements potentially toxic to cells in the apical region may explain the irritation reaction of the sinus membrane, which led to maxillary sinusitis and inflammation of the peri-implant bone with bone turnover and loss of normal structure, then implant failure.
In case 2, the fungal infection was the main cause of the failed implant and OMS. However, it is unclear whether the primary fungal infection was from the sinus cavity or an intraoral infection.
In case 3, the irregular bone structure and absence of contaminated elements suggested the failure of implant osseointegration may be due to the long perforation of the implant apical region into the sinus cavity. Each of the above phenomena can be the potential etiology of the failed implant associated with OMS and needs to be confirmed with further clinical study and analysis of a larger number of failed implants and accompanying human tissue samples.
