Section 2 Maxillofacial

#### **Chapter 5**

## Sino-Nasal Changes Associated with Midfacial Expansion: An Overview

*G. Dave Singh*

#### **Abstract**

The concept of palatal expansion can be viewed as an anachronism since the delivery and scope of this clinical technique has changed dramatically over the past few decades. Indeed, since the palatal complex does not exist in isolation, clinicians ought to be cognizant of how palatal expansion affects contiguous midfacial structures. Because of this structural arrangement, surgical and non-surgical palatal expansion can have clinical consequences on the dentoalveolar structures, which are dependent on bony remodeling of the maxillo-palatine complex. In addition, it can also be suggested that morphologic alterations of the maxillary air sinus might lead to functional and clinical improvements of inflammatory changes associated with rhinosinusitis. Furthermore, enhancements in the nasal airway could affect a host of other conditions, including nasal breathing and obstructive sleep apnea, etc. Therefore, the aim of this chapter is to review the effects of midfacial expansion techniques on contiguous structures, including the paranasal sinuses.

**Keywords:** Maxillary sinus, nasal airway, sinusitis, palatal expansion, midfacial development

#### **1. Introduction**

The human air sinuses are enigmatic in that numerous functional attributes have been associated with them, including humidification, warming, and cleaning of inhaled air; biosynthesis, storage, and concentration of nitric oxide (NO); an anterior 'crumple zone' to withstand frontal trauma, and lightening of the skull, presumably for flight in extinct dinosaurs and extant birds. Recent evidence even goes on to suggest that the paranasal sinuses might be vestigial organs of breathing [1]. In any case, originally, clinical palatal expansion was pioneered as an orthodontic technique to widen the upper dental arch in attempt to improve jaw relations and/or tooth alignment. However, the maxillary air sinuses also lie above and lateral to the hard palate, while the dentoalveolar structures, such as the roots of the maxillary molars, can project into the sinus floor. Medially, the nasal airway communicates with the maxillary sinuses, including the ostio-meatal complex. Because of this diverse structural arrangement, non-surgical and surgical palatal expansion techniques might have clinical consequences on the maxillary air sinuses, which are dependent on bony remodeling and subsequent pneumatization of the maxillo-palatine complex. Therefore, an overview of various midfacial expansion

procedures that might induce anatomic alterations of the maxillary air sinus, that may in turn lead to functional and clinical changes, is warranted.

#### **2. Sinus changes associated with non-surgical midfacial expansion**

Numerous studies have deployed 3D cone-beam computed tomography (CBCT) scans to quantify morphologic changes associated with rapid maxillary expansion (RME). For example, Lanteri et al. [2] evaluated midfacial changes after slow maxillary expansion and RME in 8 yr-old children. They found that the volumes of the nasal cavity and maxillary sinuses increased after treatment in both protocols. Conversely, Garrett et al. [3] had earlier reported that RME in 14 yr-olds was associated with an increase in nasal width but a decrease in maxillary sinus width, implying that the increase in nasal functional space was gained by displacing the maxillary air sinus volume, although clinical consequences of these changes were not noted. However, in a similar study on 13 yr-olds treated with banded and bonded maxillary expanders, Pangrazio-Kulbersh et al. [4] found that both appliances induced anterior and posterior skeletal widening of the hard palate via the midpalatal suture, and their study demonstrated increases in both nasal cavity volume and maxillary sinus volume. On the other hand, Almuzian et al. [5] provided further details of the RME approach in 13 yr-olds. Over a period of 2–3 weeks, an average palatal width-increase of 3.7 mm was noted in males and 2.8 mm in females. These linear changes were found to be correlated with maxillary sinus volume changes. Therefore, it can be surmised that anatomical differences in the outcome of RME might simply be explained by differences in the design, materials and protocols of the devices used.

A non-surgical variant of RME, maxillary protraction, deploys the use of facemasks (FM), particularly in cases of Class III malocclusion that exhibit a maxillary deficiency. Pamporakis et al. [6] assessed midfacial alterations, including the volume of the maxillary air sinuses in 10-yr-old children, associated with an RME-FM protocol for 10 days. Using this technique, they reported an overall increase in maxillary sinus volume post-treatment. However, the authors also noted that the RME-FM protocol did not affect all the maxillary sinuses, indicating that there may be a range of responses, presumably related to individual craniofacial morphology. In another variation of RME, alternate RME and constriction is sometimes deployed followed by FM. Onem-Ozbilen et al. [7] used this protocol on 10-yr-old children with a skeletal Class III phenotype, exhibiting maxillary retrognathia, over 10–12 months. It was found that the maxillary sinus volumes increased. Therefore, the authors concluded that different expansion devices and protocols can effect disparate changes in maxillary sinus volume. This deduction was borne out by the study of Erdur et al. [8] who used symmetric and asymmetric rapid maxillary expansion (ARME) treatments in patients aged 12-15 yrs. While maxillary sinus volume changes were greater in the RME group post-treatment, in the ARME group, no changes in sinus volume were found. Since bilateral symmetry is a feature of human development, these results are not perhaps surprising as the craniofacial system may regress to homeostasis once the devices are removed.

The age at which these various palatal expansion protocols are applied may also be pertinent. Most of these types of studies have been undertaken in pediatric populations but the efficacy of palatal expansion in older individuals is also worth considering. In fact, Machado-Júnior and Crespo [9] opine that maxillary expansion in adults requires further due diligence. In this regard, Kavand et al. [10] studied maxillary expansion with bone- and tooth-borne appliances in adolescents. They reported that both groups showed an increase in nasal cavity volume, but not

*Sino-Nasal Changes Associated with Midfacial Expansion: An Overview DOI: http://dx.doi.org/10.5772/intechopen.99052*

maxillary sinus volume, even though the maxillary bone width increased. This is an interesting finding because by age 15 yrs. the second maxillary molars are often fully erupted and root formation is typically completed, giving little or no room for continued pneumatization until the maxillary third molars evacuate the body of the maxilla, which is rare, since unerupted, impacted wisdom teeth is a common finding on radiographs. Thus, in adolescents, RME is unlikely to result in an increase in maxillary sinus volume. In contrast, Singh and Kim [11] found that a biomimetic approach to palatal expansion increased maxillary sinus volume by some 6.5% in adults (mean age approx. 25 yrs.) accompanied by a mean palatal width increase of approx. 3 mm, which is similar to that achieved in teenagers as noted above. Therefore, while morphologic differences in the outcome of non-surgical RME might be explained by disparate designs, materials and protocols of the devices used, if the laws of biologic control, such as sutural homeostasis and pneumatization, are not violated, enhancement of maxillary sinus morphology might be possible even in adults, perhaps leading to improved clinical outcomes.

#### **3. Functional sinus changes associated with non-surgical midfacial expansion**

One of the roles of the paranasal sinuses is the biosynthesis of nitric oxide (NO). It is known that NO plays important roles in a diverse range of physiologic and patho-physiologic processes, including antimicrobial activity, pulmonary vascular resistance, alveolar oxygen transfer, neurotransmission, respiration, as well as its anti-inflammatory activities [12, 13]. Lundberg et al. [14] were some of the first to report that NO originates from the paranasal sinuses and that NO synthase is expressed in healthy sinus pneumocytes. In addition, Andersson et al. [15] found extremely high concentrations of NO in the paranasal sinuses, suggesting that the antra may act as NO reservoirs. Furthermore, Runer et al. [16] noted that NO is likely to be a regulator of mucociliary activity in the nasal airway. In contrast to these healthy states, Deja et al. [17] found significantly reduced NO production in maxillary sinuses of patients with sinusitis diagnosed using radiologic methods. Similarly, Naraghi et al. [18] reported that NO metabolites are higher in patients with chronic sinusitis and concluded that NO metabolites may play an important role in the pathogenesis of rhinosinusitis. In view of these findings, Degano et al. [19] investigated changes in NO concentration during the treatment of maxillary sinusitis. Using a protocol that included drainage, daily lavage, etc., a significant increase in the levels of maxillary and nasal NO was noted. Therefore, morphologic and functional optimization of the paranasal sinuses using non-surgical palatal expansion might be beneficial in the management of some sinus diseases.

In pediatric rhinitis, Wen et al. [20] consider that NO is a useful biomarker for both nasal inflammation and sinus ostial patency. In their study, they determined that obstruction of NO sino-nasal flow is likely associated with rhinosinusitis since NO concentrations returned to normal levels following antibiotic therapy. On the other hand, in a case series, Hwang et al. [21] reported their findings on pediatric rhinosinusitis during biomimetic oral appliance therapy (BOAT). **Figures 1a**–**3b** summarize their findings. In 3 consecutive pediatric patients (mean age 9 yrs.), Hwang et al. [21] used 3D cone-beam CT scans to show inflammatory maxillary sinus disease with circumferential mucosal thickening, obstructed ostio-meatuses, and enlarged inferior turbinates (**Figures 1a, 2a** and **3a**) prior to treatment. All 3 cases were treated using BOAT for approx. 10 months. Post-treatment, the sinuses were aerated without mucosal thickening; the sinus walls were intact, and the ostiomeatal units were patent (**Figures 1b, 2b** and **3b**). Although enhancement of maxillary air sinus structure

#### **Figure 1.**

*a: Case 1: Pre-treatment nasal floor width is 17.7 mm; b: Post-treatment nasal floor width increased to 19.5 mm.*

#### **Figure 2.**

*a: Case 2: Pre-treatment nasal floor width is 17.6 mm; b: Post-treatment nasal floor width increased to 19.3 mm.*

#### **Figure 3.**

*a: Case 3: Pre-treatment nasal floor nasal floor width is 15.3 mm; b: Post-treatment width increased to 18.7 m.*

and function through non-surgical remodeling is presumed, there is no clear mechanism of how the sinuses improved during BOAT in these cases. It is possible that the sinusitis resolved through the natural immune response, seasonal changes, through

normal craniofacial growth or the placebo effect. However, enlargement of the ostium (>20 mm2 ) is thought to decrease sinus NO concentration, as the size of the ostium shows correlation to NO levels [22]. Since the width of the nasal floor increased in these 3 cases (**Figures 1b, 2b** and **3b**), the notion that BOAT involved remodeling of the ostia to within normal limits is yet to be determined.

#### **4. Surgical midfacial expansion**

Aside from non-surgical palatal expansion, a plethora of surgical maxillary expansion procedures has become available. One study [23] compared the effects of non-surgical RME with surgically assisted rapid maxillary expansion (SARME). Surprisingly perhaps, there were no differences between the two protocols since nasal cavity width and volume, as well as maxillary width, increased with a concomitant decrease in nasal airway resistance. If non-surgical and surgical techniques yield similar results, one of the questions that currently remains unanswered is, how to minimize or avoid (orthognathic) surgery? To address this subject, Lee et al. [24] described the use of orthodontic screws for mini-screw-assisted rapid maxillary expansion (MARME), since some mistakenly believe that non-surgical palatal expansion relies on unwanted dental tipping rather than actual skeletal expansion. Bearing this in mind, Carlson et al. [25] treated a 19-year-old using MARME. Post-treatment, they reported enlargement in the zygomatic regions and nasal bone regions in association with widening of the circum-maxillary sutures. Indeed, MARME utilizes forces to split the midpalatal suture, which precipitates a midline diastema, an unwanted dental effect. However, insufficient force application may render MARME unsuccessful. Therefore, Suzuki et al. [26] deployed cortical punctures along the midpalatal suture followed by mini-screw insertion to fracture the midpalatal suture by 3-4 mm in an adult patient.

Despite the above variations, the impact of MARME on the upper airway and breathing is not clear. Recently, Abu-Arqub et al. [27] reviewed the effects of MARME on the upper airway in pediatric patients aged 10-17 yrs. They concluded that while short-term improvements were identifiable, no correlation was observed between upper airway morphology and functional parameters, such as nasal airflow and nasal resistance. Similarly, in older patients (mean age 20 yrs.), Yi et al. [28] found that although MARME produced both skeletal and dento-alveolar expansion, there were no changes in the oropharyngeal, palatopharyngeal, and glossopharyngeal regions and the total airway volume remained unaltered on 3D CBCT scans. In another study [29], it was reported that MARME produced an increase in nasal cavity and nasopharyngeal volumes, associated with bony expansion of the nasal floor and maxillary width in young adults (mean age 22.5 yrs.). Thus, when assessing changes on 3D CBCT scans after MARME, the association between skeletal changes and the upper airway remain unclear. Despite these assertions, Singh et al. [30] tested the hypothesis that the upper airway can be improved non-surgically in adults using BOAT. The mean treatment time was 16.5mos. and CBCT scan measurements were taken with no device in the patient's mouth. Their multivariate tests confirmed a significant treatment effect on the upper airway parameters (p = 0.012), suggesting that both craniofacial architecture and upper airway morphology can be non-surgically enhanced even in adults. However, this novel approach remains overlooked although further evidence is emerging.

To enhance orthopedics effect induced by MARME, 4 mini-implants with palatal and nasal cortical engagement are sometimes positioned in the palate, when using the maxillary skeletal expander (MSE) technique. Cantarella et al. [31] investigated the effects of this particular protocol on the midpalatal and pterygopalatine

sutures in young adults (mean age 17 yrs.). Using CBCT scans, it was found that the midpalatal suture was split slightly asymmetrically, being wider anteriorly than posteriorly. Moreover, pterygopalatine disjunction was revealed in over half of the cases studied, as the pyramidal process of the palatine bone was dislocated from the pterygoid processes. In a similar later study, Cantarella et al. [32] assessed facial changes associated with MSE, again using CBCT scans. Here, it was reported that the zygomatico-maxillary complex showed centrifugal changes with a "center of rotation" located at the fronto-zygomatic suture. Consequently, the inter-zygomatic distances and the fronto-zygomatic angles increased using MSE, but no data on any associated nasopharyngeal airway changes were reported in these particular studies. However, to further locate the center of rotation for the zygomatico-maxillary complex associated with MSE, Cantarella et al. [33] reported that the center of rotation for the zygomatico-maxillary complex could be found more inferiorly, posteriorly and laterally (near the zygomatic process of the temporal bone) compared with their other study [32]. In contrast, Paredes et al. [34] concluded that the center of rotation for the zygomatico-maxillary complex is located at the most infero-lateral point of the zygomatic process of the frontal bone. This variation in the center of rotational displacement could be due to bone deformations that are thought to occur during MSE, which might also explain the occurrence of pterygopalatine dislocation. In fact, Colak et al. [35] evaluated pterygopalatine disarticulation patterns after MSE. The vast majority of cases (> 80%) exhibited pterygopalatine disjunction without direct surgical intervention at this site. The clinical consequences of this iatrogenic fracture, if any, remain undetermined, at least as yet.

Recently, in order to avoid the potential risk of damaging anatomical structures, Cantarella et al. [36] suggested that the deployment of 3D virtual surgical planning using digital data might be advantageous prior to undertaking MSE. Elkenawy et al. [37] were also interested in the biomechanics of MSE. In their study, they noted that over half of approx. 30 adult patients exhibited an asymmetric response following splitting of the midpalatal suture. This result is perhaps not surprising since the midline vomero-maxillary suture would presumably provide an impediment to a symmetric split based *a priori* on fluctuating asymmetry [38]. Indeed, Schwarz et al. [39] examined adult patients for the incidence of nasal septal deviation following SARME. Although no post-operative changes in nasal septal positioning were found, maxillary rotation was associated with an inferior 'rotation' of the palatal vault with a concomitant increase in nasal airway space, although these authors attributed the increases to a decreased thickening of the pre-operative inflamed nasal mucosa. Nonetheless, Abedini et al. [40] were also interested in the soft tissue facial changes induced by MSE. Using 3D stereophotogrammetry, they computed mean 3D soft tissue geometries using techniques similar to those first described by Singh et al. [41, 42] for craniofacial data (**Figure 4**), and were able to demonstrate changes in the paranasal, upper lip, and zygomatic regions of the face associated with MSE. Therefore, clinicians and patients ought to be cognizant of the facial effects associated with MSE prior to embarking upon a treatment plan that putatively targets upper airway inadequacy.

Distraction osteogenesis maxillary expansion (DOME) is another technique that aims to improve the nasal airway changes through widening of the maxilla. Using this approach, Kunkel et al. [43] were able to enlarge the nasal airway volume by 23% on average without pterygomaxillary disjunction being a part of the surgical procedure, which occurs in any case. Despite this drawback, DOME is currently viewed as a reliable procedure to widen the nasal floor in adults with OSA. Using this protocol, the mean apnea-hypopnea index (AHI) was improved, nasal airflow velocity decreased and the mean negative pressures in the nasal, retropalatal, oropharyngeal, and hypopharyngeal airway were reduced, which correlated with a

*Sino-Nasal Changes Associated with Midfacial Expansion: An Overview DOI: http://dx.doi.org/10.5772/intechopen.99052*

#### **Figure 4.**

*Using CBCT data, the maxillary complex has been rendered in 3D virtual space and dense correspondence of (colored) landmarks has been computed using the ten homologous landmarks (1–10).*

reduction in the AHI, according to Iwasaki et al. [44]. These findings are, however, similar to the well-known results of non-surgical RME using fixed appliance in children. For example, in pediatric cases, Cozza et al. [45] reported that there was a reduction in nasal resistance with increased nasal airflow after RME. Indeed, RME is thought by some to be a comparatively non-invasive, economic treatment option to improve nasal respiration in patients up to at least 30 years of age. Gray [46] considers the medical indications for RME are a deficient nasal airway, septal deformity, recurrent ear infection, and allergic rhinitis, *inter alia*. In a series of over 300 consecutive selected cases, 80% changed their mode of oral breathing to nasal breathing. Thus, the advantages of MSE over RME in terms of nasal airway resistance and anatomical changes in the nasal cavity require further clarification.

#### **5. Nasal airway space, resistance and breathing**

In an early study, Warren et al. [47] assessed the effects of non-surgical RME and surgical expansion on nasal airway size. While both procedures improved the nasal airway, approx. 30% of subjects in both groups were unable to eliminate the need for mouth breathing, suggesting that neither RME nor surgical maxillary expansion is justified for nasal breathing purposes alone, likely due to individual variation in response. Bicakci et al. [48] were one of the first to assess the effect of RME on nasal cross-sectional area using acoustic rhinometry, confirming that the overall increase in the cross-sectional area was greater in the RME-treated groups when compared to controls. Around the same time, Ceroni-Compadretti et al. [49] also reported that RME increased both the width of the maxilla and the nasal volume, as measured with acoustic rhinometry. Furthermore, Compadretti et al. [50] deployed rhinomanometry and acoustic rhinometry to assess the function and size of the nasal cavities associated with RME in children. Compared to a control group, the RME treatment group showed an increase in nasal cross-sectional area and volume, as well as a decrease in nasal airway resistance, but the study was unable to confirm the clinical mode of breathing. Likewise, Palaisa et al. [51], using CT scanning, explored the relationship between morphologic changes in nasal area and volume following RME in young patients (8-15 yrs). They reported symmetric increases in both nasal cavity area and volume although the variance in response was again large. Similarly, Oliveira de Felippe et al. [52] concluded that

post-expansion, while nasal cross-sectional area increased when measured using acoustic rhinometry, and nasal cavity volume increased using 3D imaging, only 60% of subjects reported subjective improvement in nasal respiration. Therefore, Enoki et al. [53] correctly concluded that RME may lessen nasal resistance but subtle differences in nasal geometry, such as shape changes as opposed to size-changes, may influence success in switching from mouth breathing to nasal respiration.

Currently there is a lack of consensus on the reliability of RME-related procedures in improving nasal functional behaviors, such as changing mouth breathing to nasal breathing predominantly. Hershey et al. [54] noted that patients' subjective opinions on changes in the ability to breathe nasally are not correlated to reductions in treatment-induced nasal resistance, even though RME is effective in reducing nasal resistance to levels consistent with nasal respiration. For example, Doruk et al. [55] found that nearly 60% of 13-yr-olds considered their nasal breathing had improved following RME using subjective evaluation. Earlier, using rhinomanometry, Timms [56] measured nasal airway resistance prior to and after RME in patients aged 10 to 19.5 yrs. On average, a 36% reduction in nasal resistance was reported but this did not correlate with the transpalatal or trans-alar width increases post-expansion. Similarly, Hartgerink et al. [57] surmise that individual variation in nasal resistance values is considerable and that average response variability renders RME unpredictable in terms of decreasing nasal resistance despite evidence of expansion at the anterior nares. In this regard, White et al. [58] reported a mean reduction in nasal airway resistance of approx. 50% after about one-year post-RME. Moreover, they noted that the reduction in nasal airway resistance was correlated to the initial nasal resistance level prior to RME, and that individuals with greater resistance preexpansion tended to have greater reductions post-treatment. This notion had earlier been investigated using a multidisciplinary approach [59]. Utilizing a combination of RME and oral myofunctional assessment using rhinomanometric measurements, two phenotypes were identified: first, predominantly mouth breathers, showing an average nasal airway resistance decrease of 34%; and second, predominantly nasal breathers with an average nasal airway resistance decrease of <5%. Notably, 75% of predominantly mouth breathers were converted to nasal breathing. Thus, it appears that maxillary deficiency allied with functional deficits needs a tailored approach to be adopted to address the mode of respiration.

It is thought that nasal surgery alone can fail to restore nasal breathing in various cases with maxillary restriction, which is associated with closure of the internal and external nasal valves. In addition, although some now generally agree that RME in both children and adults increases upper airway volume, it remains uncertain whether maxillary expansion improves nasal function. Thus, recently, Iwasaki et al. [60] investigated the efficacy of three RME appliances on nasal ventilation in 10-16 yr. old patients. They reported that RME reduced nasal pressure and nasal airflow velocity, which was accompanied by resolution of nasal obstruction. Nevertheless, Calvo-Henriquez et al. [61] undertook a systematic review on this subject, concluding that there is insufficient evidence to recommend maxillary expansion as a first-line therapy to improve nasal breathing. Despite this assertion, one aspect that remains under-investigated at this juncture is the role of nasal exercises. In the interpretation of numerous studies, it has simply been assumed that an increase or enhancement of anatomical form will result in the desired functional response. But, in their review, Levrini et al. [62] suggest that if RME is combined with functional rehabilitation, the chances of changing a mouth-breathing pattern to nasal respiration are increased. Therefore, the role of respiratory therapists and/ or oral myofunctional therapists may need to be extended to include nasal breathing exercises perhaps allied with the use of capnography for biofeedback. In any case, Kiliç and Oktay [63] are of the opinion that while RME increases nasopharyngeal

#### *Sino-Nasal Changes Associated with Midfacial Expansion: An Overview DOI: http://dx.doi.org/10.5772/intechopen.99052*

airway dimensions and nasal respiration in pediatric patients exhibiting maxillary constriction and mouth breathing, RME could also be effective on naso-respiratory and sleep-disordered breathing problems in children.

Pirelli et al. [64] evaluated the effect of RME on nasal airway patency and pediatric OSA. On postero-anterior and occlusal radiographic assessment, widening of the midpalatal suture and nasal fossae were confirmed, and restoration of nasal airflow was associated with elimination of obstructive sleep disordered breathing. Therefore, changing the anatomic structure using RME produced significant functional improvement in pediatric patients diagnosed with OSA. On the other hand, Garcez et al. [65] demonstrated the effects of MSE on respiratory function and athletic performance. Using CBCT scans they reported a 6 mm widening of the midpalatal suture and nasomaxillary structures, while the nasal and pharyngeal airways also increased in volume by 30%. In addition, all respiratory indices improved after MSE. Thus, MSE can potentially have a positive influence on both respiratory functions and athletic performance. Recently, Singh et al. [30] also reported a 14% increase in nasal cavity volume achieved non-surgically in adults using a biomimetic oral appliance. Therefore, one of the research question that needs to be addressed now is: Which procedure best suits a particular patient's requirements both safely and effectively? Taking a cohort of cases that have had the same intervention, it should be possible to compute the mean, underlying transformation for a sample of cases. If this transformation can then be applied to a naïve subject, a predictive model can be achieved, assuming the new subject behaves in the same way that the sample did on average. Therefore, the use of mathematical modeling on 3D digital data provides a promising avenue of future research in terms of virtual treatment planning, perhaps incorporating the use of artificial intelligence to inform clinical decision-making.

#### **6. Conclusion**

Non-surgical and surgical midfacial expansion techniques are associated with functional sinus changes in the paranasal sinuses as well as changes in nasal airway space, nasal resistance and the mode of breathing. To address the question of which procedure best suits a particular patient's requirements both safely and effectively, the use of mathematical modeling provides a promising approach.

#### **Conflict of interest**

Professor G. Dave Singh is Founder and Chief Medical Officer of Vivos Therapeutics, Inc., USA. He is currently collaborating with Stanford University in the development of a craniofacial facility.

*Paranasal Sinuses Anatomy and Conditions*

#### **Author details**

G. Dave Singh Institute for Craniofacial Sleep Medicine, Highlands Ranch, USA

\*Address all correspondence to: drsingh@drdavesingh.com

© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

*Sino-Nasal Changes Associated with Midfacial Expansion: An Overview DOI: http://dx.doi.org/10.5772/intechopen.99052*

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[27] Abu-Arqub S, Mehta S, Iverson MG, Yadav S, Upadhyay M, Almuzian M. Does Mini Screw Assisted Rapid Palatal Expansion (MARPE) have an influence on airway and breathing in middle-aged children and adolescents? A systematic review. Int Orthod. 2021;19:37-50.

[28] Yi F, Liu S, Lei L, Liu O, Zhang L, Peng Q, Lu Y. Changes of the upper airway and bone in microimplantassisted rapid palatal expansion: A cone-beam computed tomography (CBCT) study. J Xray Sci Technol. 2020;28:271-283.

[29] Li Q, Tang H, Liu X, Luo Q, Jiang Z, Martin D, Guo J. Comparison of dimensions and volume of upper airway before and after mini-implant assisted rapid maxillary expansion. Angle Orthod. 2020;90:432-441.

[30] Singh GD, Kim HN, Kim SH, Wang L. 3D craniofacial and upper

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airway changes after biomimetic oral appliance therapy in Korean adults. Otorhinolaryngol Head Neck Surg. 2021;6:1-7.

[31] Cantarella D, Dominguez-Mompell R, Mallya SM, Moschik C, Pan HC, Miller J, Moon W. Changes in the midpalatal and pterygopalatine sutures induced by micro-implantsupported skeletal expander, analyzed with a novel 3D method based on CBCT imaging. Prog Orthod. 2017;18:34.

[32] Cantarella D, Dominguez-Mompell R, Moschik C, Mallya SM, Pan HC, Alkahtani MR, Elkenawy I, Moon W. Midfacial changes in the coronal plane induced by microimplantsupported skeletal expander, studied with cone-beam computed tomography images. Am J Orthod Dentofacial Orthop. 2018;154:337-345.

[33] Cantarella D, Dominguez-Mompell R, Moschik C, Sfogliano L, Elkenawy I, Pan HC, Mallya SM, Moon W. Zygomaticomaxillary modifications in the horizontal plane induced by micro-implant-supported skeletal expander, analyzed with CBCT images. Prog Orthod. 2018;19:41.

[34] Paredes, N., Colak, O., Sfogliano, L. et al. Differential assessment of skeletal, alveolar, and dental components induced by microimplant-supported midfacial skeletal expander (MSE), utilizing novel angular measurements from the fulcrum. Prog Orthod. 2020;21:18.

[35] Colak O, Paredes NA, Elkenawy I, Torres M, Bui J, Jahangiri S, Moon W. Tomographic assessment of palatal suture opening pattern and pterygopalatine suture disarticulation in the axial plane after midfacial skeletal expansion. Prog Orthod. 2020;21:21.

[36] Cantarella D, Savio G, Grigolato L, Zanata P, Berveglieri C, Lo Giudice A, Isola G, Del Fabbro M, Moon W. A New Methodology for the Digital Planning of Micro-Implant-Supported Maxillary Skeletal Expansion. Med Devices (Auckl). 2020;13:93-106.

[37] Elkenawy I, Fijany L, Colak O, Paredes NA, Gargoum A, Abedini S, Cantarella D, Dominguez-Mompell R, Sfogliano L, Moon W. An assessment of the magnitude, parallelism, and asymmetry of micro-implant-assisted rapid maxillary expansion in nongrowing patients. Prog Orthod. 2020;21:42.

[38] Auffray, J.C.; Debat, V.; Alibert, P. Shape asymmetry and developmental stability. In: Chaplain MAJ, Singh GD, McLachlan JC, editors. On Growth and Form: Spatio-Temporal Pattern Formation in Biology. Chichester: Wiley; 1999. p. 309-324.

[39] Schwarz GM, Thrash WJ, Byrd DL, Jacobs JD. Tomographic assessment of nasal septal changes following surgicalorthodontic rapid maxillary expansion. Am J Orthod. 1985;87:39-45. doi: 10.1016/0002-9416(85)90172-1.

[40] Abedini S, Elkenawy I, Kim E, Moon W. Three-dimensional soft tissue analysis of the face following microimplant-supported maxillary skeletal expansion. Prog Orthod. 2018;19:46.

[41] Singh GD, McNamara JA Jr., Lozanoff S. Morphometry of the cranial base in subjects with Class III malocclusion. J. Dent. Res. 1997;76: 694-703.

[42] Singh GD, Levy-Bercowski D, Yañez MA, Santiago PE. Threedimensional facial morphology following surgical repair of unilateral cleft lip and palate in patients after nasoalveolar molding. Orthod Craniofac Res. 2007;10: 161-166.

[43] Kunkel M, Ekert O, Wagner W. [Changes in the nasal airway by transverse distraction of the maxilla]. Mund Kiefer Gesichtschir. 1999;3:12-6. [Article in German]

[44] Iwasaki T, Yoon A, Guilleminault C, Yamasaki Y, Liu SY. How does distraction osteogenesis maxillary expansion (DOME) reduce severity of obstructive sleep apnea? Sleep Breath. 2020;24:287-296.

[45] Cozza P, Di Girolamo S, Ballanti F, Panfilio F. Orthodontistotorhinolaryngologist: an inter disciplinary approach to solve otitis media. Eur J Paediatr Dent. 2007;8: 83-88.

[46] Gray LP. Results of 310 cases of rapid maxillary expansion selected for medical reasons. J Laryngol Otol. 1975;89:601-614.

[47] Warren DW, Hershey HG, Turvey TA, Hinton VA, Hairfield WM. The nasal airway following maxillary expansion. Am J Orthod Dentofacial Orthop. 1987;91:111-116.

[48] Bicakci AA, Agar U, Sökücü O, Babacan H, Doruk C. Nasal airway changes due to rapid maxillary expansion timing. Angle Orthod. 2005;75:1-6.

[49] Ceroni Compadretti G, Tasca I, Alessandri-Bonetti G, Peri S, D'Addario A. Acoustic rhinometric measurements in children undergoing rapid maxillary expansion. Int J Pediatr Otorhinolaryngol. 2006;70:27-34.

[50] Compadretti GC, Tasca I, Bonetti GA. Nasal airway measurements in children treated by rapid maxillary expansion. Am J Rhinol. 2006;20: 385-393.

[51] Palaisa J, Ngan P, Martin C, Razmus T. Use of conventional tomography to evaluate changes in the nasal cavity with rapid palatal expansion. Am J Orthod Dentofacial Orthop. 2007;132:458-466.

[52] Oliveira De Felippe NL, Da Silveira AC, Viana G, Kusnoto B, Smith B, Evans CA. Relationship between rapid maxillary expansion and nasal cavity size and airway resistance: short- and long-term effects. Am J Orthod Dentofacial Orthop. 2008;134: 370-382.

[53] Enoki C, Valera FC, Lessa FC, Elias AM, Matsumoto MA, Anselmo-Lima WT. Effect of rapid maxillary expansion on the dimension of the nasal cavity and on nasal air resistance. Int J Pediatr Otorhino laryngol. 2006;70:1225-1230.

[54] Hershey HG, Stewart BL, Warren DW. Changes in nasal airway resistance associated with rapid maxillary expansion. Am J Orthod. 1976;69:274-284.

[55] Doruk C, Sökücü O, Sezer H, Canbay EI. Evaluation of nasal airway resistance during rapid maxillary expansion using acoustic rhinometry. Eur J Orthod. 2004;26:397-401.

[56] Timms DJ. The effect of rapid maxillary expansion on nasal airway resistance. Br J Orthod. 1986; 13:221-228.

[57] Hartgerink DV, Vig PS, Abbott DW. The effect of rapid maxillary expansion on nasal airway resistance. Am J Orthod Dentofacial Orthop. 1987;92:381-389.

[58] White BC, Woodside DG, Cole P. The effect of rapid maxillary expansion on nasal airway resistance. J Otolaryngol. 1989;18(4):137-143.

[59] Wollens AG, Goffart Y, Lismonde P, Limme M. [Therapeutic maxillary expansion]. Rev Belge Med Dent (1984) 1991;46:51-8. [Article in French]

[60] Iwasaki T, Papageorgiou SN, Yamasaki Y, Ali Darendeliler M, Papadopoulou AK. Nasal ventilation and rapid maxillary expansion (RME): *Sino-Nasal Changes Associated with Midfacial Expansion: An Overview DOI: http://dx.doi.org/10.5772/intechopen.99052*

a randomized trial. Eur J Orthod. 2021 Feb 10:cjab001.

[61] Calvo-Henriquez C, Megias-Barrera J, Chiesa-Estomba C, Lechien JR, Maldonado Alvarado B, Ibrahim B, Suarez-Quintanilla D, Kahn S, Capasso R. The impact of maxillary expansion on adults' nasal breathing: A systematic review and meta-analysis. Am J Rhinol Allergy. 2021:1945892421995350. doi: 10.1177/1945892421995350. Epub ahead of print.

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[63] Kiliç N, Oktay H. Effects of rapid maxillary expansion on nasal breathing and some naso-respiratory and breathing problems in growing children: a literature review. Int J Pediatr Otorhinolaryngol. 2008;72:1595-1601.

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[65] Garcez AS, Suzuki SS, Storto CJ, Cusmanich KG, Elkenawy I, Moon W. Effects of maxillary skeletal expansion on respiratory function and sport performance in a para-athlete – A case report. Phys Ther Sport 2019;36:70-77.

#### **Chapter 6**

## Maxillary Sinus in Dental Implantology

*Nikolay Uzunov and Elena Bozhikova*

#### **Abstract**

Dental implants have significantly increased prosthetic options for the edentulous patient. Implant placement in the posterior maxilla may often be hampered due to anatomical limitations, inadequate height and width, and poor bone quality. After tooth extraction, three-dimensional physiological resorption and sinus expansion take place and reduce the volume of the alveolar ridge. The concomitant actions of alveolar atrophy and sinus pneumatization reconstruct the subantral alveolar segment into a low, shallow, and sloped ridge which is incapable to accommodate dental implants and bear the functional strains. Advanced maxillary resorption can be managed by several surgical options, the most popular of which is maxillary sinus floor elevation. The chapter discusses recent advancements in bone biology and biomechanics in the light of alveolar atrophy and the impact of anatomy on maxillary sinus floor elevation as a treatment modality for the partially or totally edentulous patient.

**Keywords:** maxillary sinus floor elevation, dental implants, maxillary atrophy, maxillary pneumatization, maxillary edentulism

#### **1. Introduction**

Dental implants (DI) have significantly increased prosthetic options for the edentulous patient. However, implant placement in the posterior maxilla is often hampered by anatomical limitations such as inadequate vertical and buccopalatal dimensions, poor bone quality, thin or missing cortex, and undercuts. Following tooth extraction, three-dimensional resorption of the alveolar ridge takes place and reduces its' dimensions; in addition, the periosteum of the maxillary sinus (MS) can exhibit an increase in osteoclastic activity. The latter can aggravate the physiological process of maxillary sinus pneumatization (MSP) or aeration. The concomitant actions of postextraction alveolar atrophy (AA) and MSP worsen the subantral alveolar dimensions in short terms and makes doubtful the prosthetic rehabilitation with DIs, as adequate bone height and width are mandatory to implant treatment [1–4]. The principal solution for alveolar insufficiency is to augment the distal maxilla. Several surgical approaches have the potential to improve the subantral osseous environment to prepare the edentulous segment for the accommodation of DI, and the most popular is maxillary sinus floor elevation (MSFE).

#### **2. Alveolar atrophy after tooth extraction**

Alveolar atrophy is defined as loss or diminution of supportive alveolar bone due to loss of teeth or to function, trauma, reduced blood supply, or unknown cause [5]. The most common reason for AA is the alveolar resorption after tooth loss [6]. Removal of a tooth is followed by remodeling and reduction of the buccolingual and apicocoronal dimensions of the edentulous segment and results in a shorter and narrower alveolar ridge [6–10]. Unaddressed, postextraction AA develops through the whole lifespan of the person (**Figure 1**). Jaws with progressive bone loss are subjected to continuing anatomical make-over that alters normal orofacial tissue configuration which may affect the social integration and realization of the affected individuals. In advanced AA cases, adequate anatomical, functional, and esthetic rehabilitation is highly complicated.

#### **2.1 Physiology and biomechanics of bone atrophy**

In 1881 Wilhelm Roux suggested that the natural forces acting on the alveolar ridge are reduced after tooth loss. As result, less bone is needed to maintain function, and, consequently, the body gets rid of the non-functioning structures. It was concluded that loss of alveolar bone after tooth removal is an example of disuse atrophy. Eleven years later Wolff's law stated that bone tissue adapts its mass and architecture to the mechanical demands [10].

It was understood that loads play a key role in bone biology. The principles of biomechanics were applied to present bone mass maintenance and resorption as a reaction to continuously repeated loading impetus. The daily stress stimulus theory of bone adaptation was formulated to describe the loading conditions necessary to support bone mass and recognized the stress/strain magnitude and loading cycle number as sufficient to define an appropriate maintenance loading signal [11]. Frost [12] published a hypothesis on a provisional general model of the skeleton's mechanostat. According to this hypothesis, the mechanostat spans the biological distance

**Figure 1.** *Advanced maxillary and mandibular alveolar atrophy in a 64-year-old male.*

#### *Maxillary Sinus in Dental Implantology DOI: http://dx.doi.org/10.5772/intechopen.99780*

between organs and macromolecules and can be applied to "all organs and tissues, including bone, made wholly or in part from the basic tissues". It was proposed that "interlocking negative feedback loops" provide mechanical-usage-dedicated message traffic routes on which nonmechanical agents could act to optimize postnatal skeletal adaptations to varied mechanical and nonmechanical challenges, and treatments of disease [12]. The understanding that mechanical stimuli can be transferred to the bone by a signaling network was further developed by Burger and Klein-Nulend in the mechanotransduction concept. They pointed that the osteocytes function as mechanosensory cells of osseous tissues and explained the capacity of bone to change its mass and structure in response to mechanical demands within specific cellular mechanisms [13].

For a long time, the contribution of osteocytes to bone biology was undervalued as they were accepted as terminal stage cells of the osteoblastic lineage. Recent investigations addressed the osteocytes and their role in bone orchestration and revealed that they may have mechanosensory, endocrine, and homeostatic activity.

Osteocytes are the most abundant bone cells and the only cells embedded in the bone mineral matrix. After being entrapped in bone, the osteocytes are housed within lacunae and connect to each other by cytoplasmic processes hosted in channels called canaliculi. The lacunae and the canaliculi form a three-dimensional (3D) network named the lacuno-canalicular network (LCN). In the light of mechanotransduction, the strains in bone accumulated under loads may induce a strainderived flow of interstitial fluid through the LCN which mechanically activates the osteocytes to respond to the loading stimuli and ensure the transport of cell signaling molecules, nutrients, and waste products. This explains local bone gain, loss, and remodeling, in response to fatigue damage, as cellular and intercellular activity supervised by the mechanosensitive osteocytes [13]. The LCN is a negative imprint of the cellular network in the bone and its morphology is considered to play a central role in bone mechanosensation and mechanotransduction [14]. Within the LCN, the osteocytes can transport nutrients, biochemical signals, and hormonal stimuli, enabling the integration of the information between and interaction with other bone cells [15].

The general existence and micro-anatomy of the LCN have been known for a long time. The connections of the osteocyte network with other regions of the body [16] and its importance for phosphate metabolism [13, 15] were debated in recent research [17, 18]. As endocrine cells, osteocytes have an impact on many organs [16]. They communicate with the kidney through the factor FGF23 [19], and with the brain, through the expression of leptin [20]. The osteocytes could be regulators of bone resorption by secreting the Receptor activator of NF-κB ligand (RANKL) [21] and control bone formation by producing WNT1 glycoprotein [22, 23]. They contribute to fat metabolism by secreting sclerostin, which promotes the increase of beige adipogenesis [22], and influence hematopoiesis by the adjustment of the endosteal microenvironment through the release of soluble factors [24].

The connectivity between osteocytes themselves is of crucial importance to understand bone health [17]. Within the complex communication between cells, the osteocyte network acts as a mechano-sensory organ [25]. Through sensing the fluid flow in LCN and sclerostin expression, the osteocytes regulate bone's mechanobiological adaptation and remodeling [26]. The hypothesis of the LCN connectome, paralleling the neurosensory connectome, is emerging from the complex LCN organization and wealth of connections within the bone and with other organs [17].

It is important to distinguish between the LCN and the osteocyte network as a connected cell network. However, most of the functions of the osteocyte network can only be understood in the interplay between the "biological" cell network and the "material" porosity in the mineralized matrix [25]. In human osteons, canaliculi that are not oriented towards the Haversian canal were found to be co-aligned with the preferred matrix orientation. The pericanalicular matrix in the immediate vicinity of the cell processes was shown to be disordered and more mineralized with increased thickness of the mineral particles incorporated in the collagen matrix. This higher mineral content around the canaliculi is remarkable in the context of the osteocytes' contribution to calcium and phosphate metabolism. Recent evidence revived the almost forgotten idea of osteocytic osteolysis. Due to the high surface area of the LCN and the small distance from the LCN to any point in the bone matrix, osteocytes have easy access to the bone mineral and can demineralize bone. The role of osteocytes as mechanosensors and orchestrators of bone remodeling depends crucially on the interaction between cell network and porous network.

The fluid flow hypothesis assumes that mechanical loads squeeze interstitial bone fluid through the pericellular space between the cell processes and bodies in the canaliculi and lacunae. The osteocytes and their processes sense the shear forces caused by the fluid flow, and it seems that the cell processes are more mechanosensitive than the cell body. The details of the fluid flow and the resulting shear forces do not only depend on the connectivity and the irregular shape of the canaliculi, but also on how the cells deform due to the flow and how the cell processes are anchored on the canaliculi walls [17]. More recently, a newly discovered cell type, osteomorphs, was proved to participate in bone resorption and remodeling. It was shown that osteoclasts recycle via osteomorphs and that the latter may be targeted for the treatment of resorptive skeletal diseases [27].

#### **2.2 Biomechanics of alveolar bone**

It was confirmed that the grounds of understanding bone physiology are the osteocyte reactions to stress stimuli, inducing bone resorption, remodeling, and adaptation, on one hand, and biomechanics, on the other. Several investigations addressed the biomechanics of bone adaptation. Qin et al. examined a turkey ulna model of disuse osteopenia to determine whether the daily stress theory of bone adaptation can be applied to conditions of very high numbers of loading cycles at very low strain magnitudes [28]. They found that the strain stimulus needed per day to maintain bone mass could be expressed by the formula

$$y = \mathbf{10}^{\text{res}} \left( \mathbf{5.6} - \log \mathbf{10} \mathbf{x} \right)^{\text{tr}} \tag{1}$$

where *x* is the number of loading cycles per day and *y* is the strain magnitude. The results proved the strong antiresorptive influence of mechanical loading identifying a threshold for a daily loading cycle regimen near 70 microstrain of approximately 100,000 strain cycles, and suggest that the strain frequency or strain rate associated with the loading stimulus must also play a critical role in the mechanism by which bone, as a tissue, responds to mechanical loads.

In 2012 Hansson and Halldin tested such experiments and investigated, in the light of mechanics of materials, the correlation between established principles of bone physiology and the changes in the dimensions of the alveolar ridge after tooth extraction [10]. Their considerations were based on the mathematical presentation of principal stresses and strains acting on the mandible as a beam subjected to loads and, also, the differences in the response of cancellous and cortical bone to strains. Data analysis from clinical and experimental investigations on the effects of strains on lamellar organization and orientation of cancellous bone [29–31], the alignment of the Haversian systems in cortical bones [32], and bone mass dependence on the magnitude

#### *Maxillary Sinus in Dental Implantology DOI: http://dx.doi.org/10.5772/intechopen.99780*

of strains, was integrated with experimental findings on the healing of postextraction sockets and resorption of the empty alveolar ridge. One month after tooth extraction the empty socket is filled with woven bone. Three months later the woven bone is substituted by a cortical ridge-like structure consisting of lamellar and woven bone which, in turn, is substituted in the sixth month by an alveolar ridge constructed of lamellar bone and bone marrow [33]. It was also pointed that the resorption of the buccal and lingual alveolar walls occurs in two overlapping phases; in the first phase, the bundle bone is resorbed and replaced with woven bone, while the second phase includes resorption from the outer surface of both bone walls, and that the resorption is larger at the buccal aspect of the ridge than at the lingual aspect [34–37].

Considering the mandible as a beam subjected to strains, i.e., bending moments, the authors speculated that the extraction socket will gradually be filled with lamellar and cancellous bone, which will make the healed extraction site stiffer both to horizontal and vertical bending. The bending moments remain unchanged and, consecutively, the bone strains will be reduced [10]. Reduced bone strains result in bone loss [28, 38]. Speculation on bone physiology and biomechanics brings the conclusion that alveolar and jaw resorption is a natural result of the fundamental physiological principle of adaptation of bone mass and bone structure to the levels and frequencies of strain [10].

#### **3. Practical aspects of alveolar atrophy of the distal maxilla**

#### **3.1 Alveolar atrophy and dental implants**

Masticatory forces are distributed to the skull through the fronto-maxillary (frontonasal), the zygomatico-maxillary, and the pterygomaxillary pillars, and the palatine arch [38, 39]. DI placement requires bony structures with adequate volume, and [1] therefore, the volume of the alveolar crest is a principal consideration for DI treatment. In the distal maxilla, the subantral height, i.e., the height of the inferior MS wall, and width of the alveolar span are of crucial importance in treatment planning.

After tooth loss, the alveolar bone undergoes fast remodeling that leads to horizontal and vertical decrease of crestal dimensions [6, 40]. When, after tooth extraction, the alveolus is occupied by bone, or by DI and bone, the stiffness of the edentulous span will be increased. With unchanged loads, increased stiffness implies reduced strains, and the strain stimulus needed to maintain bone mass is no longer reached. The biological response to this is to remove bone and reduce the bony volume. Therefore, placing a DI in the empty alveolus will increase alveolar stiffness, and, theoretically, immediate DI placement into fresh extraction sockets should not be expected to prevent the dimensional reduction of the alveolar ridge [10].

Clinical trials and systematic reviews demonstrated that horizontal and vertical resorption is more pronounced at the buccal aspect of the ridge than at the lingual aspect [34, 35, 37, 41–43] and that the horizontal reduction is greater than the loss in height [34]. The consequence of a greater vertical bone loss buccally than lingually is a ridge that is sloped in the lingual to the buccal direction (**Figure 2**). A new "tug-of-war" hypothesis explains the more pronounced buccal resorption with the forces acting at the empty socket after tooth loss and the activity of the myofibroblasts as their pull is directed from the buccal and palatal edges towards the center of the alveolus. Since the balance depends on the relative mass of the two edges, the thin buccal wall would be the one to cede under the tension of the granulation tissue [44].

**Figure 2***. Advanced alveolar atrophy of the mandible resulting in a sloped alveolar ridge.*

**Figure 3.** *The sloped alveolar ridge does not allow for placement of DI without ridge augmentation.*

In cases with a sloped alveolar ridge, the insertion of standard DI might not be optimal (**Figure 3**). Implant placement in level with the lingual bone margin may result in compromised esthetics. If DI instead is placed at a level with the buccal margin, the lingual marginal bone is at risk to be resorbed due to insufficient strain stimulus. In a clinical study, DI with a sloped marginal contour was used in cases with an alveolar crest sloped in lingual to buccal direction. Both the mean buccal marginal bone level change and the mean lingual marginal bone level change after 16 weeks amounted to −0.2 mm. Thus, the installation of a DI with a sloped marginal contour may be a treatment option in cases where the alveolar ridge is sloped in lingual to the buccal direction [10, 45].

#### **3.2 Atrophy of the distal maxilla**

The above line of arguments can be applied to the maxilla with its complicated anatomy, lesser bone density, and aeration. Disuse atrophy creates a sloped and

#### *Maxillary Sinus in Dental Implantology DOI: http://dx.doi.org/10.5772/intechopen.99780*

reduced in height alveolar profile, constructed mostly from soft trabecular bone. Moreover, the edentulous maxillary posterior sextants were shown to have the least amount of residual bone height compared with other edentulous regions of the maxilla and, therefore, represent one of the most critical areas to be rehabilitated by an implant-supported prosthesis [46]. In addition, the postextraction bone resorption in the distal maxilla may be associated with MSP, which may contribute to a further decrease of the available bone volume for DI placement [47].

#### **3.3 Residual alveolar height of the distal maxilla and maxillary sinus pneumatization**

The aeration of the paranasal cavities is a physiological process the effect of which is an increase in sinus volume and decrease in the volume of the surrounding bone during growth. MSP adds additional three-dimensional reduction to the postextraction alveolar resorption in the distal maxilla (**Figure 4**) [2, 40].

The MS begins its development in the 10th week. At the time of birth, the sinus is already pneumatized and increases in size through continuous MSP during the whole life of the individual [48, 49]. With the eruption of the permanent dentition, MSP is paused, and the sinus reaches 4–5 mm below the nasal cavity as an alveolar recess [50]. The variations in MS volume and dimensions among individuals and tooth position are significant. The alveolar recess can project between adjacent teeth or between the roots of the same tooth [51]. This is often observed between the roots of the first and the second molar which have a very close relationship to the sinus floor [52–55]. Tooth loss unlocks sinus aeration again and its effect is added to the effect of the postextraction alveolar resorption.

Several studies reported significant MSP after tooth extraction and accepted that alveolar bone height in the edentulous distal maxilla is a result of the concomitant actions of crestal atrophy and apical sinus enlargement. The anatomical and pathological peculiarities of the distal maxilla contribute to the MS expansion after removal of the first and the second upper molars. The ultimate anatomical

#### **Figure 4.**

*Advanced alveolar atrophy and pneumatization of the distal maxilla. Note that the subantral height is 1 mm on the left and even less on the right (white arrows). The sinus pneumatization extends into the premolar region and lies beneath the nasal floor bilaterally approximating the canines. A well-defined sinus floor septum is found in the right (yellow arrow). The sinus drainage is doubtful on both sides, due to thickened mucosa.*

consideration is the proximity between the root apices of these teeth and the sinus floor [2, 40, 55–57]. This means that the height of the bony roofs of the alveoli of the upper molars, i.e., the thickness of the inferior sinus wall, is anatomically small, and, in turn, can be more readily reduced by AA and MSP even in cases without preceding pathology in or trauma to this region. The same is the cause for asymptomatic cortical bone fractures of the alveolar roof during upper molar extraction. Extensive ridge atrophy and MSP can be provoked by the removal of teeth which roots elevate the sinus floor or are enveloped by a superiorly curving floor. Multiple extractions within the same segment initiate more aggressive AA and MSP and reduce considerably ridge volume and resistance to the loading stimuli. Considering that the causes for tooth loss are mainly periapical and/or periodontal pathology, and trauma, it becomes clearer why postextraction alveolar resorption is often accelerated at the distal maxilla and why the loss of maxillary molars is considered to provoke excessive MSP [2, 40, 57–60]. It is not still completely understood how much atrophy and MSP contribute actually to the total loss of bony height [2, 61, 62].

Other studies could not confirm MS expansion after tooth loss [63, 64]. The role of residual ridge resorption and MSP was recently addressed in the overall maxillary bony atrophy using principal components analysis [65]. They found that most of the bone loss occurring in the alveolar process is caused by disuse atrophy due to edentulism and concluded that while the alveolar crest is changed by tooth loss, the MS is not, which refers sinus depth to anatomical variation independent of dentition. Prolonged edentulism in the maxillary molar region leads to centripetal and, to minor degrees, to centrifugal ridge resorption. Minor MSP occurs in the walls thinning the buccal and palatal aspects, which may be attributed to the absence of roots or variation in force transmission to the zygomatic or the nasopalatal buttresses [65].

The reasons for MSP after tooth extraction are still debated. With tooth loss, the functional forces which are normally transferred to the bone are weakened which can cause a shift in the physiologic bone remodeling to a resorptive pattern [58]. Previous studies demonstrated a downward expansion of the MS after tooth loss and showed that it was larger if the extracted tooth was surrounded by a superiorly curved sinus floor [2, 66–68].

In conclusion, advanced alveolar resorption constitutes a sloped alveolar ridge with inadequate bone volume and quality that limits conventional DI treatment. The bone density in the distal maxilla is the lowest in comparison to other jaw regions. The edentulous upper molar alveolar ridge presents with a thin cortex and a loose trabecular subcortical bone. This means that the biomechanical properties and the healing potential of this segment may be insufficient to secure primary DI stability and graft consolidation.

#### **4. Maxillary sinus floor elevation**

Treatment limitations present functional and esthetic impairments to the affected individuals. In such cases, the rehabilitation of the altered jaw segments necessitates the reconstruction of the missing dentoalveolar tissues. An increasing number of patients with edentulous posterior maxilla needs bone and soft tissue augmentation procedures to allow proper DI placement and achieve satisfactory results [46].

Maxillary sinus floor elevation (MSFE) is a treatment concept the purpose of which is volume augmentation of the distal maxilla to enhance the prosthetic rehabilitation of partial or total maxillary edentulism with DI. The goal is achieved with two basic surgical techniques and their variations that share a common key point which is to intrude the subantral alveolar ridge, or part of it, into the sinus,

#### *Maxillary Sinus in Dental Implantology DOI: http://dx.doi.org/10.5772/intechopen.99780*

thus establishing a new sinus bottom at a higher level and creating an empty space between it and the alveolar crest. Various grafting techniques are applied at the empty space to induce new bone formation and convert it into a newly constructed ridge allowing placement of DI. The two main surgical approaches of MSFE are the lateral window (external) approach and the transalveolar (internal) approach [69].

*The lateral window technique (external approach)* was first presented by Tatum at the Birmingham, Alabama, implant meeting of 1976 [70]. The first publication on the technique was made by Boyne and James in 1980 [71]. The classical operation consists of the preparation of a top hinge door in the lateral sinus wall, which is luxated inward and upward together with the Schneiderian membrane to a horizontal position forming the new sinus bottom. The space below the new sinus bottom is filled with graft material. In cases with sufficient alveolar height (±4 mm) for primary stability, the DI can be inserted simultaneously with the MSFE (**Figure 5**). In cases with doubtful primary stability (bone height < 4 mm), the DI is inserted in a second procedure (**Figure 6**) when bone remodeling of the graft has taken place [1, 72].

Although safe and predictable, complications and morbidity can be associated with the lateral MSFE. Several surgical techniques have been proposed to minimize these problems with the use of specialized trephine burrs, piezosurgical devices, balloons, and hydrostatic pressure.

*The transcrestal approach (internal approach)* was also presented by Tatum. A "socket former" for the selected DI size was used to prepare the implant site. A green-stick fracture of the sinus floor was then created by hand-tapping the socket former towards the sinus cavity [70]. The internal approach is considered less invasive than the external lateral window approach.

*The osteotome technique* is a development of the transcrestal approach used for MSFE and site development by compressing the soft maxillary bone to improve the mineral density intraalveolarly by osseous deformation and trabecular microfracture [73, 74]. Summers used specialized osteotomes with increasing diameters to intrude the sinus bottom and compress the adjacent bone optimizing its density. The green-stick fractured bottom together with the sinus membrane is displaced step-by-step into the MS cavity to form a "tent" above the original sinus floor level.

**Figure 5.** *MSFE with lateral approach, one-stage procedure.*

**Figure 6.** *MSFE with lateral approach, two-stage procedure.*

**Figure 7.** *MSFE with transcrestal approach, one-stage procedure.*

The space within the "tent" is filled with grafting material and blood clot and the DI may be inserted into the tented space through the osteotomy opening (**Figure 7**). In cases when initial stability is doubtful the placement of the DI is postponed until the end of the healing period.

Several surgical techniques have been proposed to minimize the complications and postoperative morbidity of MSFE procedures.

*Interradicular bone intrusion with MSFE* is advocated in cases when sufficient in quantity (4–5 mm) interradicular septum is present after tooth removal. The central portion of the septum is freed with a standard osteotome, then a round osteotome is used to upfracture and intrude the alveolar fragment into the MS. This way, the socket is extended into the MS creating a new sinus floor at a higher level. Implant

#### *Maxillary Sinus in Dental Implantology DOI: http://dx.doi.org/10.5772/intechopen.99780*

placement is carried out if adequate bone height and primary implant stability can be achieved, otherwise, the DI is inserted after a healing period of 4 months [75].

*The trans-alveolar sinus elevation with ridge expansion* is applicable at sites with prominent MS with horizontal alveolar resorption. The procedure combines in a single surgery MSFE with buccal ridge expansion and implant placement. The crestal distraction develops an expanded intrabony space within the cancellous bone with intact periosteal blood supply followed by immediate gentle upfracture and displacement of the floor segment into the MS [76, 77].

Other options for augmentation of the distal maxilla include:

*On-lay bone grafts and MSFE.* In patients with insufficient subantral bone height and unfavorable interarch relations due to advanced horizontal and vertical resorption, the MSFE procedure may be conducted simultaneously with on-lay block grafts for vertical and/or horizontal ridge augmentation. The grafting material can be harvested from extra- and intraoral donor sites or allogenous, xenogenous, and alloplastic blocks can be used [78–80].

*Le Fort I downgraft with MSFE.* Cases with nearly total alveolar atrophy and unfavorable maxillo-mandibular interrelations can be treated with the Le Fort I downgraft osteotomy and interpositional bone graft from the iliac crest [81–84].

*Le Fort I and alveolar distraction osteogenesis with bone grafting.* A moderately atrophic, retro displaced edentulous maxilla can be distracted to Class I jaw relation when combined with sinus bone grafting. When a sinus bone grafted maxilla is anteriorized via distraction osteogenesis, the repositioned sinus floor bone mass allows for axial implant development throughout the arch, especially in the canine, premolar, and first molar areas [85].

Alternative procedures were proposed to avoid the more complex MSFE surgery.

*Alveolar ridge preservation* is a surgical technique developed to resist postextraction ridge resorption to simplify the treatment plan for DI insertion and to decrease the need for advanced surgical procedures. Recent systematic reviews with metaanalysis confirmed the effectiveness of this approach in reducing postextraction horizontal and vertical alveolar ridge resorption when compared to spontaneous socket healing. Alveolar ridge preservation after the extraction of a maxillary molar could be regarded as a preventive treatment, in cases where a DI-supported restoration is planned, allowing a standard DI placement without additional regenerative procedures. Today alveolar ridge preservation is the most common, easy to perform, and cheap procedure aiming to control crestal bone resorption after tooth loss [47].

Other alternatives that may avoid MSFE procedures are tilted, short, zygomatic, and pterygomaxillary implants.

#### **5. The impact of maxillary sinus anatomy on maxillary sinus elevation procedures**

All MSFE techniques share common features:


As seen from above, the MSFE operations use the inferior and lateral MS walls to enter the sinus cavity and to reconstruct its bottom into an alveolar ridge competent enough to accept, integrate, and keep DI capable to bear masticatory loads, and to oppose alveolar atrophy.

#### **5.1 The maxillary sinus floor**

All MSFE procedures insert DI through the inferior sinus wall. The transcrestal approach with its variations uses the sinus floor to approach and elevate the Schneiderian membrane. Thus, the inferior MS wall is assigned a key role in MSFE.

The floor of the antrum in dentate adults is approximately 1 cm below the nasal floor. Anteriorly the sinus extends in general to the canine and the premolar region. There is, however, a large variety in size and shape of the sinuses even within the same person. The convex sinus floor usually reaches its deepest point at the first molar region. Roots of the maxillary teeth frequently cause convolutions in the floor of the sinus [1].

*Primary alveolar bone height and width.* It is believed that the concomitant actions of AA and MSP determine the bone quality and quantity of the subantral ridge. The subantral alveolar dimensions should be examined before MSFE to assure that the conditions are suitable for DI accommodation and primary stability. The prerequisites are enough height, width, bone thickness, and intermaxillary relations that permit adequate functional loading and biomechanics. These features are of crucial importance to decide whether DI can be inserted in one or a twostage procedure. The ridge dimensions necessary for conventional DI placement are 1.5 mm of intact bone on the buccal and the palatal side to resist the horizontal AA and tension, and 2 mm above the apical tip of the implant to withstand functional loads and spare neighboring anatomical structures, if any. When planning a one-stage MSFE for an implant with a 4 mm diameter the recommended ridge dimensions must be at least 4 mm bone height and 5 mm width. The bone density must also be considered. Soft bone cannot guarantee primary stability. Otherwise, when bone quality and quantity cannot meet the needed osseous environment for a one-stage procedure, the DI should be placed in a second stage 4 to 6 months after sinus floor grafting [1]. In conclusion, when sufficient alveolar height (±4 mm) for primary stability is present, the DI can be inserted simultaneously with the MSFE. In cases with doubtful primary stability (bone height < 4 mm), the DI is inserted in a second procedure when bone-remodeling of the graft has taken place [1, 72].

*Subantral dimensions as indications for MSFE procedures.* The decision concerning DI size and number should rest not only on the available bone volume but should also take into consideration the prosthetic and biomechanical aspects. The classification of the International Team of Implantology categorizes the atrophic maxilla

#### *Maxillary Sinus in Dental Implantology DOI: http://dx.doi.org/10.5772/intechopen.99780*

into groups, and each group requires a different surgical approach to achieve ideal bone volume and three-dimensional interarch relations. These groups are [86]:

*Group 1:* Insufficient subantral bone height, adequate alveolar width, acceptable vertical and horizontal interarch relations. *Surgical approach*: MSFE with bone substitute and/or autogenous bone from intraoral bone sight.

*Group 2:* Insufficient subantral bone height, inadequate alveolar width, acceptable vertical and horizontal interarch relations. *Surgical approach*: MSFE with horizontal ridge augmentation. Autogenous horizontal block graft (from intra- or extraoral site according to the extent of AA) may be combined with a bone substitute and barrier membrane.

*Group 3.* Insufficient subantral bone height, adequate alveolar width, acceptable horizontal but unfavorable vertical interarch relations due to advanced crestal resorption. *Surgical approach*: MSFE and vertical ridge augmentation. Autogenous vertical block graft (from intra- or extraoral site according to the extent of AA) may be combined with a bone substitute and barrier membrane.

*Group 4.* Insufficient subantral bone height, unfavorable interarch relations due to advanced horizontal and vertical crestal resorption. *Surgical approach*: MSFE with vertical and horizontal ridge augmentation. Autogenous vertical block graft (from intra- or extraoral site according to the extent of AA) may be combined with a bone substitute and barrier membrane.

More detailed classifications have been proposed by Misch [87] and Chiapasco et al. [88].

#### **5.2 The lateral (buccal) wall and trap-door preparation**

The external MSFE enters the MS by preparing a hinge trapdoor osteotomy in it which is intruded into the sinus (**Figure 8**).

The lateral sinus wall is covered by muscle-periosteal tissue, containing the facial artery and vein, the lymphatic system, and the infraorbital nerves [69, 89]. The wall usually is thin, semi-transparent and the grayish blue Schneiderian membrane can be seen through it. The thin wall facilitates door preparation and intrusion; if this is not the case, it should be thinned out to ease the mobilization of the membrane from the inner aspect of the MS. A trapdoor that follows the inner

**Figure 8.** *Lateral MSFE, trapdoor preparation and intrusion.*

shape of the MS with a wide cranial hinge base and rounded corners is advocated. Three-dimensional cone-beam computed tomography and clinical inspection will provide information on the form, the curvature, the extent, and the circumference of the sinus. The rounded corners help door mobilization and intrusion and reduce the incidence of Schneiderian membrane perforations. After the preparation of the door is finished the Schneiderian will be visualized. Normal MS anatomy will allow the trapdoor to be intruded and lifted to a horizontal position. This is possible if only the Schneiderian membrane is sufficiently mobilized from the sinus floor. The too convex outer aspect of the lateral wall (the zygomatic process of the maxilla) restricts the door base to function as a hinge because the hinge line would cause a membrane tear during door luxation. This can be avoided by the transformation of the hinged door into a hatch door; after that, the whole bone fragment can be dislocated cranially [1].

#### **5.3 The Schneiderian membrane**

Normal antral mucosa is thin (1 mm thick) and less vascular than the nasal mucosa. The ciliated respiratory epithelium transports fluids like mucus and pus towards the internal ostium. The healthy membrane is grayish blue, with traces of blood vessels. In smokers, it may be atrophic, extremely thin, and fragile even to the slightest touch. During MSFE the membrane should be kept intact to secure hermetic graft seal. Only when the whole caudal membrane is prepared free from the sinus bottom the door can be lifted to the new horizontal position; the graft material must be placed until this level. Overfilling and tension may cause necrosis of the Schneiderian membrane, loss of graft, and sinusitis [1].

The most common complication during MSFE is the Schneiderian membrane perforation (**Figure 9**). Mobilization difficulties are met in detaching it from septa, longitudinal floor rims, convolutions, and root tip expressions. Certain anatomical features such as narrow sinuses and sharp sinus opening angles have also been recognized to increase the risk of membrane perforation. Adhesions between the oral and sinus mucosa in places with totally missing alveolar bone, as well, as scars from previous MS surgery may be a contraindication for MSFE because the membrane cannot be kept intact. Small perforations located in areas where the elevated mucosa forms multiple folds usually do not necessitate treatment because the folded membrane tends to close the perforation which heals spontaneously. Larger and/or unfolded perforations need closure and must be covered with resorbable membranes and biologic glues. In cases with very large perforations, further sinus elevation should be abandoned. Re-entry might be considered 6–8 weeks after the first surgical attempt [1].

#### **5.4 Maxillary sinus septa**

Maxillary sinus septa, or Underwood's septa, complete and incomplete, arise manly from the floor but can spur from other walls. Incomplete septa divide the floor into compartments known as recesses (**Figure 9**), while complete septa may intercept the sinus into smaller sinuses (**Figure 10**). It is assumed that floor septa function as struts bearing the masticatory forces during the dentate phase of life and slowly disappear after tooth loss.

The presence of sinus floor septa determines the shape of the osteotomy. Short floor septa have no serious impact on the lateral MSFE as they cannot block the trapdoor intrusion, but the mobilization of the Schneiderian membrane is usually difficult. With high septa the door design must either follow the floor contour, outlining it in a W-shaped or any suitable form (**Figure 14**), or two trapdoors must

#### **Figure 9.**

*A one-stage procedure consisting of extraction of the periodontally compromised right first and second maxillary molars, and lateral MSFE with simultaneous DI placement. The cause for the sinus membrane perforation is the inflammatory adhesion to the well-defined sinus floor septa and the lateral wall due to the long-lasting chronic periodontal lesions.*

be performed, or the entry must be located at that side of the septum that corresponds to a recess (medial usually) in which the DI will be placed. Another option is to remove the septum through an antrostomy after the sinus mucosa has been prepared [1].

#### **5.5 The narrow sinus**

Narrow MS can only be recognized on a CT scan [90–92]. The narrow sinus, similarly, to high antral septa, will not allow for the upward intrusion of the trapdoor to the appropriate level (**Figure 11**), because the sharp MS opening angle is a predisposition to a Schneiderian membrane perforation.

The solutions to this situation are either to make an antrostomy, removing the osteotomized segment of the lateral sinus wall, or convert the trapdoor into a hatch door, mobilized all around and kept attached to the sinus membrane peduncle only.

#### **Figure 10.**

*Complete septa may divide the sinus into smaller sinuses.*

#### **Figure 11.** *The narrow sinus will not allow for the upward intrusion of the trapdoor.*

#### **5.6 Anterior (buccal) wall and the infraorbital foramen**

The anterior wall is made of thin compact bone, containing the neurovascular canals to the anterior teeth if present. The structure that must be avoided cranially is the infraorbital foramen. Not only might the preparation of the door be a threat

*Maxillary Sinus in Dental Implantology DOI: http://dx.doi.org/10.5772/intechopen.99780*

**Figure 12.** *Canalis sinuosus, ending in the canine area.*

to the neuro-vascular bundle but also the possibility of mechanical damage by the wound retractor should be regarded. Normally however there is no reason for such high preparations because there is no need for such a high "door". It might even cause the door to be too large for the width of the sinus, making it impossible to raise it to a horizontal level. This problem may also be encountered with the combination of "normal" sized doors and very narrow sinuses [1].

Canalis sinuosus is a small canal running through the anterior wall of the maxilla and then along the lateral wall of the nasal cavity, residing in the alveolar process of the maxilla (**Figure 12**). Its nerves and vessels supply anterior teeth and adjacent soft tissues. In rare cases, the small canal could be damaged if the anterior edge projection of the trapdoor goes too far anteriorly above the first maxillary premolar [93].

#### **5.7 The internal or nasal wall and maxillary ostium**

The internal wall has a rectangular shape and forms the bony septum between the nasal cavity and MS. The inferior part of the wall corresponds with the inferior meatus of the nasal cavity, marked by the tuberosity of the inferior concha at the top. At the cranial side of this wall a fragile bony structure, the so-called sinus hiatus or ostium, can be recognized, which drains the sinus into the middle nasal meatus. The architecture of the MS drainage is complex and consists of three passages. The first one is the ostium, which leads into the second passage, the ethmoid infundibulum, that conducts mucus from the maxillary sinus into the middle meatus via the third passage, the hiatus semilunaris. The obstruction of any of the three interconnected passages may lead to retention of the sinus secretions [94]. The competence of the ostium must be evaluated before and after MSFE and kept intact because arrests on drainage during the healing period may compromise the postoperative result (**Figure 13**).

An accessory ostium may sometimes be found on the medial wall. When this occurs, it should be identified before any maxillary sinus elevation procedure is performed to avoid detaching the mucosa up to this point.

**Figure 13.** *Competent MS drainage.*

#### **Figure 14.**

*Lateral MSFE with hatch door design and additionally enlarged window to follow the floor topography due to the presence of a floor septum. Note the neurovascular structures attached to the Schneiderian membrane. At the top, the membrane is traversed by the medial alveolar nerve, the bottom is crossed by the alveolar antral artery and its accompanying vein is seen in the middle.*

#### *Maxillary Sinus in Dental Implantology DOI: http://dx.doi.org/10.5772/intechopen.99780*

Normal sinus physiology could be threatened if the function of the ciliated epithelium of the ostium is impaired after MSFE, but there is no clinical evidence for changed antral mucosal function after surgery [1].

#### **5.8 Blood supply**

The blood supply of the MS derives from the infraorbital artery, the greater palatine artery, and the posterior superior alveolar artery. Several anastomoses between the posterior superior alveolar artery and the infraorbital artery can be found inside the bony lateral antral wall, which also supplies the Schneiderian membrane as well as in the epiperiosteal vestibular tissues. The major intraosseous anastomosis, called the alveolar antral artery (**Figure 14**), passes through the area of the bony window [95]. In its course, the artery can lie strictly within the sinus wall, or it may occupy the inner surface of the bony window, or even may be attached to the outer

#### **Figure 15.**

*Heavy chronic odontogenic sinusitis on both sides due to extensive endodontic and periodontal lesions. The interradicular septum of 16 is fully destroyed. The apical lesion around the mesio-vesibular root of 26 perforates the sinus floor and drains directly into the sinus.*

aspect of the Schneiderian membrane. The mean distance between the intraosseous anastomoses and the alveolar ridge is 19 mm. The epiperiosteal vestibular anastomosis is situated at a more cranial level [1]. Hemorrhages during sinus grafting are rare since the main arteries are not within the surgical area. However, small vessels might be damaged. If they are located in the exposed Schneiderian membrane, they should best be left to stop spontaneously or stopped by slight gauze pressure. Electro-surgery will cause necrosis of the membrane and therefore can threaten the coverage of the graft.

The posterior teeth are supplied by neurovascular branches coming from the maxillary tuberosity. This must be kept in mind because a surgical approach too close to the apexes of vital neighboring teeth might devitalize them.

#### **6. Maxillary sinus elevation and odontogenic sinus infections**

Odontogenic infection of the MS, odontogenic sinusitis, accounts for about 10–25% of all cases suffering MS sinusitis. The primary cause usually is periapical or periodontal infection from maxillary molars and premolars, as the inflammatory exudate can easily erode through the thin floor to drain into the sinus (**Figure 15**). The etiology is predominantly bacterial, but, fungal infections must also be suspectedbecause filamentous fungi from endodontically and periodontally compromised teeth can invade the sinus. Such teeth can serve as reservoirs for most common fungal infections as candidiasis, aspergillosis, and mucormycosis (zygomycosis). Allergic conditions may also lead to chronic reactive mucosal changes and can block normal sinus drainage. Obstruction of the osteomateal unit is thought to be pivotal in the development and persistence of sinusitis (**Figure 15**) [96, 97].

In many patients, the disease is asymptomatic or causes minor inconveniences which explains why its role in MSFE is underestimated [97]. It must be emphasized that retention of secretions may compromise the short-term and long-term treatment success. The careful clinical and roentgenological examination is mandatory before MSFE, with no regard to the chosen approach. Chronic sinusitis is recognized as a thickening of the Schneiderian membrane and presents a contra-indication for sinus elevation. Even asymptomatic forms of infection cause serious complications. The operation should be postponed until the condition is placed under control.

#### **Author details**

Nikolay Uzunov1 \* and Elena Bozhikova<sup>2</sup>

1 Private Practice, Plovdiv, Bulgaria

2 Medical University Plovdiv, Plovdiv, Bulgaria

\*Address all correspondence to: nouzoun.nu@gmail.com

© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

*Maxillary Sinus in Dental Implantology DOI: http://dx.doi.org/10.5772/intechopen.99780*

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### *Edited by Balwant Singh Gendeh*

This book discusses selected topics on the anatomy of paranasal sinuses and related conditions, providing insight into advancements in the field. The first section covers morphological aspects of the maxillary sinus, infectious causes of acute and chronic sinusitis, posterior ethmoidal artery, and paranasal sinuses anatomy and anatomical variations. The second section covers sinonasal-associated midfacial expansion and maxillary sinus in dental implantology. Chapters present new clinical and research developments as well as future perspectives on ever-expanding upper airway and jaw problems.

Published in London, UK © 2022 IntechOpen © stockdevil / iStock

Paranasal Sinuses Anatomy and Conditions

Paranasal Sinuses Anatomy

and Conditions

*Edited by Balwant Singh Gendeh*