Definisi

The group decided by consensus to use the term rhinosinusitis instead of sinusitis throughout
this document. This decision was based on the fact that sinusitis is almost always
accompanied by concurrent nasal airway inflammation, and, in many cases, sinusitis is
preceded by rhinitis symptoms. Therefore, it was believed that the use of the term
rhinosinusitis more accurately describes the spectrum of infectious and inflammatory
conditions previously grouped under the term sinusitis. The group endorsed and adopted the
previously developed definition of the Sinus and Allergy Health Partnership Task Force for
Rhinosinusitis: “Rhinosinusitis is a group of disorders characterized by inflammation of the
mucosa of the nose and the paranasal sinuses.” 1
Maxillary sinusitis (acute or chronic) is defined as a symptomatic inflammation of the
maxillary sinus, usually caused by viral, bacterial, allergic or fungal rhinitis. 2
Klasifikasi
Acute rhinosinusitis (ARS) is defined according to symptom duration as follows: infectious
ABRS, with purulent nasal discharges, obstruction, and pain with sensation of fullness within
4 weeks; subacute rhinosinusitis (SRS) between 4 and 8 weeks; and CRS with symptoms
lasting more than 8 weeks despite treatment with medications. Rhinosinusitis has been also
classified into allergic or non-allergic, occupational, and other types of rhinitis syndrome
Etiologi
OMS has basic polymicrobial characteristics, with predominantly anaerobic bacteria in both
the oral cavity and upper respiratory tract. Aerobic Staphylococcus aureus and Streptococcus
pneumonia (S. pneumonia) and anaerobic Peptostreptococcus and Prevotella spp. are found
in more than 75% of cases, while methicillinresistant Staphylococcus aureus is found in 10–
12% of OMS patients
About the main tooth involved, the molar region standed out with a maxillary sinusitis
frequency of 47,68%. The fi rst molar tooth was the most frequently affected with an
incidence of 22.51%, followed by the third molar tooth (17.21%) and the second molar tooth
(3.97%). Regarding the premolar region, it was only affected in 5.96% of the cases, being the
second premolar tooth the most frequently involved (1.98%). The canine only participated in
0.66% of the cases of maxillary sinusitis (3). 3
Acute bacterial rhinosinusitis is caused by various factors (Table 1). 5,6 However, it is most
often the result of a viral etiology associated with upper respiratory infection.1-4,7 Sinus
mucosa edema, sinus ostia obstruction, and decreased mucociliary activity are three key
factors in the pathophysiology of rhinosinusitis. As a result, secretions stagnate, providing a
favorable environment for bacterial growth
Patofisiologi
The pathological characteristics of odontogenic maxillary sinusitis and chronic sinusitis are
different [18, 30]. It is viewed that the pathophysiology of rhinogenic sinusitis has various
reasons leading to the inflammation of the sinus ostium complex, which spreads to the tissues
around the ostium, and finally to other maxillary sinus locations, blocking the ability of
maxillary sinus mucosal clearance. The cascade of inflammation will lead to damage by the
infiltrating cells, causing edema, fluid extravasation, mucus production, engorgement, and
sinus obstruction in the process (such as Figures 1(a)–1(d)). The origin of odontogenic
maxillary sinusitis is the pathogenic teeth; from the teeth, it diffuses to the maxillary sinus
floor, then from the maxillary sinus floor, it spreads to the maxillary sinus ostium and finally
to the tissues around the maxillary sinus ostium and other accessory sinuses. The
microorganisms even scatter over the orbital and brain [20, 28, 31–35]. The odontogenic
maxillary sinusitis can be used as an important basis for distinguishing odontogenic maxillary
sinusitis from nonodontogenic maxillary sinusitis (such as Figures 2(a)– 2(d)
Maxillary sinusitis is the dysfunction of the host mucosal epithelium under environmental
pressure to initiate an inflammatory response. The inflammatory response cascade amplifies
the process along corresponding inflammatory mediator
The pseudostratified ciliated columnar epithelium, known as SM, lines the inner respiratory
mucosa of the maxillary sinuses. The SM produces mucus that moves to the ostium for
drainage into the nasal cavity against normal gravity, with movement of cilia around the
maxillary sinus occurring in a synchronized pattern (Fig. 1). This mucus, passing from the
nasal cavity to the nasopharynx, is swallowed and passes into the esophagus and stomach.
Any interruption of these basic movements of mucus by reduced ciliary activity or
obstruction of ostia can result in sinus disease and symptoms. Each ostium of the anterior
ethmoidal sinus, frontal sinus, and maxillary sinus is closely approximated in the middle
nasal meatus, and together, these comprise the osteo-meatal unit (OMU). Thus, any
inflammation or blockage of the OMU will induce sinusitis, including cases involving several
sinuses, referred to as pan-sinusitis.
The epithelial cells of SM play essential roles in mucociliary clearance (MCC) and keeping
the upper airway clean by driving continuous ciliary beating to move inhaled foreign bodies,
bacteria, fungi, and viruses toward the oropharyngeal airway. These basic protective
functions are aided by the airway epithelium with mucin secretions that create ion or fluid
transport to maintain mucous viscosity. Several chemokines are secreted according to
pathogen exposure levels to activate inflammatory or protective immune pathways by
recruitment of macrophages, dendritic cells, eosinophils, neutrophils, T cells, and NK cells
(Fig. 2) [4, 5]. Several cytokines, including IL-1β, IL-6, TNFα, IL-8, and monocyte
chemotactic protein 1, are also released. These epithelial cells of SM are connected by tight
junctions to form a physical defensive wall, and mucociliary transport is managed by the
formation of reactive oxygen and nitrogen species through control of antimicrobial peptides
such as lactotransferrin, lysozyme, and defensins
The mean distance between the maxillary molar and premolar roots and the maxillary sinus is
1.97 mm, which suggests that the tips of the roots might project into the floor of the sinus,
causing small elevations or prominences along the SM [17, 18]. These intimate anatomical
relations of the upper molar teeth to the maxillary sinus facilitate the development of
periapical or periodontal odontogenic infection inside the maxillary sinus [19] (Fig. 3).
Manifestasi klinis
The main symptoms related to OMS are facial pain or pressure, nasal congestion,
purulent rhinorrhea that may be unilateral, cacosmia, and postnasal drip. Hoskison et
al.7 reported that 21 (81%) and 19 (73%) out of 26 patients with OMS complained of
rhinorrhea and cacosmia, respectively. In a study13 that included 27 patients with OMS,
rhinorrhea was found in 66.7% of cases, cheek pain in 33.3% and cacosmia in 25.9%.
However, these symptoms do not distinguish OMS from other causes of sinusitis, as
some patients experience sinusitis-like symptoms, such as dental pain and nasal
congestion, whereas others present with minimal sinusitis symptoms and dental pain,
because the osteomeatal complex is not obstructed and allows drainage and relief of
pressure.4,6,40e42 Longhini and Ferguson20 reported that dentists did not diagnose dental
infection causing OMS in 6 (85%) out of 7 cases; similarly, 56 (55%) out of 99 of OMS cases
were missed on routine dental examination including dental X-ray.43 Less than half of
patients presenting with OMS report a recent dental procedure42; this is because, for
example, OMS can appear within 1 year after augmentative dental surgery following graft
infection. OMS may also occur after a latency period of almost 4 years as a late complication
of dental implantology due to progressive peri-implantitis.
Diagnosis
intranasal examination with anterior rhinoscopy or nasal endoscopy may
demonstrate findings of unilateral purulent rhinorrhea or edema but remains less
sensitive in the detection of odontogenic sinusitis as compared to imaging
modalities
penunjang
komplikasi
Generally, the complications of sinusitis are classified into three types: local
(osseous), orbital, and intracranial complications [2, 3]. The most common
complication is the orbital type (60–75%), followed by the intracranial (15–
20%) and the local type (5–10%)
Orbital
The Chandler classification system of orbital complications includes five stages of increasing
severity14: I, preseptal edema; II, orbital cellulitis; III, subperiosteal abscess; IV, orbital
abscess; and V, cavernous sinus thrombosis
Preseptal cellulitis, Chandler group I, is a bacterial infection of the eyelid and periorbital soft
tissues, which causes local erythema and induration, and often presents with fever, pain,
conjunctival injection, epiphora, and blurry vision.
orbital cellulitis, Chandler group II, involves infection of the soft tissues of the orbit posterior
to the septum and is associated with a significant morbidity, including the possibility of
permanent blindness. Patients present with erythema and induration of the eyelids, proptosis
and gaze impairment due to limited mobility of the eye, eye pain, conjunctival chemosis, and
fever
Subperiosteal abscess, Chandler group III, which forms between the orbital wall and the
periorbita, can create mass effect, which displaces orbital content laterally or downward, and
contributes to proptosis and impaired mobility of the eye, with chemosi
Orbital abscesses, Chandler group IV, may be a result of subperiosteal abscess rupture or
progression of orbital cellulitis. An orbital abscess may cause severe proptosis,
ophthalmoplegia, and visual loss
cavernous venous thrombosis, Chandler group V, is often a complication of sphenoid,
ethmoid, or frontal sinusitis and/or orbital cellulitis, and results from infectious spread from
the orbit through valveless veins. Classic signs of cavernous sinus thrombosis include ptosis,
proptosis, chemosis, and cranial nerve palsy

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