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 Table of Contents  
REVIEW ARTICLE
Year : 2018  |  Volume : 13  |  Issue : 4  |  Page : 264-272

Oral manifestations of autoimmune connective tissue diseases


1 Consultant Rheumatologist, Department of Rheumatology and Clinical Immunology, Apollo Hospitals, Indore, Madhya Pradesh, India
2 Consultant Oral Medicine and Radiology, My Dentist Indore, Indore, India
3 Department of Medicine, MGM Medical College, Indore, Madhya Pradesh, India
4 Consultant Rheumatologist, Centre for Rheumatology, Calicut, Kerala, India

Date of Web Publication18-Nov-2018

Correspondence Address:
Dr. Akshat Pandey
A-4 MIG Colony, Behind Hotel Amaltas, Indore - 452 001, Madhya Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/injr.injr_51_18

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  Abstract 


Autoimmune connective tissue diseases possess difficulty in diagnosis and treatment due to uncertainty in etiology, a wide array of clinical presentation, and unpredictable disease course. Many such diseases like Sjögren syndrome, Rheumatoid arthritis, Systemic Lupus Erythematosus, Systemic Sclerosis, have characteristic oral findings, the identification of which may allow for early diagnosis and treatment. For the purpose of this narrative review we searched the databases such as MEDLINE the Embase and Cochrane library using search terms including “rheumatic” “autoimmune,” “connective tissue diseases,” “dental,” “oral,” and “manifestations” and the names of individual known diseases and also a manual search of bibliographies of these articles and of previously published reviews and animal studies. In this review, we describe the oral manifestation and dental considerations associated with these diseases which will allow the practitioner in holistic management of these patients.

Keywords: Autoimmune, connective tissue, dental, gingivitis, oral manifestations, rheumatoid arthritis


How to cite this article:
Pandey A, Pandey M, Pandey VP, Ravindran V. Oral manifestations of autoimmune connective tissue diseases. Indian J Rheumatol 2018;13:264-72

How to cite this URL:
Pandey A, Pandey M, Pandey VP, Ravindran V. Oral manifestations of autoimmune connective tissue diseases. Indian J Rheumatol [serial online] 2018 [cited 2019 Mar 24];13:264-72. Available from: http://www.indianjrheumatol.com/text.asp?2018/13/4/264/238099




  Introduction Top


Autoimmune connective tissue diseases such as systemic lupus erythematosus (SLE), systemic sclerosis (SSc), rheumatoid arthritis (RA), and Sjögren's syndrome (SS) have an abnormality in structure or function of one or more of the elements of connective tissue, that is, collagen, elastin, (and cells) or the mucopolysaccharides.[1] Collagen develops from the mesoderm and is present in almost all parts of the body. The word “collagen” comes from the Greek, means “glue producing.” It is fibrous in nature and triple helical structure (Madras helix). It is the main component of fascia, cartilage, ligaments, tendons, blood vessels, bone, and teeth.[2]

In oral tissue, collagen is present in alveolar bone, periodontal ligament, pulp, cementum, temporomandibular joint, dentin, gingiva, and basal bone as shown in [Table 1].
Table 1: Distribution and function of collagen fibers in oral tissues

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Any disease which affects collagen will affect directly or indirectly oral tissues and its functioning. In this article, we present a review of connective tissue diseases which have characteristic oral findings, the early identification of which would help the clinicians in the early diagnosis and prompt treatment.

In this review, we discuss the oral manifestations of several common rheumatological conditions. For this, we searched the available literature by screening of primary sources MEDLINE (1966 to date) and old MEDLINE (1949–1965) using the PubMed interface, as well as secondary sources, the Embase, and Cochrane library without any time limits. Appropriate combinations of search terms including “rheumatic” “autoimmune,” “connective tissue diseases,” “dental,” “oral,” and “manifestations” and the names of individual known diseases were used with limits “(English, Human).” Relevant keyword variations for different databases were used. This was supplemented by a manual search of bibliographies of these articles and of previously published reviews.


  Sjögren's Syndrome Top


SS is a chronic autoimmune disease characterized by dysfunction and destruction of the exocrine glands associated with lymphocytic infiltration and immunological hyperactivity.[6] Etiology of SS is not yet fully understood, but certain genetic traits, stress, hormonal factors, and infections such as viruses or bacteria may act as a triggering factor in the pathogenesis of Sjogren's syndrome.[7]

It is subclassified into primary and secondary About 88% of SS participants are reported to have reduced salivary flow rate, followed by complaints of xerostomia in the 75%–92%.[8] Patients complain of dry mouth, difficulty in swallowing, difficulty in speaking, difficulty in eating dry foods, and difficulty in wearing dentures. Other symptoms such as burning, tingling sensations, especially on the tongue, abnormal taste sensations (dysgeusia), fissures, and sores at corners of lips.[9] Oral mucosa may show drying of lips, erosive lesions, pale and corrugated buccal mucosa, depapillation on the tongue, dental caries, periodontitis, erythematous candidiasis, and angular cheilitis [Figure 1]. Non-Hodgkin lymphoma and neuropathy are its possible complications.[9]
Figure 1: (a) Depapillation on anterior two-third and lateral border of the tongue. (b) Angular cheilitis of left commissural area. (c) Erythematous candidiasis on the right buccal mucosa.

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A study to asses symptoms and risk factors associated with xerostomia found that patients with xerostomia were three times more likely to drink water to swallow food than were patients without xerostomia.[10] Older individuals taking one or more drugs were significantly higher compared to medication-free patients and increased with increasing numbers of medications used, and individuals with a nervous or mental disorder, or who wore removable dentures were five times more likely to develop xerostomia than patients without disorder or dentures.[10]


  Dental Considerations Top


Dental treatment is mainly preventive, symptomatic, and supportive. Therapies designed to stimulate secretion, whether local or systemic, have the great advantage of providing the benefits of natural saliva.

Preventive therapy is aimed to prevent oral complications from the low salivary output, frequent oral examination once in every 4–6 months and radiographs should be performed annually.

  • Dental caries: Meticulous oral hygiene, a low-sugar diet, and regular use of topical fluoride are recommended. Fluorides and remineralizing solutions are available as varnishes, dentifrices, gels, and rinses, which can be used with or without applicator trays
  • Oral candidiasis: A number of topical antifungal agents, in the form of rinses, ointments, and pastilles are effective therapeutics. Systemic antifungal therapy should be reserved for cases refractory to topical therapy and for immunocompromised patients
  • Denture users should prevent fungal colonization through daily immersion of prostheses in benzoic acid, chlorhexidine 0.12% solution, or 1% sodium hypochlorite. Angular cheilitis can be treated with topical antifungal and anti-inflammatory agents.


Symptomatic treatment aimed to alleviate discomfort and pain as well as to prevent complications of xerostomia.[11] A number of saliva substitutes in liquid, spray, or gel form have moistening and lubricating properties, and prolonged wetness of the oral mucosa. Adequate hydration of the oral mucosa is essential. Patients should be encouraged to sip water throughout the day. Patients should be cautioned to avoid dry and bulky foods, spicy or acidic foods, beverages-containing alcohol, sugar, caffeine, or strong flavorings that may irritate sensitive, dry mucosa. Commercial available artificial saliva contains carboxymethyl cellulose, mucin, xylitol or sorbitol, mineral salts, fluorides, and preservatives. It helps in the coating and moisturizing oral mucosa and teeth, but it is for a short period.[12]

A Cochrane review of 36 randomized controlled trials comparing topical interventions such as lozenges, sprays, mouth rinses, gels, oils, chewing gum, or dentifrices for the treatment of xerostomic symptoms was published in 2011.[13] The Cochrane collaboration asserts that while there is no strong evidence that any topical treatment is effective for relieving the sensations of xerostomia, oxygenated glycerol triester saliva substitute spray was found to be more effective than water-based electrolyte spray.[13]

Since no commercial saliva substitute has been developed which accurately replicates all essential qualities of natural saliva, attempts should be made to increase the natural flow of saliva as much as possible. Salivary stimulation is done through topical and systemic agents. Local stimulation includes sugar-free chewing gums and candies, citric acid, acupuncture, and electrostimulation. Electrostimulation using transcutaneous electrical nerve stimulation (TENS) enhances the patient's ability to generate saliva by augmenting normal physiologic salivary reflexes.

Systemic stimulation may be considered in cases of severe xerostomia.[14] Two muscarinic acetylcholine receptor agonists such as pilocarpine and cevimeline used to stimulate the muscarinic acetylcholine receptors M1 and M3 present on salivary glands, leading to increased secretory function. There side effects are sweating, increased urinary frequency, and flushing. However, these drugs are contraindicated in cardiovascular and pulmonary disease patient. Other therapeutics agents include bethanechol, anetholetrithione, bromhexine and mucolytic agents, cytokines or immunoregulators (e.g., rituximab or hydroxychloroquine), or systemic steroids.[10],[11],[12]

Dentists must recognize the signs and symptoms of SS and communicate those findings and concerns to other health--care providers, including the primary care physician, rheumatologist, and ophthalmologist for evaluation in a timely fashion.


  Rheumatoid Arthritis Top


RA is chronic autoimmune inflammatory disease affecting the synovial membrane of diarthrodial joints. Systemic weight loss, fever, and fatigue may be the first presentation of RA. The classic features of this disease are chronic, bilateral and symmetric polyarthritis, joint pain, and inflammation that can result in deformity, instability, and destruction of synovial joints.[15] It is etiology multifactorial. Combination of infection, autoimmunity, and strong genetic factors is associated with the incidence of RA.

Temporomandibular joint (TMJ) involvement occurs in about more than 50% of RA patients. It can occur at an early age and may result in mandibular growth disturbance, facial deformity, and bilateral/unilateral TMJ ankylosis, retrognathic mandible, and malocclusion giving typical bird facies appearance.[16],[17] In Juvenile idiopathic arthritis, shortening of mandibular rami and narrowing of space results in narrow oropharyngeal airway and hypotonicity of oropharyngeal muscles can result in complication such as upper airway obstruction.[18]

TMJ is usually among the last joint to be involved and is associated with many clinical signs and symptoms of which pain is a major problem later leading to inflammation, limited movements, swelling (joint stiffness), and muscle spasm. Radiographic findings include narrowed joint spaces, flattened condyles, erosions, subchondral sclerosis, cysts, and osteoporosis [Figure 2]. A recent study reported that in patients with RA, the predominant finding was erosion of condyle (85%) followed by condylar sclerosis.[16] Sclerosis is a sign of healing of joint in contrast to erosion, which indicated active bone disease.
Figure 2: Panoramic view showing reduced joint space, erosion of condylar surface

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Patients with long-standing active RA may have an increased incidence of periodontal disease, including an increase in pocket depths, furcation involvement, loss of alveolar bone, and teeth [Figure 3].
Figure 3: (a) labial view and (b) lingual view suggestive of periodontitis

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About one-third of RA patients have secondary SS. A study including 604 RA patients showed a decrease in salivary flow in 43% of participants. Its prevalence estimates between 3% and 30%.[15] Patients with secondary SS have chronic xerostomia, aphthous ulcer, oral candidiasis, angular cheilitis, glossitis, multiple caries, gingivitis, and periodontitis. Long-term use of methotrexate and other antirheumatic agents such as gold, D-penicillamine, and nonsteroidal anti-inflammatory drugs (NSAIDs) can cause lichenoid reaction and stomatitis. Prolonged use of cyclosporine may lead to gingival overgrowth [Figure 4].
Figure 4: Drug-induced gingival hyperplasia

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  Dental Considerations Top


It is necessary for the dentist to have awareness about patient's current RA medication. It is possible side effects and interactions with other drugs. Before recommending any additional NSAIDs, the clinician must assess the patient's current medication schedule to avoid renal or gastric toxicity. Gastrointestinal-protective agents such as misoprostol may help to reduce these side effects. Replacement therapy is essential in a patient with long-term use of glucocorticoids to prevent secondary adrenal insufficiency.

In patients with severe RA who have had joints surgically replaced with prosthetic joints may require prophylactic antibiotic therapy before undergoing any invasive dental procedures.[9],[17] It is important to assess the status of the patient's condition carefully, as even mild cases of RA may adversely affect the patient's ability to maintain good oral hygiene.[9]


  Systemic Lupus Erythematosus Top


SLE is a multisystem autoimmune disease characterized by the formation and deposition of autoantibodies and immune complexes leading to inflammation and vasculopathy.[19] Autoantibodies to nuclear components and immune complexes are produced, which lead to inflammation and/or destruction of organs and tissues.[1]

SLE has a wide range of mucocutaneous, renal, neuropsychiatric, cardiovascular, infectious, and hematologic manifestations. The most common extraoral lesion in SLE is the appearance of erythematous patches crossing the bridge of the nose and malar regions of the face appears as butterfly rash.[20] Involvement of eye in SLE may be the initial sign and manifest as proptosis, enophthalmos, orbital pain, blurred vision, chemosis, and restriction of extraocular motility.[21]

The prevalence of oral lesions in patients with SLE varies between 6.5% and 21%. Oral ulcerations are frequent and listed among the minor criteria for SLE diagnosis and characteristically shallow in appearance with a tendency to occur in crops on the hard palate.

They are typically 1–2 cm in diameter and painless unless secondary infected.[16] The associated oral ulcerations may persist for years or occur intermittently with cyclical remissions and exacerbations. SLE patients may also experience lupus cheilitis, honeycomb plaque, lichen planus such as lesion and stomatodynia, dysgeusia, xerostomia, candidiasis, and periodontal disease.[22]

Lupus cheilitis has variable clinical presentations ranging from atrophic plaques to white/keratotic, purpuric, bullous, and verrucous lesions. The most common areas for lesions are buccal mucosa followed by hard palate and lower lip. Chronic lip enlargement or macrocheilia may also occur.[23]

Clinically, lesions of LE most often resemble erosive oral lichen planus (OLP) but tend to be less symmetrically distributed. The keratotic striae of LE are much more delicate and subtle than Wickham's striae and show characteristic radiation from the central focus. While in OLP, lesion appears as bilaterally interlacing white radiating striae at the periphery mostly on the posterior buccal mucosa and biopsy reveals typical subepithelial T cell band infiltration [Figure 5].[24]
Figure 5: (a) Right buccal mucosa and (b) Left buccal mucosa showing bilaterally interlacing white radiating striae suggestive of oral lichen planus

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However, salivary gland (parotid or submandibular) involvement is usually associated with SS, in which lymphocytic acinar infiltrates and fibrosis predominate histologically.[25]

Cases of trigeminal sensory neuropathy have been reported with SLE.[26] Facial numbness, paresthesia, dysesthesia, and pain have been reported most frequently; however, other cranial nerves may also be involved. Trigeminal neuropathy may be the initial feature of SLE or may follow the onset of the disease, usually developing slowly over the course of the illness.[27] Salivary gland infection and conditions unique to SLE, such as focal parotid necrosis and LE profundus (presenting as a bilateral submandibular mass), have also been reported.[19]

In a study of 182 patients with SLE, oral mucosal ulceration found in 47 patients (26%) and it was usually painless (82%), and most often involved the hard palate (89%). Oral ulceration was associated with an increase in overall clinical activity, although this was not accompanied by significant changes in the levels or titers of C3, anti-Deoxyribonucleic acid antibodies, and antinuclear antibodies. Necrotizing vasculitis was not observed.[28] In another series of 90 patients with SLE, 10 patients had oral lesions related to the disease.[29] Oral ulcerations accompanied by white irradiating striae was found in five patients, erythema was noticed in five patients and a white homogeneous plaque in one patient. Fifteen lesions demonstrated vacuolar basal degeneration and 12 thickening of the basement membrane histologically.[29]


  Dental Considerations Top


Platelet count should be estimated before oral surgical procedure to evaluate the severity of thrombocytopenia. Due to cardiac involvement in these patients, precautions like antibiotic prophylaxis must be considered for all patients with SLE who are undergoing surgical dental procedures.[30] Patients are susceptible to shock and infection as they are medicated with adrenal suppressing doses of corticosteroid or cytotoxic drugs.[15]


  Systemic Sclerosis (Scleroderma) Top


SS is characterized by small vessel vasculopathy, autoantibody production, and excessive deposition of collagen in the skin and internal organs. Overproduction and accumulation of collagen and other extracellular matrix proteins are the hallmark of this disease, resulting in fibrosis, and tissue dysfunction.[6] Its etiology may be secondary to immunologic mechanisms, vascular endothelial cell injury, and activation of fibroblasts. It has been classified into two groups as groups: limited cutaneous disease and diffuse cutaneous disease.[31],[32],[33]

Localized scleroderma includes CREST syndrome (Calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia). It manifests in two forms as morphea and linear scleroderma. Morphea is characterized by localized thickening of the skin and starts as violaceous or purplish-brown oval skin patches that enlarge become indurated and eventually lose hair and the ability to sweat. Linear scleroderma is a condition which can run through the entire length of an extremity as a thin band of sclerosis involving underlying muscle, bones, and joints. When there is involvement of head and face, it is called as en coup de sabre and may result in facial hemiatrophy.[34]

Specifically, one of the most frequently experienced oral manifestations of SSc is microstomia or difficulty in opening the mouth as a result of sclerosis of the perioral tissues [35] [Figure 6]. A study of 21 patients with SSc found that 80% of the patients were unable to open their mouth beyond 40 mm.[36] Many patients also experience xerostomia and loss of mobility to the tongue, which may result in difficulty swallowing, accelerated dental decay, and increased predisposition to low-grade erythematous oral candidiasis. Loss of expression lines of the facies leading to a mask-like an appearance and thinned lips is yet another complication causing a “purse-string” appearance to the mouth.[22],[33] Pseudoankylosis (fixation of a joint) may also develop owing to fibrosis of the soft tissues around the TMJ. Other findings include effacement of the lingual papillae, pallor with blanching of the mucous membranes, and fibrosis of the buccal mucosa with loss of normal elasticity.[33] Orthopantomogram shows generalized widening of periodontal ligament space [Figure 7]. It could be due to increase in the collagen synthesis in the periodontal ligament or due to the involvement of the masticatory muscle, which becomes bulky, leading to an increased occlusal load, and primary trauma from occlusion.[37]
Figure 6: Microsomia in scleroderma

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Figure 7: Intraoral periapical radiograph of 47, 48 regions showing widening of periodontal ligament space

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One study investigated the prevalence of oral manifestations and TMJ temporomandibular disorders (TMD) in SSc patients compared with healthy people in 80 patients.[38] The assessment of TMD was based on the standardized research diagnostic criteria for (RDC/TMD) through a questionnaire and clinical examination. More patients (78.8%) had oral symptoms (xerostomia, dysgeusia, dysphagia, and stomatodynia) than controls (28.7%). TMD symptoms (muscle pain on chewing, difficulty in mouth opening, and headaches) were complained by 92.5% of SSc patients and by 76.2% of controls. On clinical examination, 85% of SSc patients showed restricted opening versus 20.0% of controls, 81.2% of SSc showed reduced the right lateral excursion versus 50% of controls; 73.8% of SSc showed limited left lateral excursion versus 53.8% of controls; and 73.8% of SSc had narrow protrusion versus 56.2% of controls.[38] Mandibular resorption in SSc is relatively rare and reported only in 10% of cases. For early detection of resorption, panoramic radiographs of the mandible are essential to prevent possible consequences such as pathological fractures, osteomyelitis, and occasional neuropathies.[39]

In a case-based review of three cases of orofacial manifestations in scleroderma, one of the cases showed orofacial appearance with mask-like or mouse-facies as taut facial skin, loss of wrinkles and skin folds, pinched nose, thin lips, and puckered mouth.[34]

The differential diagnosis for scleroderma is oral submucous fibrosis (OSMF) associated with betel quid chewing characterized by juxta-epithelial inflammatory reaction followed by fibroblastic changes in the lamina propria, with epithelial atrophy. Clinically, scleroderma and OSMF patients show reduced mouth opening, pale mucosa but in OSMF blanching, leathery texture, depapillation, sunken cheeks, and bud-shaped uvula. In advanced stages, the fibrous band is palpated in buccal mucosa as a thick vertical band and circular band in perioral tissue [Figure 8].[40]
Figure 8: Oral submucous fibrosis showing (a) leathery texture buccal mucosa, (b) reduced mouth opening and (c) bud-shaped uvula

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  Dental Considerations Top


SS can give rise to various oral problems, most commonly restricted mouth opening. Mouth stretching exercises, facial grimacing, use of an increased number of tongue blades between posterior teeth to stretch facial tissues probably is the best possible solution for reduced mouth opening. Good oral care is essential to keep free of dental caries and periodontal diseases. It is advised that patients with scleroderma should visit a dentist at least once in 3 months for the maintenance of oral health.[33]


  Other Autoimmune Diseases Top


Ankylosing spondylitis

TMJ may be involved with ossification of the ligament, bony erosions, condylar flattening, destruction of the disk, and reduced range of motion. As such, true ankylosis is rare, till now only 10 cases have been reported. The involvement of TMJ has not been very well investigated, and there has been always a dispute with its incidence. Previously, studies have reported the involvement of the TMJ in AS between 4% and 32%. However, these were either only radiological or used only insufficient clinical or radiological examination methods.[41] Mehdizadeh et al found TMJ involvement in 6% of 200 patients.[42] Resnick reviewed 1000 patients in which TMJ involvement was only 1%.[43] NSAIDs are recommended as first-line pharmacological treatment in patients who present with symptoms of temporomandibular pain and dysfunction. Nonpharmacological management of AS includes fabrication of intraoral splint, physiotherapy, and patient education. Physiotherapy includes ultrasound, TENS, and home exercises.[44]

Vasculitis

There have not been many studies and case reports on oral manifestation of vasculitis. Oral involvement of granulomatous with polyangitis has been observed in approximately 6%–13% of patients and its manifestation includes oral mucosal ulcerations and nodules. However, the most characteristic oral lesion is hyperplastic gingivitis presenting with a “strawberry-like” appearance. Occasionally, oral lesions are observed before multiorgan involvement occurs. Local topical agents can be used for the treatment of ulcers and immunosuppressants such as corticosteroids and azathioprine are used for management of disease.[45],[46]

Behcet's syndrome

Recurrent oral ulcers are the most common lesions and they will be considered with Behcet's syndrome. The mucocutaneous syndrome may involve a combination of two or more of the following sites: mouth, genitals, conjunctiva, and skin. Topical and systemic corticosteroids have been commonly used. Azathioprine, cyclophosphamide, and chlorambucil are some common immunosuppressants that are used. Levamisole has also been used in the treatment of recurrent oral ulcers associated with Behcet's syndrome.[47]

Mouth and genital ulcers with inflammed cartilage syndrome

Mouth and genital ulcers with inflamed cartilage (MAGIC) syndrome is a rare autoimmune syndrome with very few cases reported in the literature. Presentation of MAGIC syndrome includes both features of Behcet's disease (oral/genital ulcers, ocular disease, and cutaneous vasculitis) and years later develop symptoms of relapsing polychondritis (Auricular chondritis and polyarthritis). Treatment as per literature includes use of methotrexate and pentoxifylline to control oral ulcers, erythema nodosum, and arthritis.[48]


  Conclusion Top


Autoimmune connective tissue disorder often presents with oral signs and symptoms. For clinicians and dentists, it is important to aware of these manifestations. When health-care professionals work together as a team, they can improve patient outcomes and quality of life. Various oral manifestations and dental management of common autoimmune disorders are shown in [Table 2].
Table 2: Oral manifestations of 4 common rheumatic diseases and their management

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Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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    Figures

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Abstract
Introduction
Sjögren'...
Dental Considera...
Rheumatoid Arthritis
Dental Considera...
Systemic Lupus E...
Dental Considera...
Systemic Scleros...
Dental Considera...
Other Autoimmune...
Conclusion
References
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