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Sjogren's Syndrome: A review

Article · March 2014

DOI: 10.4103/0976-433X.129070

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Review Article

Sjogren’s syndrome: A review

Mallika Kishore, Sunil Ramchandra Panat, Ashish Aggarwal, Nupur Agarwal,
Nitin Upadhyay, Ritika Garg
Department of Oral Medicine and Radiology, Institute of Dental Sciences, Bareilly, Uttar Pradesh, India

ABSTRACT
Sjogren’s syndrome (SS) is a chronic autoimmune disease characterized by the lymphocytic
infiltration of salivary and lacrimal glands leading to xerostomia and keratoconjunctivitis
sicca. Prevalence of primary SS in the general population has been estimated to be around
1-3%. SS is an under-recognized disease in which most of the significant progress has
been made in the past 25 years. The herald of newer diagnostic tools could help clinicians
and thereby provide significant relief to patients through earlier treatments. The treatment
of SS is limited to symptomatic management, and involves the use of solutions to replace
salivary secretion and afford a measure of hydration. The purpose of present paper is to
highlight the difficulties and complexities that are inherent in the diagnosis of SS and the
important role that dental practitioners can play in the management of its oral manifestations.

Key words: Diagnosis, oral, Sjogren’s syndrome

INTRODUCTION EPIDEMOLOGY

Sjogren’s syndrome (SS) is a chronic autoimmune disease
characterized by lymphocytic infiltration and subsequent
destruction of the exocrine glands, including those found in
the nose, ears, skin, vagina, respiratory and gastrointestinal
systems.[1] It is among the group of diseases overseen by
rheumatologists; however, its diagnosis and management
require 3 areas of specialty practice: rheumatology,
ophthalmology, and oral medicine.[2]
Therefore, this paper aims to review and critically address the
recent advances on the aetiopathogenesis of the SS, taking
into account the attained clinical features, with particular
relevance given to the oral involvement.
SS is estimated to affect 1-3% of the general population.[3]
A cautious but realistic estimate from the studies presented
so far will be that primary SS(pSS) is a disease with a
prevalence not exceeding 0.6% of the general population
(6/1000). [4] In an epidemiologic study, the calculated
prevalence of SS in 705 randomly selected women aged
ranges from 52-72 years was 2.7%.[5] SS, although a common
disorder in Western countries with an estimated prevalence
of 3 in 100 to 1 in 1000, has rarely been reported from
India.[6] This report highlights the rarity of this disease in
our geographic region.
ETIOLOGY AND PATHOGENESIS

Even if tremendous progress in the field of research has been

Address for correspondence:
Dr. Mallika Kishore, made to unveil the different mechanistic processes underlying
Department of Oral Medicine and Radiology, Institute of Dental the development of SS, the initial triggering events of the disease
Sciences, Bareilly, Uttar Pradesh, India. have yet to be unearthed. Central to the pathophysiology of SS
E-mail: dr.mallika.kishore01@gmail.com is chronic perpetual stimulation of the autoimmune system.
Access this article online Both B and T cells are implicated in the pathogenesis of the SS,
Quick Response Code: even though the mechanisms underlying humoral and cellular
Website: abnormalities are not yet known.[7,8]
www.srmjrds.in
It is probably the result of an environmental stimulus that
DOI: promotes an autoimmune reaction in genetically susceptible
10.4103/0976-433X.129070
persons. Infectious agents most commonly sialotropic viruses
have been postulated to trigger the syndrome; however,
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Kishore, et al.: Sjogren’s syndrome
associations with most of the potential viral candidates,
including cytomegalovirus and Epstein-Barr virus, are
weak.[9] The putative role of different viruses in SS can be
viewed in the light that salivary glands are a site of latent
viral infections.[10]
A genetic predisposition to SS has been suggested because
of multiple reports of two or more members of the same
family developing the syndrome. Affected individuals of
different ethnic origins carry different human leucocyte
antigen susceptibilities.[4]
The high percentage of females with SS compared to
males suggests that the immune regulatory properties
of sex hormones are involved in its development. [11]
Androgen deficiency, both locally and systemically, has
also been pointed out to be a key factor prompting
SS. Reduced plasmatic levels (up to 40 - 50%) of
dehydroepiandrosterone sulfate, the precursor sex steroid
hormone produced in the adrenal cortex, has been
identified in SS-affected individuals, comparing to age
and sex matched controls.[12]
CLINICAL FEATURES
Glandular manifestations
Xerostomia
The dry mouth is often manifest as the ‘cream cracker’ sign
an inability to swallow dry dental caries is a common feature
that may prompt a referral from a dentist. About half of the
patients complain of recurrent parotid swelling, particularly
relatively young patients in whom the inflammatory phase
predominates.[13]
In advanced disease, the oral mucosa appears dry and glazed
and tends to form fine wrinkles. Extreme dryness of the
mouth, causing the tongue to stick to the palate, may lead
to a “clicking” quality in the speech of patients with SS. In
general, the surface of the tongue becomes red and lobulated,
with partial or complete depapillation.[14]
Ocular manifestations
Diminished tear production due to lacrimal gland
involvement leads to the destruction of both corneal and
bulbar conjunctival epithelium and a constellation of clinical
findings termed keratoconjunctivitis sicca (KCS).[15]
Symptoms of dry eye may include sensations of itching,
grittiness, or soreness, even though the eyes’ appearance
is normal. Ocular complaints may include photosensitivity,
erythema, eye fatigue, decreased visual acuity, a discharge
in the eyes, and the sensation of a film across the visual
field.[14]
In more severe disease, functional disability with visual
impairment occurs. Complications of KCS include
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SRM Journal of Research in Dental Sciences | Vol. 5 | Issue 1 | January-March 2014
corneal ulcerations that can lead to perforations and
iridocyclitis.[16]
Extraglandular manifestations
Musculoskeletal involvement
Joint disease associated with SS is commonly a polyarticular
arthropathy which intermittently affects small joints.
Evidence of joint deformity and erosion may be encountered
in primary SS-affected individuals, as well as nonerosive
arthritis. Arthralgias, myalgias and fibromyalgia-like features
are also commonly found.[17]
Pulmonary involvement
Although common, pulmonary involvement is seldom
clinically significant in patients with SS. [18] Interstitial
lung disease is a classic feature of SS. The clinical
manifestations include cough, dyspnea on exertion,
bilateral pulmonary infiltrates on plain chest radiographs
and other abnormalities on computer tomography scanner
such as wall thickening at the segmental bronchi. With
disease progression, fibrosis and neutrophilic alveolitis are
present.[19]
Renal involvement
Kidney involvement is a frequent extraglandular manifestation
of pSS. The renal involvement is rarely overt, and more often
follows a subclinical course. In some cases, it may precede
the onset of subjective sicca syndrome.[20] In SS patients who
show evidence of glomerular lesions, hematuria, proteinuria,
and renal insufficiency may be exhibited. Some patients may
progress to nephrotic syndrome.[14]
Gastroenterologic involvement
The manifestations of gastrointestinal tract are not very
specific and include esophageal dysmotility and gastro-
intestinal reflux. Patients often complain of dysphagia, nausea
and epigastric pain. Subclinical pancreatic involvement is
present in approximately 25% of cases. There are no specific
liver abnormalities, which can be attributed to SS, but
autoimmune hepatitis and primary biliary cirrhosis can be
associated diseases.[16,21]
Neurologic involvement
Neurologic disease is one of the most common manifestations
of SS, affecting cranial and peripheral nerves, and more
rarely the central nervous system. The eclectic permutation
of peripheral nervous system syndromes which occur
in SS patients are among the most common and severe
extraglandular complications.[22]
Hematologic/Oncologic involvement
Pa t i e n t s w i t h S S f re q u e n t l y h a v e l e u c o p e n i a ,
thrombocytopenia, a high erythrocyte sedimentation rate
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Kishore, et al.: Sjogren’s syndrome
and anti-nuclear antibodies.[13] Anemia of chronic disease
and hypergammaglobulinemia are the most prevalent
hematologic manifestations encountered at diagnosis and
during the course of pSS.[23]
Thyroid Involvement
Hypothyroidism seems to be common in SS.[24] A study
has shown that 45% of patients with SS also had associated
thyroid dysfunction. This is further supported by a study
suggesting that the prevalence of SS is 10 times higher in
patients with autoimmune thyroiditis.[25]
Obstetrical and gynecological involvement
Dyspareunia secondary to impaired lubrication is verified in
many premenopausal women with pSS. Other gynecological
problems include vaginal dryness, endometriosis, episodes
of amenorrhea and menorrhagia/metrorrhagia.[26]
Cardiac Involvement
Pericarditis and pulmonary hypertension can occur in SS.
Cardiovascular tests suggestive of autonomic neuropathy,
such as response of blood pressure to sustained hand grip,
valsalva maneuver, heart-rate response to deep breathing,
heart-rate and blood-pressure response to standing are
abnormal in some patients with SS.[27]
Diagnosis
The diagnosis of SS is not straightforward as many of the
symptoms are subjective and vague and can be dismissed
initially as other conditions or effect of medications.[28]
Although minor salivary gland biopsy has been traditionally
considered “the gold standard” for the diagnosis of SS,
newer criteria have emerged to assist on this disease
identification.
The revised diagnostic criteria established in 2002 by
the American-European Consensus Group are listed
in [Table 1]. [4] Early recognition of SS may prevent
complications such as dental caries, corneal ulceration,
chronic oral infection, and sialadenitis, and it allows
for clinical surveillance for the development of serious
extraglandular systemic manifestations.[14]
Diagnostic Tests
Oral diagnostic tests
Sialometry
Patients with clinically overt SS have reduced flow rate.
Measuring submandibular/sublingual flow rates may
contribute to an early diagnosis of SS. In contrast, parotid
flow rates are decreased in SS and Non-SS sicca patients.[29]
The test should therefore be standardized; the unstimulated
whole saliva collection test is performed for 15 min, and
the test is considered positive when <1.5 ml whole saliva
is collected.[4]
SRM Journal of Research in Dental Sciences | Vol. 5 | Issue 1 | January-March 2014
Sialography
The sialography typically shows sialectasias in contrast to the
fine arborization seen in normal parotid ductules. Diagnosis
is generally based on the classification given in [Table 2].[30]
Scintigraphy
In the scintigraphic test, 99mTc-pertechnate is given
intravenously, and in SS patients the typical finding is
decreased uptake in response to stimulation of the parotid
and submandibular salivary glands. This test is a sensitive
and valid method to measure abnormalities in salivary gland
function in the hands of skilled personal.[31]
Sialochemistry
SS is a mixture of increased inflammatory proteins and
decreased acinar proteins when compared with healthy
controls.[32] Furthermore ionic changes were observed in SS-
affected individuals, namely regarding the levels of chloride,
potassium, calcium, sodium and magnesium.[29]
Magnetic Resonance (MR) and ultrasonography (US)
MR imaging (MRI), MR sialography and US are noninvasive
methodologies that allow the imaging of salivary glands
in their physiological state without artefacts induced by
intraductal contrast media or biopsy procedures. MRI was
shown to provide a reliable imaging procedure to evaluate
glandular alterations. It allows multiplanar evaluation and
Table 1: Diagnostic criteria of Sjögren’s syndrome
Clinical and Histopathological findings
Ocular symptoms: at least one of the following
Daily dry eyes for >3 months
Persistent sensation of sand or gravel
Use of tear substitutes >3 times daily
Oral symptoms: at least one of the following
Dry mouth daily >3 months
Recurrent salivary gland swellings
Use of liquid to aid in swallowing food
Ocular signs: at least one of the following
Schirmer’s I test (≤5 mm in 5 min)
Rose Bengal score (≥4)
Histopathology
Focal lymphocytic sialoadenitis with focus score ≥1 per 4 mm2 of tissue
Salivary gland involvement: at least one of the following
Unstimulated salivary flow ≤1.5 ml⁄15 min
Abnormal parotid sialography
Abnormal salivary scintigraphy
Autoantibodies
Presence of Ro(SSA) or La(SSB) or both,
Table 2: Sialographic staging
Stages Diagnostic information
Stage 0 (normal) corresponds to no contrast media collection
Stage 1 (punctate) refers to contrast media collection ≤1 mm
in diameter
Stage 2 (globular) refers to contrast media collection between
1 and 2 mm in diameter
Stage 3 (cavitary) refers to contrast media collection ≥2 mm
in diameter
Stage 4 (destructive) refers to the complete destruction of the
gland parenchyma
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Kishore, et al.: Sjogren’s syndrome

processes a high contrast tissue resolution. Characteristically, CONCLUSION

in SS, MRI reveals an inhomogeneous internal pattern on
both T1 and T2 sequences, with multiple hypo- and hyper- People with SS may be more susceptible to drug allergies
intense nodules of different sizes.[33] and care is needed to monitor their condition if medication
is required. Like all chronic diseases it is important to
Serologic tests have regular contact with your doctor and eye specialist
Serology is used to establish the presence of anti-SS-A/Ro to monitor your condition. Regular dental checkups are
and anti-SS-B/La auto-antibodies,based on (enzyme-linked essential. Although SS is not life threatening, careful
immunosorbent assay). Anti-SS-A/Ro antibodies can also be attention to the problems it causes can help minimize the
detected in other autoimmune processes such as rheumatoid “nuisance” aspect of this condition and assist in a more
arthritis and systemic lupus erythematosus; for this reason, relaxed way.
anti-SS-B/La antibodies are considered to be more specific
of SS. Anti- SS-A/Ro can be isolated in 25-65% of cases, and
Table 4: Management of SS
anti- SS-B/La in 13-48%.[34]
Topical and systemic management
XEROPHTHALMIA
Ocular Diagnostic tests Artificial tears & ointmnets
1. Schirmer test Commercially Available Preparations of Artificial Tears
2. Rose Bengal Staining and Ocular Ointments
3. Tear break up time (BUT) Hydroxyethyl cellulose (Adsorbotear)
White petrolatum (Duratears, Lacrilube)
Polyvinyl alcohol (HypoTears, Liquifilm Forte, Tears Plus)
HISTOPATHOLOGY Polyethylene glycol (AquaSite)
Hydroxypropyl methylcellulose (Bion Tears, Tears Naturale)
Salivary gland Biopsy Methylcellulose (Murocel)
Carboxymethylcellulose (Refresh Plus)
A positive biopsy is defined as at least one focus of dense,
Soft contact lenses
inflammatory infiltrate containing at least 50 lymphocytes/4 ‘Punctal occlusion’ by using a variety of ‘plugs’ to occlude the
mm2. The lip biopsy may be useful in ambiguous cases or when punctal openings at the inner aspects of the eyelids eye for
therapy beyond symptom management is being considered.[35] longer time.
Muscarinic agonists
Pilocarpine (Salagen)- Oral pilocarpine, at a dosage of 5 mg
Differential Diagnosis twice daily
The differential diagnosis of SS includes conditions and Cevimeline (Evoxac)- Dosage of 30 mg three times daily
medications that can produce KCS, xerostomia, and parotid Anti-inflammatory medications
gland enlargement [Table 3].[14] Steroids
Cyclosporine
XEROSTOMIA
Management Maintenance of good oral hygiene
At present, treatment for most patients is essentially Use of sugarless sweets and chewing gums to stimulate residual
symptomatic.The patient should regularly visit a salivary flow
rheumatologist as well as an ophthalmologist and dentist Artificial saliva products
Commercially Available Preparations of Artificial Saliva and Oral
in order to prevent and treat the consequences of mucosal Lubricants
dryness, in addition to extraglandular manifestations and Salivart
other associated complications [Table 4].[4,36-39] Biotène Mouthwash
MouthKote
Xero-Lube
Table 3: Differential Diagnosis Saliment
Xerostomia Special toothpaste
Amyloidosis Fluoride supplementation
Diabetes mellitus Eradication of oral candidiasis
Sarcoidosis Antimicrobial mouth rinses
Viral infections Sugar substitutes-Xylitol
Trauma Pilocarpine -dosage of 5 mg four times daily
Irradiation Cevimeline at a dosage of 30 mg three times daily
Psychogenic Natural human interferon alfa- 150 IU 3 times daily
Drugs like antihypertensive, parasympatholytic, for 12 weeks
and psychotherapeutic agents Nystatin in tablets or solution (100,000 IU 4-6 times a day), or
Dry Eyes miconazole gel 4 times a day
Allergic conjunctivitis SYSTEMIC MANAGEMENT
Blepharitis Corticosteroids (hydroxychloroquine 6-7 mg/kg/day
Pemphigoid Prednisone 1-2 mg/kg/day)
Stevens-Johnson syndrome Nonsteroidal antiinflammatory drugs
Sarcoidosis Immune regulators
Toxicity (burns or drugs) Immune suppressors reserved for severe cases (azathioprine)

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