Sjögren's Disease and Dry Eye

Sjögren’s is a systemic autoimmune disease. In autoimmune disease, the immune system mistakenly targets the body’s own tissues. Sjögren’s has a particular tendency to affect the lacrimal glands, which produce much of the aqueous component of tears, and the salivary glands, which produce saliva. This is why two of its best-known manifestations are:

• •dry eyes
• •dry mouth

But Sjögren’s is not simply a “dryness disease.” It can affect other parts of the body as well, and its presentation varies considerably from person to person.

In Sjögren’s, immune-mediated inflammation can disrupt the normal function of the lacrimal glands. If the lacrimal glands produce less aqueous tear fluid, the result can be aqueous-deficient dry eye. But, as we have seen throughout this guide, the ocular surface is a connected system. Reduced aqueous secretion can contribute to tear-film instability, increased concentration of the tear film, inflammation and ocular-surface damage.

And a person with Sjögren’s can simultaneously have other dry-eye drivers. So even in someone with a confirmed systemic disease, the eye problem may still be multifactorial. TFOS DEWS III emphasizes this broader etiological approach to dry eye rather than assuming one abnormality explains the whole disease.

Aqueous Deficiency

No. This distinction is essential. Sjögren’s can cause aqueous-deficient dry eye. But aqueous-deficient dry eye is not the same as Sjögren’s disease.

Aqueous tear production can be reduced for other reasons. This is why a low Schirmer result alone cannot diagnose Sjögren’s. In fact, in the current ACR/EULAR classification criteria, an abnormal Schirmer test contributes only one part of a multi-component assessment.

The Schirmer Test: what it measures and what it doesn't

Not by itself. The severity of eye symptoms does not identify their cause.

Someone can have severe dry eye from MGD, ocular-surface inflammation, exposure, neural abnormalities or several overlapping problems. Likewise, symptoms and clinical signs do not always correspond neatly. What makes Sjögren’s more relevant is the whole pattern rather than simply how bad the eyes feel.

One of the most important clues is persistent dry mouth. People may notice that they need frequent sips of water, have difficulty with very dry foods or experience other problems related to reduced saliva. But Sjögren’s is systemic, so manifestations can extend beyond dryness. Depending on the individual, the disease may involve joints, skin, lungs, nerves and other organs.

Not everyone has the same combination of symptoms. And importantly, modern Sjögren’s classification recognizes that systemic manifestations can matter even when classic eye or mouth dryness is not the dominant presentation.

There is no single test that answers the question for every patient. Evaluation may involve several different kinds of evidence:

• •blood tests
• •tests of tear production and ocular-surface damage
• •measurement of saliva production
• •and sometimes assessment or biopsy of the salivary glands

The pieces are interpreted together. This is very different from:

“Take one blood test and find out whether you have Sjögren’s.”

How Dry Eye Is Diagnosed

One particularly important antibody is anti-SSA/Ro. Anti-SSA positivity is given substantial weight in the 2016 ACR/EULAR classification criteria. Other laboratory tests may also be ordered in clinical practice depending on the patient’s presentation, but it is worth knowing that the current classification criteria specifically use anti-SSA/Ro rather than simply treating any positive ANA or rheumatoid factor as evidence of Sjögren’s. That distinction matters because many immune markers are not specific to one disease.

This is where the subject becomes more nuanced. A negative anti-SSA/Ro result means that one important piece of evidence for Sjögren’s is absent. It does not, by itself, function as a universal rule-out test. The ACR/EULAR framework itself demonstrates why: strong evidence can also come from a minor salivary-gland biopsy showing focal lymphocytic sialadenitis. Anti-SSA positivity and a qualifying biopsy each receive three points in the classification system.

So a negative anti-SSA is not automatic proof that Sjögren’s is impossible. But equally, negative anti-SSA plus dry eyes is not a reason to assume “seronegative Sjögren’s.” Whether further investigation is appropriate depends on the rest of the clinical picture.

The Schirmer test measures tear production under particular testing conditions. As we discussed in our diagnostic section, it is not a perfect test and should not be interpreted in isolation. But markedly reduced tear production can become one useful piece of evidence when Sjögren’s is being investigated. The 2016 ACR/EULAR criteria use Schirmer ≤5 mm in 5 minutes in at least one eye as one objective criterion.

But notice the weighting: Schirmer is 1 point. Anti-SSA/Ro is 3 points. A qualifying salivary-gland biopsy is 3 points. That helps illustrate why a low Schirmer result is supportive information, not a diagnosis.

Sjögren’s-related aqueous deficiency can lead to ocular-surface damage. Doctors can use dyes to reveal areas of epithelial disruption. The ACR/EULAR criteria therefore also include an ocular staining score as one of the objective items.

Again, staining does not tell us “This damage was caused by Sjögren’s.” Many forms of dry eye can produce staining. It becomes useful when interpreted alongside the rest of the evidence.

Because Sjögren’s frequently affects salivary glands as well as lacrimal glands. One objective test measures unstimulated whole salivary flow, essentially how much saliva is produced without stimulation. A very low salivary-flow rate is another component of the ACR/EULAR criteria.

This illustrates something important: Sjögren’s evaluation is not just an eye evaluation. The doctor is looking for evidence of a systemic autoimmune process affecting glandular function.

Small salivary glands are present inside the lower lip. A minor salivary-gland biopsy removes a small sample of this tissue so it can be examined under a microscope. Pathologists look for a characteristic pattern called focal lymphocytic sialadenitis and calculate a focus score.

A qualifying biopsy carries substantial weight in the ACR/EULAR classification criteria: the same number of points as anti-SSA positivity. This can be particularly relevant when the clinical suspicion remains meaningful but antibody testing has not provided the answer. It is an invasive test, however, so whether it is appropriate is a clinical decision rather than something every dry-eye patient needs.

Ultrasound of the major salivary glands is increasingly used as a non-invasive way of looking for structural abnormalities associated with Sjögren’s. Research suggests that adding salivary-gland ultrasound can improve diagnostic assessment in some settings. However, it is not one of the five items in the original 2016 ACR/EULAR criteria, and studies have evaluated different ways of incorporating it. So it is useful to distinguish between:

• •tests clinicians may use in real-world evaluation
• •the formal classification criteria

They are not necessarily identical.

You may encounter these criteria when researching Sjögren’s online, so they are worth understanding. The 2016 ACR/EULAR classification system assigns weighted points to five objective findings:

• •anti-SSA/Ro antibodies: 3 points
• •characteristic minor salivary-gland biopsy: 3 points
• •abnormal ocular-surface staining: 1 point
• •Schirmer ≤5 mm/5 min: 1 point
• •very low unstimulated salivary flow: 1 point

A score of 4 or more, in an appropriate patient meeting the criteria’s entry requirements and without specified exclusions, satisfies the classification criteria.

But there is an important caveat: classification criteria are not the same thing as a DIY diagnostic calculator. They were developed to create a standardized way of classifying patients, particularly for research, and were validated against expert clinical judgment. A real diagnostic evaluation also considers the patient’s history, examination, alternative explanations and broader clinical context.

The disease does not present identically in everyone. Modern criteria also recognize the systemic nature of Sjögren’s rather than requiring every patient to fit the classic picture of obvious eye and mouth dryness. So absence of one textbook symptom should not be turned into an absolute rule. At the same time, this does not mean every unexplained dry-eye patient should assume they have an unusual form of Sjögren’s.

The degree of clinical suspicion still matters.

Because Sjögren’s is a systemic autoimmune disease, evaluation often involves a rheumatologist. But eye doctors can play an important role. They may identify significant aqueous deficiency, ocular-surface staining or a combination of findings that makes a systemic evaluation appropriate. Dentists, oral-medicine specialists and other clinicians may also identify signs of salivary-gland dysfunction.

Ideally, the information from different parts of the body is considered together.

Not necessarily. This is worth repeating because it fits the central idea of our entire guide. A person with Sjögren’s can also have:

• •MGD
• •blepharitis
• •ocular rosacea
• •incomplete blinking
• •exposure
• •or other ocular-surface problems

A systemic diagnosis is extremely important. But it should not stop clinicians from asking what is actually happening in the eyes. TFOS DEWS III’s etiological approach specifically encourages identifying the individual drivers of dry eye rather than stopping at a broad disease label.

Dry Eye Is Often Mixed