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Oral health alterations: Glimpse into its connection to inflammatory rheumatic diseases

1 Department of Physiology, Medical College for Women and Hospital, Dhaka, Bangladesh
2 The Unit of Pharmacology, Faculty of Medicine and Defence Health, Universiti Pertahanan Nasional Malaysia (National Defence University of Malaysia), Kuala Lumpur, Malaysia

Date of Submission29-Jan-2023
Date of Acceptance31-Jan-2023
Date of Web Publication16-Feb-2023

Correspondence Address:
Mainul Haque,
The Unit of Pharmacology, Faculty of Medicine and Defence Health, Universiti Pertahanan Nasional Malaysia (National Defence University of Malaysia), Kem Perdana Sungai Besi, Kuala Lumpur
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/aihb.aihb_11_23

How to cite this URL:
Ahmad R, Haque M. Oral health alterations: Glimpse into its connection to inflammatory rheumatic diseases. Adv Hum Biol [Epub ahead of print] [cited 2023 Mar 31]. Available from: https://www.aihbonline.com/preprintarticle.asp?id=369799

Chronic inflammatory rheumatic disease (IRD) is suffered by approximately 3% of global citizens and includes rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and Sjögren's syndrome.[1],[2] There are several systemic complications, including complications of cardiovascular, renal, respiratory and neurological systems. There are also oral manifestations of rheumatic disease in some patients [Figure 1].[3] Oral symptoms along with other typical clinical manifestations may lead to the suspicion of the rheumatic disease since oral changes may be one of the early signs of these systemic disorders. Condition like oral aphthous has been noted in about 50% of individuals suffering from SLE.[4],[5] About 90% of individuals with Sjögren's syndrome suffer from hyposalivation and xerostomia. Microcheilia and microstomia have been noted in those suffering from systemic sclerosis (SSc) which interferes with the opening of the mouth. Other oral manifestations in chronic IRD include strawberry-like gum disease and jaw claudication.[3]
Figure 1: The different oral complications that may result from inflammation and altered immune response in inflammatory rheumatic diseases. This figure has been drawn with the premium version of BioRender (https://biorender.com/) with license number JB24XLKAMQ. Image Credit: Rahnuma Ahmad.

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  Oral Changes in Rheumatic Diseases Top

Oral aphthous ulcer

The frequent appearance of oral aphthous ulcers has been included in the 2012 Systemic Lupus International Collaborating Clinics SLE classification criteria. This is because individuals with IRDs and SLE patients suffer from repeated oral aphthous ulcer.[6] About 50% of SLE patients suffer from aphthous ulcer, and examination shows peripheral keratotic striae and whitish plaque with central erythema.[4],[5],[7] There have also been reports of lesions in the oral cavity like discoid lesions and lichenoid mucositis in gingival and buccal mucosae and lips.[7],[8] Basement membrane with linear deposition of immunoglobulin M, G and C3 has been observed by direct immunofluorescence study. The presence of CD4+ T-lymphocytes has also been noted in the site of lesion.[7],[9]


Both muscles of the oropharynx and the wall of the oesophagus are responsible for swallowing, impairment of which may result in dysphagia.[10] In about 90% of SSc cases, there is an impairment of oesophageal movement causing dysphagia as well as stricture of oesophagus, gastro-oesophageal reflux and retrosternal burn. Hypotonia of the lower sphincter of the oesophagus and reduced functioning of the lower one-third of the oesophagus have been noted in individuals with SSc.[11],[12]

Dermatomyositis and polymyositis are rare rheumatic diseases that affect the muscles of the body and are characterised by weakness of muscle and high level of creatine kinase and affect organs such as joints, skin, gastrointestinal, cardiovascular and respiratory systems. The anti-nuclear antibodies are found often in these conditions.[3],[10] The proximal one-third of oesophagus as well as the posterior wall of the pharynx muscles suffer myopathies, which is immune mediated causing dysphagia.[10],[13] There has been a report of dysphagia in 12% and 54% of individuals suffering from dermatomyositis and polymyositis.[14] The time of transit through the pharynx to the upper sphincter of the oesophagus has been observed to be raised.[15] An association between a rise in internal malignancy incidence and dysphagia in individuals having dermatomyositis has been reported.[16] Hypersalivation observed in a number cases due to impairment of swallowing as well as salivation reflex precipitated through oesophageal reflux. Systemic symptoms such as loss of weight, fever which is low grade, joint pain or arthritis and fatigue may also be present.[17],[18],[19]

Microcheilia, microstomia and inflammatory rheumatic disease

Patients with SSc may suffer from microstomia (decreased aperture of lips) and microcheilia (small lips) along with radial folds periorally, telangiectasias of body, face and mucosa, thickening of skin and Raynaud's phenomenon.[3],[20] The opening of the mouth is limited in microstomia and is suffered by 70% of individuals suffering from SSc. Microstomia results from soft tissue fibrosis periorally.[21] There is deposition of collagen subcutaneously in the skin of the face giving it an appearance of a smooth mask.[22],[23] Telangiectasias of the labia, tongue and perioral region may also be present.[3] Since the incidence of carcinoma of the tongue in individuals suffering from SSc is high, the mucosa of the oral cavity of these individuals should be examined regularly to identify any lesion at an early stage and provide treatment.[24],[25] Dentists must refer SSc patients with oral lesion to a rheumatologist as early as possible since the involvement of the organ occurs rapidly.[26] Exercises may cause an improvement of the opening of the mouth and grafting of fat may be helpful in case of microstomia.[21],[27],[28]


Xerostomia or dry mouth may be complained by patients with Sjögren's syndrome along with swelling of the salivary gland due to inflammation. This syndrome is an autoimmune disorder which affects the exocrine glands giving rise to ocular and oral dryness which is accompanied by systemic signs and symptoms.[3],[29] The primary Sjögren's syndrome criteria of classification acknowledged widely are the American-European Consensus Group classification, and four or more of the mentioned criteria need to be present: (1) symptom of xerostomia, (2) symptoms of dry eye, (3) objective dryness of mouth-positive salivary sialography and scintigraphy or <0.1 mL/min unstimulated rate of flow of saliva), (4) objective dryness of eye (Schirmer's test <5 mm in 5 min), (5) biopsy of labial gland showing focal sialadenitis of lymphocyte and (6) positive anti-SSB/La or anti-SSA/Ro.[30]

Another systemic fibroinflammatory disease related often to swelling of the salivary gland and dry mouth is a disease related to immunoglobulin G4 (IgG4). There is the presence of high level of IgG4 in serum with inflammation of multiple organs, including the lacrimal gland, periorbital structures, thyroid, pancreas, lungs, pituitary gland, biliary tree, retroperitoneal cavity and salivary gland.[31]

Periodontal disease

Periodontal disease leads to the destruction of the gingiva and supporting tissue of tooth with eventual loss of tooth.[32],[33],[34] The immune system of the host often affected through genetic make-up, infectious diseases, and environmental factors results in this chronic inflammatory condition. Individuals having RA often suffer from periodontitis. Several studies have noted an association between RA and periodontitis in which a greater prevalence of periodontitis was noted in subjects with RA when compared to those without RA.[35],[36] There is raised production of inflammatory cytokines like tumour necrosis factor-alpha, interleukin (IL)-8, IL-6 and IL-1β in case of both RA and periodontal disease.[33] In about 50%–70% of patients with RA, there is the presence of anti-citrullinated peptide antibodies and rheumatic factors, which is related to symptoms and damage of joints more in severity and greater mortality rate.[37],[38] An oral microbiota commonly related to periodontitis is Porphyromonas gingivalis which may aggravate the conversion of arginine to citrulline by means of type IV peptidyl arginine deiminase with ultimate production of ACRAs [Figure 2].[33] Studies have shown a decrease in RA severity in individuals who underwent non-surgical management of periodontal disease.[39],[40]
Figure 2: The vicious cycle of chronic inflammation, citrullination, immunity dysregulation and periodontal pathogens along with genetic and environmental factors cause periodontal damage and lead to periodontitis. This figure has been drawn with the premium version of BioRender (https://biorender.com/) with license number YC24Y151CF. Image Credit: Rahnuma Ahmad.

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Periodontitis has also been observed in patients with SSc. In 40% of SSc patients, a typical periodontitis radiographic sign of widening of space of the periodontal ligament was noted.[41],[42] This may have resulted from raised deposition of collagen,[43] decreased vascular endothelial growth factor and lowered periodontal capillary number with eventual greater tooth loss prevalence in patients with SSc.[44],[45] Periodontitis has also been noted in about 70% of individuals with SLE.[46] A meta-analysis of eight studies observed that periodontitis risk was higher than those without SLE.[47]

Overgrowth of the gingiva

Although overgrowth of the gingiva (gingiva enlargement resulting from raised cell number and extracellular matrix accumulation) may result from gingivitis related to poor maintenance of hygiene of oral cavity, different systemic disorders may also aggravate it.[3],[48] In granulomatosis with polyangiitis, there may be an overgrowth of the gingiva that is swollen, reddened with small punctate lesions and petechia-covered granular tissue which is strawberry-like gingivitis.[49],[50] Necrotising granulomatous vasculitis affects upper respiratory tracts in 90% of cases and, if not treated, may result in mandibular and maxillary bone destruction.[3],[51] Other conditions of the oral cavity include lingual necrosis and ulceration of the mucosa.[52]

Claudication of jaw

Pain of muscle of mastication during chewing is claudication of the jaw and occurs when function is impaired due to ischaemia with lactate accumulation of lactate in skeletal muscles.[53] A common manifestation of giant cell arteritis affecting large blood vessel is claudication of the jaw in Western subjects above the age of 50 years.[54] The temporal artery is affected by giant cell arteritis which when palpated is tender.[55] Giant cell artery symptoms include low-grade fever, depression, weight loss, temporal headaches, dental pain, dysarthria, dysphagia and rare occasion lip and tongue necrosis.[53] Individuals with claudication of the jaw need to be assessed by a rheumatologist for giant cell arteritis exclusion.[56]

Involvement of temporomandibular joint

A frequent condition suffered by patients of IRD is temporomandibular joint inflammation.[57] The individual suffers from pain of the jaw, restriction of motion, malocclusion and swelling. Involvement of the temporomandibular joint may take place in 90% of cases of juvenile idiopathic arthritis.[58],[59]

Rheumatic disease is frequently associated with different manifestations of the oral cavity for which patients seek the doctor's consultation initially. There are non-specific symptoms such as xerostomia and oral ulcers while other symptoms such as microstomia and strawberry-like gingivitis are characteristic of rare IRD like SSc and granulomatosis with polyangiitis, respectively. In IRDs, there are alterations in the immunological response, and inflammation. These deleterious process often influenced by lifestyle. Additionally, with erroneous healthcare intervention. There needs to be a collaboration between physicians and dentists to help early diagnosis and management of rheumatic disease complications both systemic and that of the oral cavity.

Consent for publication

The author reviewed and approved the final version and has agreed to be accountable for all aspects of the work, including any accuracy or integrity issues.


The author declares that they do not have any financial involvement or affiliations with any organisation, association or entity directly or indirectly with the subject matter or materials presented in this article. This includes honoraria, expert testimony, employment, ownership of stocks or options, patents or grants received or pending or royalties.

Data availability

Information is taken from freely available sources for this editorial.

Authorship contribution

All authors contributed significantly to the work, whether it be in the conception, design, utilisation, collection, analysis and interpretation of data or in all these areas. They also participated in the article's drafting, revision or critical review, gave their final approval for the version that would be published, decided on the journal to which the article would be submitted and made the responsible decision to be held accountable for all aspects of the work.

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