Periodontal disease is a biofilm-induced chronic inflammatory condition that affects the tooth-supporting tissues, which in its severe form may lead to tooth loss and negatively affect systemic health. Although host immune and inflammatory responses are crucial in the control of this biofilm, their persistence and dysregulation may lead to destruction of periodontal tissues, where neutrophils and macrophages might play an important role. Moreover, it has been shown that periodontitis is associated with several chronic inflammatory diseases, among which inflammatory bowel disease has raised special attention . Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the gastrointestinal tract, which comprises two main forms, Crohn’s disease and ulcerative colitis .
The pathogenesis of IBD involves genetic and environmental factors, such as diet, smoking, stress, and microorganisms , and it is characterized by intestinal inflammation and epithelial injury . Crohn’s disease (CD) is characterized by macrophage aggregation, frequently forming noncaseating granulomas and transmural inflammation. The terminal ileum is the most common site affected, but the disease can involve any site of the gastrointestinal tract.
Ulcerative colitis (UC) is characterized by a significant infiltration of neutrophils within the lamina propria and the crypts, forming micro-abscesses and superficial mucosal ulceration. The distal colon is the most affected region . As previously mentioned, both cell types, macrophages and neutrophils, are also relevant to the pathogenesis of periodontal disease, suggesting that under a similar cytokine signalling, these diseases might share similar pathways. Indeed, the presence of periodontal disease is more frequent in patients with IBD when compared to controls.
In addition, greater severity and extent of periodontitis have been found in IBD patients when compared to healthy controls . This might be related to a higher expression of IL-18 in the serum of IBD patients with periodontitis . However, different cytokine clustering patterns were observed in gingival tissues in comparison to those found in intestinal tissues. This might suggest that although a common pathway may exist in serum, local cytokine behaviour may be slightly different. Considering the complexity of both periodontal disease and IBD, it is very challenging to comprehend the possible pathways involved in their coexistence.
Dental management of patients with IBD should include the following: \
• Frequent preventive and routine dental care to prevent destruction of hard and soft tissue.
• Evaluation of hypothalamic/pituitary/adrenal cortical function to determine the patient’s ability to undergo extensive dental procedures.
• Avoid prescribing non-steroidal anti-inflammatory drugs (NSAID), as they can trigger a flare-up. The use of paracetamol is recommended, although it can also adversely affect patients.
• Early diagnosis and treatment of oral infections to enhance the gastroenterologist’s ability to manage the IBD.
• Diagnosis (biopsy if necessary) and treatment of oral inflammatory.
Conclusions Mucosal changes of UC in the oral cavity include stomatitis, glossitis, cheilitis, aphtous ulcerations, and pyostomatitis vegetans. The latter represents a specific marker of ulcerative colitis. Macrocheilia, cobblestoning of oral mucosa, deep linear ulcers of buccal vestibules, and polypoid mucosal tags are considered specific and pathogonomic for CD . Nonspecific changes include angular cheilitis, aphthous stomatitis and pyostomatitis vegetans
In dental treatment of patients with IBD, it is important that they undergo frequent dental revisions and preventive care to avoid oral infections and hard and soft tissue destruction; it is also important to diagnose and treat all inflammatory, infectious or granulomatous oral lesions. We also have to avoid NSAID prescriptions and evaluate hypothalamic/pituitary/adrenal cortical functions.
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