The arthritis may also involve the spine, leading to ankylosing spondylitis if the entire spine is involved, or simply sacroiliitis if only the sacroiliac joint is involved. The symptoms of arthritis include painful, warm, swollen, stiff joints, and loss of joint mobility or function.Crohns disease increases the risk of osteoporosis or thinning of the bones. Individuals with osteoporosis are at increased risk of bone fractures. Dermatological
Crohns disease may also involve the skin, blood, and endocrine system. Erythema nodosum is the most common type of skin problem, occurring in around 8% of people with Crohns disease, producing raised, tender red nodules usually appearing on the shins. Erythema nodosum is due to inflammation of the underlying subcutaneous tissue, and is characterized by septal panniculitis.Pyoderma gangrenosum is a less common skin problem, occurring in under 2%, and is typically a painful ulcerating nodule.Clubbing, a deformity of the ends of the fingers, may also be a result of Crohns disease. Other very rare dermatological manifestations include: Pyostomatitis vegetans, Psoriasis, Erythema multiforme, Epidermolysis bullosa acquista (described in a case report), and Metastatic CD (the spread of Crohns inflammation to the skin). It is unknown if Sweets Syndrome is connected to Crohns disease.Neurological
Crohns disease can also cause neurological complications (reportedly in up to 15%). The most common of these are seizures, stroke, myopathy, peripheral neuropathy, headache, and depression.Central and peripheral neurological disorders are described in patients with IBD and include peripheral neuropathies, myopathies, focal central nervous system defects, convulsions, confusional episodes, meningitis, syncope, optic neuritis, and sensorineural loss.
All this new knowledge in the pathogenesis of Crohns disease allows us to put this multifactorial disease in the group of autoinflammatory syndromes.Some examples of how the innate immune system affects bowel inflammation have been described. A meta-analysis of CD genome-wide association studies revealed 71 distinct CD-susceptibility loci. Interestingly, three very important CD-susceptibility genes (the intracellular pathogen-recognition receptor, NOD2; the autophagy-related 16-like 1, ATG16L1 and the immunity-related GTPase M, IRGM) are involved in innate immune responses against gut microbiota, while one (the X-box binding protein 1) is involved in regulation of the [adaptive] immune pathway via MHC class II, resulting in autoinflammatory inflammation. Studies have also found that increased ILC3 can overexpress major histocompatibility complex (MHC) II. MHC class II can induce CD4+ T cell apoptosis, thus avoiding the T cell response to normal bowel micro bacteria. Further studies of IBD patients compared with non-IBD patients found that the expression of MHC II by ILC3 was significantly reduced in IBD patients, thus causing an immune reaction against intestinal cells or normal bowel bacteria and damaging the intestines. This can also make the intestines more susceptible to environmental factors, such as food or bacteria.The thinking is, that because Crohns disease has strong innate immune system involvement and has NOD2 mutations as a predisposition, Crohns disease is more likely an autoinflammatory disease than an autoimmune disease. Immunodeficiency theory
A substantial body of data has emerged in recent years to suggest that the primary defect in Crohns disease is actually one of relative immunodeficiency.