Diffuse idiopathic skeletal hyperostosis (DISH) and axial spondyloarthritis (axSpA) are diseases with inflammatory involvement of the axial skeleton that can result in new bone formation that may lead to total ankylosis of the spine and functional impairment of different extent in individual patients. In these diseases, the new bone formation may lead to total ankylosis of the spine and impaired mobility with functional impairment. This review will highlight the similarities and differences of these two conditions. In axSpA, the genetic background with the association with human leukocyte antigen-B27 (HLA-B27) is known for 50 years, while in DISH, a genetic contribution is not yet proven. The phenotype of new bone formation and its anatomic features are different between these diseases. In axSpA symmetric, thin and marginal syndesmophytes representing an ossification of enthesitic inflammation at the area of the attachment of the annulus fibrosus that may extend to the adjacent deeper layers anterior longitudinal ligament and are typical, while in DISH the so-called “chunky bridging osteophytes” grow as an additional layer on the anterior longitudinal ligament. Besides distinct anamnestic and clinical features, magnetic resonance imaging is helpful differentiating the two diseases since inflammatory changes with the typical pattern of axSpA are reliably visualized. Similar in both diseases is the high prevalence of vertebral fractures, which are mainly caused by the local osteoporosis and decreased flexibility of the affected bones, and therefore may occur even after minor traumata. The presence of extraarticular manifestations like uveitis, inflammatory bowel disease or psoriasis are only linked to axSpA. In contrast, DISH is associated with obesity, diabetes mellitus, and other metabolic diseases. Although DISH and axSpA are distinct conditions, the cooccurrence of these two diseases exists in some patients. Various therapeutic options are becoming available for axSpA, but no therapy has been approved for DISH yet.

Rheumatoid arthritis (RA) is an inflammatory arthritis that affects synovial joints, and it is not surprising that the temporomandibular joint (TMJ), a synovial joint, is also affected. However, TMJ is rarely the first affected joint in the course of RA. Often, RA patients come to the physician with more focus on complaints in other peripheral joints. Therefore, asking TMJ complaints and symptoms, and TMJ examination in RA patients is often neglected by doctors too, because they focus more on other joints. This neglect may cause serious damage to the joints and cause disability. Examination of TMJs, which is a crucial component of vital activities such as nutrition and speech, should be added to the routine. Also, further studies may be focused on adding TMJ assessment to disease activity scales and health assessment questionnaires.

Bone formation is a complex process that occurs throughout life, and is normally limited to the skeletal system. In bone formation, osteoprogenitor cells follow several developmental stages, including differentiation in osteoblasts, proliferation, matrix maturation, and mineralization. The mechanisms involved in the mineralization process of bone, such as in the new bone formation, are extremely complex and have been under intense investigation for many years. Bone formation follows two distinct processes, intramembranous and endochondral ossification; both are regulated by signaling pathways involving numerous genes. Disturbance of these signaling pathways may cause a large spectrum of skeletal diseases characterized by new bone formation and bone growth anomalies. This review will only focus on the key genetic pathways involved in heterotopic bone formation. Wingless/integrated (Wnt), hedgehog (HH), and transforming growth factor beta (TGFβ)/bone morphogenetic protein (BMP) signaling pathways are described and illustrated; their relation with new bone formation is demonstrated through their involvement in bone formation disorders.