If the greatest reduction in movement occurs upon waking then this may indicate that there is concomitant sleep bruxism. In other cases the limitation in movement gets worse throughout the day.The jaw may lock entirely.Limitation of mandibular movement itself may lead to further problems involving the TMJs and the muscles of mastication. Changes in the synovial membrane may lead to a reduction in lubrication of the joint and contribute to degenerative joint changes. The muscles become weak, and fibrosis may occur. All these factors may lead to a further limitation of jaw movement and increase in pain.Degenerative joint disease, such as osteoarthritis or organic degeneration of the articular surfaces, recurrent fibrous or bony ankylosis, developmental abnormality, or pathologic lesions within the TMJ. Myofascial pain syndrome. Referred TMD pain
Sometimes TMD pain can radiate or be referred from its cause (i.e. the TMJ or the muscles of mastication) and be felt as headaches, earache or toothache.Due to the proximity of the ear to the temporomandibular joint, TMJ pain can often be confused with ear pain. The pain may be referred in around half of all patients and experienced as otalgia (earache). Conversely, TMD is an important possible cause of secondary otalgia. Treatment of TMD may then significantly reduce symptoms of otalgia and tinnitus, as well as atypical facial pain. Despite some of these findings, some researchers question whether TMJD therapy can reduce symptoms in the ear, and there is currently an ongoing debate to settle the controversy.
This could potentially be of importance in genetically differentiating between NFJS and DPR.The disruption of the KRT14 gene in DPR suggests this gene is important during the early development of dermatoglyphics and sweat glands. Because of the aforementioned genetic similarity between NFJS and DPR, some researchers have suggested treating the disorders as a single condition. Diagnosis
Diagnosis of DPR begins with review of a patients medical history, laboratory results, and clinical examination of symptoms. Biopsy and histopathological examination can be used to test for the presence of hyperkeratosis, parakeratosis, follicular plugging, and basal cell melanization, all indicators of DPR. Furthermore, abnormalities in skin pigmentation patterns as well as the presence of palmoplantar keratoderma with yellow tinting of the skin can indicate a possible case of DPR. Despite the presence of outward indicators, routine blood testing will not yield abnormal results. While the aforementioned symptoms of DPR are outwardly identifiable, DPR is a rare genetic disease that requires genetic analysis to yield a confirmed diagnosis.The Genetic Testing Registry lists 15 clinical genetic tests used in obtaining a diagnosis of this disorder. Two of these tests utilize Targeted Variant Analysis, thirteen utilize sequence analysis of the entire coding region, and seven utilize deletion and duplication analysis. The type of test ordered may depend on the clinicians judgement or access to specific testing methods. Management
To date, there is no medical treatment specific to DPR, however symptom management of palmoplantar hyperkeratosis as well as other, secondary symptoms is possible through the use of topical steroids, keratolytics, and emollients.