Another theory is that the pain upon cold stimuli results from leak of noxious substances via the crack, irritating the pulp. Diagnosis
Cracked tooth syndrome (CTS) was defined as an incomplete fracture of a vital posterior tooth that involves the dentine and occasionally extends to the pulp by Cameron in 1964 and more recently has included a fracture plane of unknown depth and direction passing through tooth structure that, if not already involving, may progress to communicate with the pulp and/or periodontal ligament. The diagnosis of cracked tooth syndrome is notoriously difficult even for experienced clinicians. The features are highly variable and may mimic sinusitis, temporomandibular disorders, headaches, ear pain, or atypical facial pain/atypical odontalgia (persistent idiopathic facial pain). When diagnosing cracked tooth syndrome, a dentist takes many factors into consideration. Effective management and good prognosis of cracked teeth is linked to prompt diagnosis. A detailed history may reveal pain on release of pressure when eating or sharp pain when consuming cold food and drink. There are a variety of habits which predispose patients to CTS including chewing ice, pens and hard sweets etc. Recurrent occlusal adjustment of restorations due to discomfort may also be indicative of CTS, alongside a history of extensive dental treatment. Below different techniques used for diagnosing CTS are discussed. Clinical examination
Cracks are difficult to see during a clinical exam which may limit diagnosis.
Any of these muscles can be involved or spasm with a painful and dysfunctional sacroiliac joint. The SI joint is a pain-sensitive structure richly innervated by a combination of unmyelinated free nerve endings and the posterior primary rami of spinal segments L2-S3. The wide possibility of innervation may explain why pain originating from the joint can manifest in so many various ways, with different and unique referral patterns (see "referred pain") for individual patients. Patients with sacroiliac joint dysfunction can also develop tightness and dysfunction in the hamstring, quadriceps, iliotibial tract (see "iliotibial band syndrome") and hip flexors, including the psoas muscle. Individuals with severe and long-standing sacroiliac joint dysfunction can develop muscle deconditioning and atrophy throughout the body due to limitation of activities and exercise that bring about pain in the low back. Diagnosis
Perhaps the biggest reason for misdiagnosis or lack of diagnosis of sacroiliac joint dysfunction is based on the inability of common radiological imaging to discern the disorder. Diagnostic testing, such as X-ray, CT scan, or MRI, do not usually reveal abnormalities; therefore, they cannot reliably be used for diagnosis of sacroiliac joint dysfunction. There is a new imaging test SPECT/CT which can sometimes detect sacroiliac joint dysfunction. There is also a lack of evidence that sacroiliac joint mobility maneuvers (Gillet, Standing flexion test, and Seated Flexion test) detect motion abnormalities. Given the inherent technical limitations of the visible and palpable signs from these sacroiliac joint mobility maneuvers another broad category of clinical signs have been described called provocative maneuvers.