The involved cusp can be determined by biting on individual cusps separately. Tooth Slooth II (Professional Results Inc., Laguna Niguel, CA, USA) and Fractfinder (Denbur, Oak Brook, IL, USA) are commercially available tools. Epidemiology
Aetiology of CTS is multifactorial, the causative factors include:

previous restorative procedures. occlusal factors; patients who suffer from bruxism, or clenching are prone to have cracked teeth. developmental conditions/anatomical considerations. trauma
others, e.g., aging dentition or presence of lingual tongue studs.Most commonly involved teeth are mandibular molars followed by maxillary premolars, maxillary molars and maxillary premolars. in a recent audit, mandibular first molar thought to be most affected by CTS possibly due to the wedging effect of opposing pointy, protruding maxillary mesio-palatal cusp onto the mandibular molar central fissure. Studies have also found signs of cracked teeth following the cementation of porcelain inlays; it is suggested that the debonding of intracoronal restorations may be caused by unrecognized cracks in the tooth. Treatments
There is no universally accepted treatment strategy, but, generally, treatments aim to prevent movement of the segments of the involved tooth so they do not move or flex independently during biting and grinding (stabilisation of the crack) to prevent propagation of the crack. Provisionally, a band may be placed around the tooth or a direct composite splint can be placed in supra-occlusion to minimize flexing.
The two, however, are clinically, radiographically, and genetically distinct from one another. Treatment
People with Pyle disease are often asymptomatic. Dental anomalies may require orthodontic interventions. Skeletal anomalies may require orthopedic surgery. Epidemiology
Pyle disease is thought to be a rare disorder, although its prevalence is unknown. More than 25 cases have been described in the medical literature.It has been described in four German families originating from the same town in Bohemia and in a 7-year-old Japanese girl. Research
Cortical-bone fragility is a common feature in osteoporosis that is linked to nonvertebral fractures. Regulation of cortical-bone homeostasis has proved elusive. The study of genetic disorders of the skeleton can yield insights that fuel experimental therapeutic approaches to the treatment of rare disorders and common skeletal ailments. The study showed that Pyle’s disease was caused by a deficiency of sFRP4, that cortical-bone and trabecular-bone homeostasis were governed by different mechanisms, and that sFRP4-mediated cross-regulation between Wnt and BMP signaling was critical for achieving proper cortical-bone thickness and stability.Recently, homozygous mutations in secreted frizzled-related protein 4 gene (SFRP4) gene were found to underlie this condition. Sequencing of coding regions of SFRP4 gene from an 11-year-old female with PYL was performed. A novel homozygous nonsense variant, c.183C>G (p.Y61*) was observed. Segregation analysis in the patient revealed a germline mutation, resulting in reduced protein formation. References


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