A lack of bony support for the soft tissues in this region will subsequently produce the depression, known as paranasal hollowing. This indicates a low level antero-posterior maxillary deficiency. Maxillary deficiency usually manifests as an increased naso-labial angle, although this is not a credible indication due to factors such as a short upper lip and/or proclined incisors. Another method to predict if a patient has maxillary deficiency is by the ‘scleral show and eyelid shape.’ The lower eyelid normally rests at the inferior border of the iris, without any sclera showing. If there is any sclera showing, then this is a good sign of infraorbital rim deficiency and maxillary antero-posterior deficiency, two manifestations that are usually seen in Class III patients. Orientation
When a jaw is abnormally oriented, malrotations occur. These malrotations are classified according to the axis on which the abnormal rotation occurs. When a jaw is malrotated around the transverse facial axis, it is said to have abnormal pitch. When malrotated around the anteroposterior axis, the jaw has an abnormal roll, a condition also known as cant. Finally, when a jaw is malrotated around the vertical axis, it has abnormal yaw. It can occur in maxilla and/or mandible and could result due to abnormal growth of the jaws in itself or as compensatory growth. Shape
Shape refers to figure, the geometric characteristic of an object that is not size, position, or orientation 5. A jaw with abnormal shape is said be distorted. Completeness
Completeness means the wholeness of the jaw.
Individuals with the complete form of CSNB (CSNB1) have highly impaired rod sensitivity (reduced ~300x) as well as cone dysfunction. Patients with the incomplete form can present with either myopia or hyperopia. Cause
CSNB is caused by malfunctions in neurotransmission from rod and cone photoreceptors to  bipolar cells in the retina. At this first synapse, information from photoreceptors is divided into two channels: ON and OFF. The ON pathway detects light onset, while the OFF pathway detects light offset. The malfunctions in CSNB1 specifically affect the ON pathway, by hindering the ability of ON-type bipolar cells to detect neurotransmitter released from photoreceptors. Rods, which are responsible for low-light vision, make contacts with ON-type bipolar cells only, while, cones, which are responsible for bright-light vision, make contacts with bipolar cells of both ON an OFF subtypes. Because the low-light sensing rods feed only into the ON pathway, individuals with CSNB1 typically have problems with night vision, while vision in well-lit conditions is spared. In CSNB2, release of neurotransmitter from photoreceptors is impaired, leading to involvement of both ON and OFF pathways. The electroretinogram (ERG) is an important tool for diagnosing CSNB. The ERG a-wave, which reflects the function of the  phototransduction cascade in response to a light flashes, is typically normal in CSNB patients, although in some cases phototransduction is also affected, leading to a reduced a-wave. The ERG b-wave, which primarily reflects the function of ON-bipolar cells, is greatly reduced in CSNB2 cases, and completely absent in CSNB1 cases.