Palate cleft can occur as complete (soft and hard palate, possibly including a gap in the jaw) or incomplete (a hole in the roof of the mouth, usually as a cleft soft palate). When cleft palate occurs, the uvula is usually split. It occurs due to the failure of fusion of the lateral palatine processes, the nasal septum, or the median palatine processes (formation of the secondary palate). The hole in the roof of the mouth caused by a cleft connects the mouth directly to the inside of the nose. Note: the next images show the roof of the mouth. The top shows the nose, the lips are colored pink. For clarity the images depict a toothless infant. A result of an open connection between the mouth and inside the nose is called velopharyngeal insufficiency (VPI). Because of the gap, air leaks into the nasal cavity resulting in a hypernasal voice resonance and nasal emissions while talking. Secondary effects of VPI include speech articulation errors (e.g., distortions, substitutions, and omissions) and compensatory misarticulations and mispronunciations (e.g., glottal stops and posterior nasal fricatives). Possible treatment options include speech therapy, prosthetics, augmentation of the posterior pharyngeal wall, lengthening of the palate, and surgical procedures.Submucous cleft palate can also occur, which is a cleft of the soft palate with a split uvula, a furrow along the midline of the soft palate, and a notch in the back margin of the hard palate.
Both duct widening and duct ectasia syndrome are frequently bilateral, hence systemic causes are likely involved. Diagnosis
Noninvasive methods to determine duct diameter in live patients are available only recently and it is not clear how the results should be compared with older results from biopsies. Histologically, dilation of the large duct is prominent. Duct widening with associated periductal fibrosis is frequently included in the wastebasket definition of fibrocystic disease. In plasma cell rich lesions diagnosed on core biopsies, steroid-responsive IgG4-related mastitis can be identified by IgG/IgG4 immunostaining. Duct Ectasia Syndrome
The term duct ectasia syndrome has been used to describe symptoms of nonpuerperal mastitis, possibly associated with nipple inversion and nipple discharge. In some contexts, it was used to describe a particular form of nonpuerperal mastitis coincident with fibrocystic disease, frequently involving pasty (coloured) nipple discharge, nipple retraction, retroareolar abscess and blue dome cysts. Abscessation is not very frequent but by some definitions recurrent subareolar abscess is merely a variant of duct ectasia syndrome - abscessation would be obviously more frequent with this definition. Duct ectasia syndrome has been associated with histopathological findings that are distinct from a simple duct widening. In addition to nonspecific duct widening the myoepithelial cell layer is atrophic, missing or replaced by fibrous tissue. The original cuboidal epithelial layer may be also severely impaired or missing. Characteristic calcifications are often visible on mammographic images. Periductal mastitis, comedo mastitis, secretory disease of the breast, plasma cell mastitis and mastitis obliterans are sometimes considered special cases or synonyms of duct ectasia syndrome.