(SOURCE 1) In more recent scientific literature, there is evidence in which pedigree analyses confirm autosomal dominant, autosomal recessive or even as X-linked inherited cases of the HGF trait.In 2002, researchers described the SOS1 gene and proved for the first time that a single-nucleotide–insertion mutation of the SOS1 gene on codon 1083 is the preliminary cause of HGF1 in humans. (Source 1) Later on in 2010, there was a case study done on a 16-year-old male with severe gingival overgrowth, almost covering all teeth. Researchers approached this issue with periodontics - a partial gingivectomy and flap surgery. This case study concluded that surgery followed by regular follow-ups is a good way to treat HGF despite the fact that the risks of re-occurrence of the condition remain high.Even more recently, a study was done in 2013 on a family that showed history of autosomal recessive inheritance of HGF. The study did not dismiss the return of HGF after treatment but did claim that general surgical intervention after scaling and root planning of teeth supplemented with good oral hygiene is good enough to prevent the re-occurrence of HGF. This case study also acknowledged how HGF can be part of a multi-system syndrome associated with disorders such as Zimmermann Laband syndrome (ear, nose, bone, and nail defects with hepatosplenomegaly), Rutherford syndrome  (microphthalmia, mental retardation, athetosis, and hypopigmentation), Murray-Puretic Drescher syndrome and Ramon syndrome. See also
Chronic periodontitis
Epidemiology of periodontal diseases
Gingivitis
Gum graft
Periodontist
Tooth loss
Gingival recession

References
External links

American Academy of Periodontology Home Page
Periodontal Disease as a Specific, albeit Chronic, Infection: Diagnosis and Treatment
Neurogenic diabetes insipidus can be a failure of production at the hypothalamus, or a failure of release at the pituitary. Genetic
The most rare form of central DI is familial neurogenic diabetes insipidus. This form of DI is due to an inherited mutation of the arginine vasopressin-neurophysin II (AVP-NPII) gene, inherited in an autosomal dominant manner. At one point, only 45 families worldwide were known to possess this genetic trait. It is now more widely recognized, although the precise number of people affected with this form of DI is unknown at the present time.There is also an X-linked familial form.Wolfram Syndrome (also called DIDMOAD) is characterised by DI, diabetes mellitus, sensorineural deafness, and optic atrophy. Diagnosis
In many respects, the diagnosis of central diabetes insipidus begins as a diagnosis of exclusion. Specifically, other more common causes of polyuria and polydipsia are ruled out. Common rule outs include: diabetes mellitus, chronic kidney disease, hypokalemia, hypercalcemia, and psychogenic polydipsia. Once these conditions have been ruled out a water deprivation test is employed to confirm the diagnosis of CDI. Treatment
The disorder is treated with vasopressin analogs such as desmopressin. Nonetheless, many times desmopressin alone is not enough to bring under control all the symptoms, and another intervention must be implemented. See also
Fluid deprivation test

References


== External links ==