Increased levels of bleeding on probing was present at 67% of sites where there is peri-implant mucositis as it is indicative of the presence of active disease and inflammation of the peri-implant mucosa. A light probing force of 0.25N should be used to probe the gingival margins so as not to damage the soft periodontal tissues. Bleeding on probing can be used in order to predict future loss of support from surrounding tissues. Microbiological testing was shown to improve the prognostic features compared to recording bleeding on probing alone as this was better for recognising the disease advancement around implants. Increased probing depths over time is linked to loss of attachment and a reduction in the supporting alveolar bone levels. When bone becomes involved, the disease has progressed to peri-implantitis and this site is no longer diagnosed with peri-implant mucositis. The presence of bleeding on probing, the probing depths measured to the base of any pocketing and suppuration should all be assessed regularly in order to correctly diagnose peri-implant mucositis. Mucosal recession, a draining sinus or fistula and swelling or hyperplasia of the gingivae surrounding the implant can all signify the presence of peri-implant disease and should all prompt further investigations to ascertain whether this is the case.Radiographs are required to distinguish between peri-implant mucositis and peri-implantitis as the supporting alveolar bone levels must be evaluated in order to decide on a diagnosis.
In up to one-third of cases no cause can be found. Brain injury
Lennox–Gastaut most often occurs secondary to brain damage. The brain damage can occur from perinatal insults, encephalitis, meningitis, tumor, and brain malformation. Genetic mutations
Other identified disorders include genetic disorders such as tuberous sclerosis and inherited deficiency of methylene tetrahydrofolate reductase. Some of these cases once thought to be of unknown cause may have definitive etiology by modern genetic testing.Progress in genome and exome sequencing is revealing that some individuals diagnosed with Lennox-Gastaut Syndrome have de novo mutations in a variety of genes, including CHD2, GABRB3, ALG13 and SCN2A. The Epi4K study consortium (2013) observed de novo mutations in at least 15% of a study cohort of 165 patients with LGS and infantile spasms using whole exome sequencing. A 2013 study found a high frequency of rare copy-number variation (CNVs) in adult patients with LGS or LGS-like epilepsy.Mutations in the IQSEC2 gene have been associated with this syndrome. This gene is located on the short arm of the X chromosome (Xp11.22). Diagnosis
The diagnosis of LGS should be suspected in children less than 8 years old with seizures of multiple types that cannot be treated with antiseizure medications. Because of high risk of irreversible brain damage in early stages of syndrome (particularly in infants and young children), early diagnosis is essential.