There may be missing teeth eruptions. If the infant is not closing down properly, the lower jaws become more noticeably deficient (micrognathia or retrognathia). The front teeth may not touch when the child closes down because the back teeth have overerrupted or because of incomplete formation of the maxilla. This condition is called an anterior open bite and has facial/skeletal implications. The saliva may be thick, or the infant may have a dry mouth. Transitional dentition
Between age 5 and 7, most children start losing their primary teeth. Occasionally, some primary teeth are slow to exfoliate (fall out), and the dentist may want to remove a primary tooth early to prevent orthodontic problems. Likewise, premature loss of primary teeth may create orthodontic problems later on. When a tooth is lost prematurely, removable or fixed spacers may be needed to prevent the shifting of teeth. Interceptive orthodontic treatment can be initiated at this stage of development to help with crowding or to help relate the upper and lower jaws. Consistent with a high palate is a narrow arch shape of the upper teeth as they line up in the mouth. This may cause the upper front teeth to flare out and become more prone to fracture if accidentally hit. Interceptive orthodontics has an important role in this situation. Appliances that expand the upper arch tend to bring the front teeth back into a more-normal position. Some appliances can even help allow the front teeth to close to normal in an open-bite situation.
Additionally, when a food substance, supplement or medicine containing a precursor (choline or carnitine) is ingested, bacteria in the gut convert a portion of those precursors to TMA. Moderate amounts of precursor are absorbed in the small intestine before reaching the gut, however if precursor rich food saturates the transport capacity of the intestine, excess precursor ends up in the gut. The proportion of precursor converted to TMA is related to the amount of specific bacteria in the gut.TMA in the gut is absorbed through the intestinal lining and enters the bloodstream, where it is filtered by the liver. The liver usually produces an abundance of the enzyme FMO3, which neutralises the TMA by oxidising it to odourless TMAO, and passes it through to the bladder. If FMO3 enzyme production is compromised, or there is too much TMA for the amount of enzyme, then TMA will continue to circulate in the bloodstream until enough enzyme is produced. While TMA is in the bloodstream, it is slowly exits the body via bodily fluids; urine, sweat, saliva, reproductive fluids and breath (See fluid balance for rates of fluid loss). TMA has no known interactions with any known internal or organ function. Although lecithin, creatinine and betaine are technically precursors to TMA, studies have shown no significant effect on the production of excess TMA/TMAO in urinary analysis at normal dietary levels of consumption. Symptoms and signs
Trimethylamine is most noticeable in urine, as it is captured, concentrated and released in intervals.