Extra Oral Halitosis

Halitosis can be subdivided into intra-oral and extra-oral halitosis, depending on the place where it originates. Most reports now agree that the most frequent sources of halitosis exist within the oral cavity and include bacterial reservoirs such as the dorsum of the tongue, saliva and periodontal pockets, where anaerobic bacteria degrade sulphur-containing amino acids to produce the foul smelling volatile sulphur compounds (VSCs), especially hydrogen sulphide (H(2)S) and methyl mercaptan (CH(3)SH). Tongue coating is considered to be the most important source of VSCs. Oral malodour can now be treated effectively. Special attention in this overview is given to extra-oral halitosis. Extra-oral halitosis can be subdivided into non-blood-borne halitosis, such as halitosis from the upper respiratory tract including the nose and from the lower respiratory tract, and blood-borne halitosis. The majority of patients with extra-oral halitosis have blood-borne halitosis. Blood-borne halitosis is also frequently caused by odorous VSCs, in particular dimethyl sulphide (CH3SCH3). Extra-oral halitosis, covering about 5-10% of all cases of halitosis, might be a manifestation of a serious disease for which treatment is much more complicated than for intra-oral halitosis. It is therefore of utmost importance to differentiate between intra-oral and extra-oral halitosis. Differences between intra-oral and extra-oral halitosis are discussed extensively. 

 

 

 

 

 

 

 

 

 

SELENBP1 ( Metabolic Halitosis ) 

An autosomal recessive malodour condition characterized by extraoral blood-borne halitosis resulting from the accumulation of sulphur-containing metabolites. In extraoral blood-borne halitosis, malodorant compounds are carried to the lungs, where they enter the breath. Affected individuals have a cabbage-like breath odour, high levels of methanethiol and dimethylsulfide in oral and nasal breath, and elevated urinary excretion of dimethyl sulfoxide in the absence of intake of dimethylsulfide-containing food or use of sulphur-containing medication, lower-gastrointestinal problems, and known metabolic defects, such as methionine adenosyl transferase deficiency and tyrosinemia.

 

Symptoms :

Mutations in SELENBP1 were found to create a characteristic cabbage - like smelling breath. Increased levels of methanethiol and dimethylsulfide in the blood are the main odorous compounds in their breath and are responsible for the malodour.

Cause :

Mutations in SELENBP1 were found in five patients with a cabbage-like smelling breath. Increased levels of methanethiol and dimethylsulfide are the main odorous compounds in their breath and responsible for the malodour. Increased urinary excretion of dimethyl sulfoxide is a diagnostic biomarker of MTO-deficiency. Patient fibroblasts showed reduced amounts of SELENBP1 protein and deficient MTO enzymatic activity which could be restored by lentiviral-mediated expression of the wild-type SELENBP1 gene. A knockout mouse line showed the same biochemical characteristics. Our data define a novel inborn error of metabolism caused by MTO-deficiency leading to a malodour syndrome. MTO deficiency may be a frequent inborn error of metabolism.

Volatile sulphur-containing compounds hydrogen sulphide (H2S), methanethiol (MT, CH3-SH) and dimethylsulfide (DMS, CH3-S-CH3) have been identified as the main contributors of halitosis or bad breath. The origin of halitosis can be intra- or extra-oral. Intra-oral halitosis is the most common form usually caused by MT and H2S produced by Gram-negative bacteria located on the dorsum of the tongue or in gingival- and periodontal crevices. Extra-oral halitosis has an estimated prevalence of 0.5-3% in the general population. Its origin is less well understood. Extra-oral bad smelling breath can be caused by conditions affecting the nose, sinuses, tonsils, and oesophagus, but evidence indicates that in some patients the extra-oral halitosis is blood-borne. In blood-borne halitosis malodorant compounds, most commonly DMS, are carried to the lungs where they enter the breath. Mouth and nose breath DMS concentrations of these patients showed a five- to six-fold increase compared to controls. The cause for increased DMS levels in these patients is unknown. DMS is produced from MT by methylation. Both compounds result from the complex microbiome-mammalian co-metabolism of volatile sulphur compounds. Under physiological conditions MT has three sources in the human body: production from sulphur containing amino acids by intestinal bacteria; formation within intestinal cells by methylation of H2S by thiol S-methyltransferase; biosynthesis from methionine by the transamination pathway in human endogenous metabolism. Under pathological conditions, it has been found that increased levels of DMS can lead to high concentrations of dimethyl sulfoxide (DMSO) and dimethyl sulfone . The enzymes involved in these conversions are largely unknown and a contribution of the gut bacteria is expected. Interestingly cancer patients were found to produce MT and DMS as prominent volatile organic compounds. DMS is produced in significant amounts by lung- and liver cancer cell lines and was found in lung tumor tissue. Recently, a methanethiol oxidase (MTO) was purified from the Hyphomicrobium strain VS. The gene encoding this enzyme was identified and showed 26% homology at the protein level to the human SELENBP1 gene, encoding a protein possessing selenium binding properties but with unknown function. Reduced expression of the human gene has been found in several tumours, and a tumor suppressor function has been suggested. We hypothesized that mutations in SELENBP1 could be causative for extra-oral halitosis. We studied five patients with extra-oral halitosis caused by elevated levels of DMS in the blood. We identified SELENBP1 as the human MTO, catalysing the conversion of MT into formaldehyde, H2S and hydrogen peroxide (H2O2). Mutations in SELENBP1 cause extra-oral halitosis and define a novel inborn error of metabolism.

Diagnosis :

Currently the only available test centre for SelenBP1 is Radboud University in the Netherlands. The test has to be ordered by your GP or Specialists consultant. Due to the location of the test centre this test is not covered by the NHS and will cost you approximately £400 and has a 4 - 8 week turnaround time.

 

Treatment :

Although there is no current cure and no diet plans available to date. Suffereres may find relief by folllowing a different malodour diet plan to try and find there trigger food groups until further research is available into this condition, there is supplementation which can help alleviate malodour symptoms and give more relief to a sufferer.

 

Vitamin B2 

Chloryphyllin 

Zinc 

Magnesium