Tuesday, 15 February 2011 22:31

Mouth and Teeth

Written By: Gobbato, F.
Rate this item
(2 votes)

The mouth is the portal of entry to the digestive system and its functions are, primarily, the chewing and swallowing of food and the partial digestion of starches by means of salivary enzymes. The mouth also participates in vocalizing and may replace or complement the nose in respiration. Due to its exposed position and the functions it fulfils, the mouth is not only a portal of entry but also an area of absorption, retention and excretion for toxic substances to which the body is exposed. Factors which lead to respiration via the mouth (nasal stenoses, emotional situations) and increased pulmonary ventilation during effort, promote either the penetration of foreign substances via this route, or their direct action on the tissues in the buccal cavity.

Respiration through the mouth promotes:

  • greater penetration of dust into the respiratory tree since the buccal cavity has a retention quotient (impingement) of solid particles much lower than that of the nasal cavities
  • dental abrasion in workers exposed to large dust particles, dental erosion in workers exposed to strong acids, caries in workers exposed to flour or sugar dust, etc.


The mouth may constitute the route of entry of toxic substances into the body either by accidental ingestion or by slow absorption. The surface area of the buccal mucous membranes is relatively small (in comparison with that of the respiratory system and gastro-intestinal system) and foreign substances will remain in contact with these membranes for only a short period. These factors considerably limit the degree of absorption even of substances which are highly soluble; nevertheless, the possibility of absorption does exist and is even exploited for therapeutic purposes (perlingual absorption of drugs).

The tissues of the buccal cavity may often be the site of accumulation of toxic substances, not only by direct and local absorption, but also by transport via the bloodstream. Research using radioactive isotopes has shown that even the tissues which seem metabolically the most inert (such as dental enamel and dentine) have a certain accumulative capacity and a relatively active turnover for certain substances. Classical examples of storage are various discolorations of the mucous membranes (gingival lines) which often provide valuable diagnostic information (e.g. lead).

Salivary excretion is of no value in the elimination of toxic substances from the body since the saliva is swallowed and the substances in it are once more absorbed into the system, thus forming a vicious circle. Salivary excretion has, on the other hand, a certain diagnostic value (determination of toxic substances in the saliva); it may also be of importance in the pathogenesis of certain lesions since the saliva renews and prolongs the action of toxic substances on the buccal mucous membrane. The following substances are excreted in the saliva: various heavy metals, the halogens (the concentration of iodine in the saliva may be 7-700 times greater than that in plasma), the thiocyanates (smokers, workers exposed to hydrocyanic acid and cyanogen compounds), and a wide range of organic compounds (alcohols, alkaloids, etc.).

Aetiopathogenesis and Clinical Classification

Lesions of the mouth and teeth (also called stomatological lesions) of occupational origin may be caused by:

  • physical agents (acute traumata and chronic microtraumata, heat, electricity, radiations, etc.)
  • chemical agents which affect the tissues of the buccal cavity directly or by means of systemic changes
  • biological agents (viruses, bacteria, mycetes).


However, when dealing with mouth and teeth lesions of occupational origin, a classification based on topographical or anatomical location is preferred to one employing aetiopathogenic principles.

Lips and cheeks. Examination of the lips and cheeks may reveal: pallor due to anaemia (benzene, lead poisoning, etc.), cyanosis due to acute respiratory insufficiency (asphyxia) or chronic respiratory insufficiency (occupational diseases of the lungs), cyanosis due to methaemoglobinaemia (nitrites and organic nitro-compounds, aromatic amines), cherry-red colouring due to acute carbon monoxide poisoning, yellow colouring in cases of acute poisoning with picric acid, dinitrocresol, or in a case of hepatotoxic jaundice (phosphorus, chlorinated hydrocarbon pesticides, etc.). In argyrosis, there is brown or grey-bluish coloration caused by the precipitation of silver or its insoluble compounds, especially in areas exposed to light.

Occupational disorders of the lips include: dyskeratoses, fissures and ulcerations due to the direct action of caustic and corrosive substances; allergic contact dermatitis (nickel, chrome) which may also include the dermatitis found in tobacco industry workers; microbial eczemas resulting from the use of respiratory protective equipment where the elementary rules of hygiene have not been observed; lesions caused by anthrax and glanders (malignant pustules and cancroid ulcer) of workers in contact with animals; inflammation due to solar radiation and found among agricultural workers and fishermen; neoplastic lesions in persons handling carcinogenic substances; traumatic lesions; and chancre of the lip in glassblowers.

Teeth. Discoloration caused by the deposition of inert substances or due to the impregnation of the dental enamel by soluble compounds is of almost exclusively diagnostic interest. The important colourings are as follows: brown, due to the deposition of iron, nickel and manganese compounds; greenish-brown due to vanadium; yellowish-brown due to iodine and bromine; golden-yellow, often limited to gingival lines, due to cadmium.

Of greater importance is dental erosion of mechanical or chemical origin. Even nowadays it is possible to find dental erosions of mechanical origin in certain craftsmen (caused by holding nails or string, etc., in the teeth) which are so characteristic that they can be considered occupational stigmata. Lesions caused by abrasive dusts have been described in grinders, sandblasters, stone industry workers and precious stone workers. Prolonged exposure to organic and inorganic acids will often cause dental lesions occurring mainly on the labial surface of the incisors (rarely on the canines); these lesions are initially superficial and limited to the enamel but later become deeper and more extensive, reaching the dentine and resulting in solubilization and mobilization of calcium salts. The localization of these erosions to the anterior surface of the teeth is due to the fact that when the lips are open it is this surface which is the most exposed and which is deprived of the natural protection offered by the buffer effect of saliva.

Dental caries is such a frequent and widespread disease that a detailed epidemiological study is required to determine whether the condition is really of occupational origin. The most typical example is that of the caries found in workers exposed to flour and sugar dust (flourmillers, bakers, confectioners, sugar industry workers). This is a soft caries which develops rapidly; it starts at the base of the tooth (rampant caries) and immediately progresses to the crown; the affected sides blacken, the tissue is softened and there is considerable loss of substance and finally the pulp is affected. These lesions begin after a few years of exposure and their severity and extent increases with the duration of this exposure. X rays may also cause rapidly developing dental caries which usually commences at the base of the tooth.

In addition to pulpites due to dental caries and erosion, an interesting aspect of pulp pathology is barotraumatic odontalgia, i.e., pressure-induced toothache. This is caused by the rapid development of gas dissolved in the pulp tissue following sudden atmospheric decompression: this is a common symptom in the clinical manifestations observed during rapid climbing in aircrafts. In the case of persons suffering from septic-gangrenous pulpites, where gaseous material is already present, this toothache may commence at an altitude of 2,000-3,000 m.

Occupational fluorosis does not lead to dental pathology as is the case with endemic fluorosis: fluorine causes dystrophic changes (mottled enamel) only when the period of exposure precedes the eruption of permanent teeth.

Mucous membrane changes and stomatitis. Of definite diagnostic value are the various discolorations of the mucous membranes due to the impregnation or precipitation of metals and their insoluble compounds (lead, antimony, bismuth, copper, silver, arsenic). A typical example is Burton’s line in lead poisoning, caused by the precipitation of lead sulphide following the development in the oral cavity of hydrogen sulphide produced by the putrefaction of food residues. It has not been possible to reproduce Burton’s line experimentally in herbivorous animals.

There is a very curious discoloration in the lingual mucous membrane of workers exposed to vanadium. This is due to impregnation by vanadium pentoxide which is subsequently reduced to trioxide; the discoloration cannot be cleaned away but disappears spontaneously a few days after termination of exposure.

The oral mucous membrane can be the site of severe corrosive damage caused by acids, alkalis and other caustic substances. Alkalis cause maceration, suppuration and tissue necrosis with the formation of lesions which slough off easily. Ingestion of caustic or corrosive substances produces severe ulcerative and very painful lesions of the mouth, oesophagus and stomach, which may develop into perforations and frequently leave scars. Chronic exposure favours the formation of inflammation, fissures, ulcers and epithelial desquamation of the tongue, palate and other parts of the oral mucous membranes. Inorganic and organic acids have a coagulating effect on proteins and cause ulcerous, necrotic lesions which heal with contractive scarring. Mercury chloride and zinc chloride, certain copper salts, alkaline chromates, phenol and other caustic substances produce similar lesions.

A prime example of chronic stomatitis is that caused by mercury. It commences gradually, with discreet symptoms and a prolonged course; the symptoms include excessive saliva, metallic taste in the mouth, bad breath, slight gingival reddening and swelling, and these constitute the first phase of periodontitis leading towards loss of teeth. A similar clinical picture is found in stomatitis due to bismuth, gold, arsenic, etc.

Salivary glands. Increased salivary secretion has been observed in the following cases:

  • in a variety of acute and chronic stomatites which is due mainly to the irritant action of the toxic substances and may, in certain cases, be extremely intense. For example, in cases of chronic mercurial poisoning, this symptom is so prominent and occurs at such an early stage that English workers have called this the “salivation disease”.
  • in cases of poisoning in which there is central nervous system involvement—as is the case in manganese poisoning. However, even in the case of chronic mercurial poisoning, salivary gland hyperactivity is thought to be, at least in part, nervous in origin.
  • in cases of acute poisoning with organophosphorus pesticides which inhibit cholinesterases.


There is reduction in salivary secretion in severe thermoregulation disorders (heatstroke, acute dinitrocresol poisoning), and in serious disorders of water and electrolyte balance during toxic hepatorenal insufficiency.

In cases of acute or chronic stomatitis, the inflammatory process may, sometimes, affect the salivary glands. In the past there have been reports of “lead parotitis”, but this condition has become so rare nowadays that doubts about its actual existence seem justified.

Maxillary bones. Degenerative, inflammatory and productive changes in the skeleton of the mouth may be caused by chemical, physical and biological agents. Probably the most important of the chemical agents is white or yellow phosphorus which causes phosphorus necrosis of the jaw or “phossy jaw”, at one time a distressing disease of match industry workers. The absorption of phosphorus is facilitated by the presence of gingival and dental lesions, and produces, initially, productive periosteal reaction followed by destructive and necrotic phenomena which are activated by bacterial infection. Arsenic also causes ulceronecrotic stomatitis which may have further bone complications. The lesions are limited to the roots in the jaw, and lead to the development of small sheets of dead bones. Once the teeth have fallen out and the dead bone eliminated, the lesions have a favourable course and nearly always heal.

Radium was the cause of maxillary osteonecrotic processes observed during the First World War in workers handling luminous compounds. In addition, damage to the bone may also be caused by infection.

Preventive Measures

A programme for the prevention of mouth and teeth diseases should be based on the following four main principles:

    • application of measures of industrial hygiene and preventive medicine including monitoring of workplace environment, analysis of production processes, elimination of hazards in the environment, and, where necessary, the use of personal protective equipment
    • education of workers in the need for scrupulous oral hygiene—in many cases it has been found that lack of oral hygiene may reduce resistance to general and localized occupational diseases
    • a careful check on the mouth and teeth when workers undergo pre-employment or periodical medical examinations
    • early detection and treatment of any mouth or teeth disease, whether of an occupational nature or not.



          Read 4148 times Last modified on Monday, 13 June 2022 00:25
          More in this category: « Digestive System Liver »

          " DISCLAIMER: The ILO does not take responsibility for content presented on this web portal that is presented in any language other than English, which is the language used for the initial production and peer-review of original content. Certain statistics have not been updated since the production of the 4th edition of the Encyclopaedia (1998)."


          Part I. The Body
          Cardiovascular System
          Digestive System
          Mental Health
          Musculoskeletal System
          Nervous System
          Renal-Urinary System
          Reproductive System
          Respiratory System
          Sensory Systems
          Skin Diseases
          Systematic Conditions
          Part II. Health Care
          Part III. Management & Policy
          Part IV. Tools and Approaches
          Part V. Psychosocial and Organizational Factors
          Part VI. General Hazards
          Part VII. The Environment
          Part VIII. Accidents and Safety Management
          Part IX. Chemicals
          Part X. Industries Based on Biological Resources
          Part XI. Industries Based on Natural Resources
          Part XII. Chemical Industries
          Part XIII. Manufacturing Industries
          Part XIV. Textile and Apparel Industries
          Part XV. Transport Industries
          Part XVI. Construction
          Part XVII. Services and Trade
          Part XVIII. Guides

          Digestive System References

          Blair, A, S Hoar Zahm, NE Pearce, EF Heineman, and JF Fraumeni. 1992. Clues to cancer aetiology from studies of farmers. Scand J Work Environ Health 18:209-215.

          Fernandez, E, C LaVecchia, M Porta, E Negri, F Lucchini, and F Levi. 1994. Trends in pancreatic cancer mortality in Europe, 1955-1989. Int J Cancer 57:786-792.

          Higginson, J, CS Muir, and N Munoz. 1992. Human Cancer: Epidemiology and Environmental Causes. In Cambridge Monographs On Cancer Research Cambridge: Cambridge Univ. Press.

          International Agency for Research on Cancer (IARC). 1987. IARC Monographs On the Evaluation of Carcinogenic Risks to Humans. An Updating of IARC Monographs Volumes 1 to 42, Suppl. 7. Lyon: IARC.

          —. 1988. Alcohol drinking. IARC Monographs On the Evaluation of Carcinogenic Risks to Humans, No. 44. Lyon: IARC.

          —. 1990. Cancer: Causes, occurrence and control. IARC Scientific Publications, No. 100. Lyon: IARC.

          —. 1992. Cancer incidence in five continents. Vol. VI. IARC Scientific Publications, No. 120. Lyon: IARC.

          —. 1993. Trends in cancer incidence and mortality. IARC Scientific Publications, No. 121. Lyon: IARC.

          —. 1994a. Hepatitis viruses. IARC Monographs On the Evaluation of Carcinogenic Risks to Humans, No. 59. Lyon: IARC.

          —. 1994b. Occupational cancer in developing countries. IARC Scientific Publications, No. 129. Lyon: IARC.

          —. 1995. Survival of cancer patients in Europe. The EUROCARE study. Vol. 132. IARC Scientific Publications. Lyon: IARC.

          Kauppinen, T, T Partanen, R Degerth, and A Ojajärvi. 1995. Pancreatic cancer and occupational exposures. Epidemiology 6(5):498-502.

          Lotze, MT, JC Flickinger, and BI Carr. 1993. Hepatobiliary Neoplasms. In Cancer: Principles and Practice of Oncology, edited by VT DeVita Jr, S Hellman, and SA Rosenberg. Philadelphia: JB Lippincott.

          Mack, TM. 1982. Pancreas. In Cancer Epidemiology and Prevention, edited by D.Schottenfeld and JF Fraumeni. Philadelphia: WB Sanders.

          Parkin, DM, P Pisani, and J Ferlay. 1993. Estimates of the worldwide incidence of eighteen major cancers in 1985. Int J Cancer 54:594-606.

          Siemiatycki, J, M Gerin, R Dewar, L Nadon, R Lakhani, D Begin, and L Richardson. 1991. Associations between occupational circumstances and cancer. In Risk Factors for Cancer in the Workplace, edited by J Siemiatycki. Boca Raton: CRC Press.