Osteonecrosis of the jaw historical perspective

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

History in Dental Medicine

ONJ is not a new disease, around 1850 various forms of "chemical osteomyelitis" resulting from environmental pollutants, such as lead and the white phosphorus used in early (non-safety) matches (Phossy jaw), as well as from popular medications containing mercury, arsenic or bismuth, were reported in the literature.[1][2][3][4][5][6][7] This disease apparently did not often occur in individuals with good gingival health, and usually targeted the mandible first.[2]It was associated with localized or generalized deep ache or pain, often of multiple jawbone sites. The teeth often appeared sound and suppuration was not present. Even so, the dentist often began extracting one tooth after another in the region of pain, often with temporary relief but usually to no real effect.[3]

Today a growing body of scientific evidence indicate that this disease process, in the cancellous bone and bone marrow, is caused by bone infarcts mediated by a range of local and systemic factors. Bone infarcts as well as damage to the deeper portion of the cancellous bone is an insidious process. It is certainly not visible clinically and routine imaging techniques such as radiographs are not effective for that sort of damage. "An important and often incompletely understood principle of radiography is the amount of bone destruction that goes undetected by routine x-rays procedures; this has been demonstrated by numerous investigators. Destruction confined to the cancellous portion of the bone cannot be detected radiographically, ad radiolucencies appear only when there is internal or external erosion or destruction of the bone cortex."[8] In fact no radiographic findings are specific for bone infarction / osteonecrosis. A variety of pathologies may mimic bone infarction, including stress fractures, infections, inflammations, and metabolic and neoplastic processes. The limitations apply to all imaging modalities, including plain radiography, radionuclide studies, CT scans, and magnetic resonance imaging (MRI). Through-transmission alveolar ultrasound, based on quantitative ultrasound (QUS) in combination with panoramic dental radiography (orthopantomography) is helpful in assessing changes in jawbone density.[9][10] When practitioners have an up to date understanding of the disease process and a good anamnesis is combined with detailed clinical findings and course of events, the diagnosis, with the help of various imaging modality, can be achieved earlier, in most patients.

In the modern dental profession, it is only recently when severe cases associated with bisphosphonates came to light, that the issue of ONJ has been brought to the attention of a majority of dentists. At present, the focus is mostly on bisphosphonates associated cases, and is sometimes referred to colloquially as "phossy jaw", a similar, earlier occupational disease.[11][12] However, the pharmaceutical manufacturers of bisphosphonates drugs such as Merck and Novartis have stated that ONJ in patients on this class of drug, can be related to a pre-existing condition, coagulopathy, anemia, infection, use of corticosteroids, alcoholism and other conditions already known to be associated with ONJ in absence of bisphosphonate therapy. The implication is that bisphosphonates may not be the initiating cause of ONJ and that other pre-existing or concurrent systemic and/or local dental factors are involved.[13][14]

Since ONJ has been diagnosed in many patients who did not take bisphosphonates, it is thus logical to assume that bisphosphonates are not the only factor in ONJ While the oversuppression of bone turnover seems to play a major role in aggravating the disease process, other factors can and do initiate the pathophysiological mechanisms responsible for ONJ. In non-bisphosphonate cases of ONj, it is mainly the cancellous portion of the bone and it’s marrow content that are involved in the disease process. The first stage is an oedema of the bone marrow initiated by a bone infarct, which is itself modulated by numerous etiological factors, leading to myelofibrosis as a result of hypoxia and gradual loss of mineral bone density characteristic of ischemic osteoporosis. Further deterioration can be triggered by additional bone infarcts leading to anoxia and a localized areas of osteonecrosis within the osteoporotic cancellous bone. Secondary events such as dental infection, injection of local anesthetics with vasoconstrictors, such as epinephrine, and trauma can add further complications to the disease process and chronic non-pus forming bone infection osteomyelitis can also be associated with ONJ. [15][16][17]

However, in patients on bisphosphonates, the cortical bone is also frequently involved as well. Spontaneous exposure of necrotic bone tissue through the oral soft tissues or following non-healing bone exposure after routine dental surgery, characteristics of this form of ONJ may be the result of late diagnosis of a disease process that has been masked by the oversuppression of osteoclastic activity, allowing pre-existing etiological factors to further aggravate bone damage.

References

  1. Bond TE Jr. A practical treatise on dental medicine. Philadelphia: Lindsay & Blakiston, 1848.
  2. 2.0 2.1 Anonymous. Necrosis of the lower jaw in makers of Lucifer matches. Am J Dent Science 1867; 1 (series 3):96-97.
  3. 3.0 3.1 Bouquot J.E. The history of maxillofacial osteonecrosis. Maxillofacial Center for Diagnostics and Research. Accessed 22 May 2006.
  4. Ferguson W. New treatment of necrosis. Am J Dent Science 1868; 1 (series 3):189.
  5. Noel HR. A lecture on caries and necrosis of bone. Am J Dent Science 1868; 1 (series 3):425, 482.
  6. Barrett WC. Oral pathology and practice. Philadelphia, S.S. White Dental Mfg Co, 1898.
  7. Black GV. A work on special dental pathology (2nd ed). Chicago, Medico_Dental Publ Co, 1915
  8. Cohen S, Burns R. Pathways of the pulp. ed. 2, St-Louis, 55-57, 1980. C.V. Mosby
  9. Imbeau J (2005). "Introduction to through-transmission alveolar ultrasonography (TAU) in dental medicine". Cranio. 23 (2): 100–12. PMID 15898566.
  10. Bouquot J, Margolis M, Shankland WE, Imbeau J. Through-transmission alveolar sonography (TTAS) – a new technology for evaluation of medullary diseases, correlation with histopathology of 285 scanned jaw sites. Presented at the 56th annual meeting of the American Academy of Oral and Maxillofacial Pathology. April 2002.
  11. PM Purcell, IW Boyd, Bisphosphonates and osteonecrosis of the jaw, ADRAC Report, MJA 2005; 182 (8): 417-418
  12. J Carreyrou, Fosamax Drug Could Become Next Merck Woe, Dow Jones (THE WALL STREET JOURNAL), Apr. 12, 2006
  13. Statement by Merck on Fosamax and rare cases of osteonecrosis of the jaws.- Accessed 21 May 2006.
  14. Information on osteonecrosis of the jaws on the Novartis web site.- Accessed 21 May 2006.
  15. Bouquot J, Wrobleski G, Fenton S. The most common osteonecrosis? Prevalence of maxillofacial osteonecrosis (MFO). J Oral Pathol Med 2000; 29:345. (abstract)
  16. Glueck CJ, McMahon RE, Bouquot JE, et al. Thrombophilia, hypofibrinolysis and osteonecrosis of the jaws. Oral Surg Oral Med Oral Pathol; 81:557-566, 1996. PMID: 8734702
  17. Gruppo R, Glueck C, McMahon R, Bouquot J, Rabinovich B, Becker A, Tracy T, Wang P (1996). "The pathophysiology of alveolar osteonecrosis of the jaw: anticardiolipin antibodies, thrombophilia, and hypofibrinolysis". J Lab Clin Med. 127 (5): 481–8. PMID 8621985.

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