Osteonecrosis of the jaw: lights and shadows in the knowledge of its pathophysiology

Gómez García, A; Gómez García, A

doi:10.4321/s1889-836x2019000200001

My SciELO

Custom services

Services on Demand

Journal

Article

Indicators

Cited by SciELO
Access statistics

Revista de Osteoporosis y Metabolismo Mineral

On-line version ISSN 2173-2345Print version ISSN 1889-836X

Rev Osteoporos Metab Miner vol.11 n.2 Madrid Apr./Jun. 2019 Epub Jan 20, 2020

https://dx.doi.org/10.4321/s1889-836x2019000200001

EDITORIAL

Osteonecrosis of the jaw: lights and shadows in the knowledge of its pathophysiology

A Gómez García¹

¹Servicio de Rehabilitación - Hospital Universitario Dr. Negrín - Las Palmas de Gran Canaria (España)

Osteonecrosis of the jaw (ONJ) was described by Marx et al.¹ in 2005. In the following years, both isolated cases and series of patients were published which, over the years, was decreasing, on the one hand, due to the saturation of the journals and the low interest that the description of new cases may cause. Furthermore, knowledge of this disease has lead to the development of preventive measures that may have diminished its incidence.

Regarding ONJ, a whole range of “fears, risks and dangers” have been developed that are largely unjustified. ONJ was indicated as a complication of prolonged bisphosphonate treatment and in this sense it was equalized to the diaphyseal fractures², when both processes most certainly have different etiopathogenic mechanisms³. Fears concerning ONJ or diaphyseal fractures developed a whole doctrine about the need to suspend treatment with bisphosphonates or denosumab, the socalled “therapeutic vacations” that in reality what it was about was simply to suspend the antiresorptive treatment, before that the possible complications of its use appear⁴-⁶. This is especially common in the field of dentists, who, in many cases, concerned about the possible development of an ONJ do not perform virtually any dental intervention in patients receiving bisphosphonates or denosumab. With this, what has been observed is an increase in the abandonment of treatment with antiresorptive drugs which produces an increased risk of fragility fractures after discontinuation of bisphosphonate therapy, a risk that has an extreme severity in the case of suspension of denosumab treatment, with the appearance of multiple vertebral fractures⁷-¹¹.

ONJ occurs mainly in patients suffering from cancer (more than 90% of the cases described) and who have received potent bisphosphonates or denosumab at doses not used in osteoporosis treatment³,¹²,¹³ and in which there has been a dental intervention¹⁴. Among patients receiving antiresorptives for the treatment of osteoporosis, the occurrence of cases, although it is true that it has been reported, is very scarce, almost exceptional¹⁵,¹⁶.

In this issue of the Revista de Osteoporosis y Metabolismo Mineral, Quintana et al.¹⁷ present the findings observed in a series of patients with ONJ in which they have carried out a complete study of both the amount of bone mass, determined by densitometry, and bone quality, estimated by the trabecular bone score (TBS) and Quantitative Ultrasound, an unfairly undervalued, harmless and simple technique that can assess bone quality and predict the risk of fracture as well as traditional densitometry¹⁸,¹⁹. The results obtained differ from the myths developed about ONJ and is that the excess suppression produced by these drugs would produce a "frozen" bone of poor quality and weakness. As can be seen in these results, it is most likely that the quantity and quality of the bone in ONJ does not show general alterations. Rather, involvement is local and influenced by multiple factors. All of this leads us to conclude that we still do not know many facts about the etiology, pathogenesis and pathophysiology of ONJ, and that we still have more shadows than lights on this matter¹²,²⁰,²¹.

Bibliografía

1 Marx RE, Sawatari Y, Fortin M, Broumand V. Bisphosphonate-induced exposed bone (osteonecrosis/osteopetrosis) of the jaws: Risk factors, recognition, prevention, and treatment. J Oral Maxillofac Surg. 2005;63(11):1567-75. [ Links ]

2 Adler RA, Fuleihan GE, Bauer DC, Camacho PM, Bart L, Clines GA, et al. Managing osteoporosis in patients on longterm bisphosphonate treatment: report of a task force of the American Society for Bone and Mineral Research. J Bone Miner Res. 2016;31(1):16-35. [ Links ]

3 Sosa-Henriquez M. Osteonecrosis de los maxilares: Documento de consenso. Rev Osteoporos Metab Miner. 2009;1(1):41-51. [ Links ]

4 Anagnostis P, Paschou SA, Mintziori G, Ceausu I, Depypere H, Lambrinoudaki I, et al. Drug holidays from bisphosphonates and denosumab in postmenopausal osteoporosis: EMAS position statement. Maturitas. 2017;101:23-30. [ Links ]

5 Brown JP, Morin S, Leslie W, Papaioannou A, Cheung AM, Davison KS, et al. Bisphosphonates for treatment of osteoporosis: expected benefits, potential harms, and drug holidays. Can Fam Physician. 2014;60(4):324-33. [ Links ]

6 Sosa Henríquez M, Gómez de Tejada Romero MJ, Malouf Sierra J. Caso clínico a debate: vacaciones terapéuticas: ¿sí o no? Rev Osteoporos Metab Miner. 2014;6(2):63-9. [ Links ]

7 Lamy O, Gonzalez-Rodriguez E, Stoll D, Hans D, Aubry-Rozier B. Severe rebound-associated vertebral fractures after denosumab discontinuation: 9 clinical cases report. J Clin Endocrinol Metab. 2017;102(2):354-8. [ Links ]

8 McClung MR. Cancel the denosumab holiday. Osteoporos Int. 2016;27(5): 1677-82. [ Links ]

9 McClung MR, Wagman RB, Miller PD, Wang A, Lewiecki EM. Observations following discontinuation of longterm denosumab therapy. Osteoporos Int. 2017;28(5):1723-32. [ Links ]

10 Popp AW, Zysset PK, Lippuner K. Rebound-associated vertebral fractures after discontinuation of denosumabfrom clinic and biomechanics. Osteoporos Int. 2016;27(5):1917-21. [ Links ]

11 Polyzos SA, Terpos E. Clinical vertebral fractures following denosumab discontinuation. Endocrine. 2016;54(1):271-2. [ Links ]

12 Ruggiero S, Gralow J, Marx RE, Hoff AO, Schubert MM, Huryn JM, et al. Practical guidelines for the prevention, diagnosis, and treatment of osteonecrosis of the jaw in patients with cancer. J Oncol Pract. 2017;2(1):7-14. [ Links ]

13 Rasmusson L, Abtahi J. Bisphosphonate associated osteonecrosis of the jaw: an update on pathophysiology, risk factors, and treatment. Int J Dent. 2014;2014:1-9. [ Links ]

14 Tsao C, Darby I, Ebeling PR, Walsh K, Brien-simpson NO, Reynolds E. Oral health risk factors for jaw osteonecrosis. J Oral Maxillofac Surg. 2013;71(8):1360-6. [ Links ]

15 Assael LA. Oral Bisphosphonates as a cause of bisphosphonate-related osteonecrosis of the jaws: clinical findings, assessment of risks, and preventive strategies. J Oral Maxillofac Surg. 2009; 67(Suppl 5):35-43. [ Links ]

16 Sosa-Henríquez M, Vicente Barrero M, Bocanegra-Pérez S. Osteonecrosis de los maxilares: nuevas evidencias sobre su etiopatogenia. Rev Osteoporos Metab Miner. 2011;3:5-6. [ Links ]

17 Quintana-González M, Quintana-Montesdeoca P, Gómez de Tejada-Romero MJ, Saavedra-Santana P, Vicente-Barrero M, Bocanegra-Pérez S, et al. Estado cualitativo y cuantitativo óseo generalizado en la osteonecrosis de maxilares. Efecto de los bifosfonatos. Rev Osteoporos Metab Miner. 2019; 11(2): 55-63. [ Links ]

18 Raum K, Grimal Q, Varga P, Barkmann R, Glüer CC, Laugier P. Ultrasound to assess bone quality. Curr Osteoporos Rep. 2014;12(2):154-62. [ Links ]

19 Glüer CC. Quantitative Ultrasound-It is time to focus research efforts. Bone. 2007;40(1):9-13. [ Links ]

20 Aspenberg P. Osteonecrosis of the jaw: what do bisphosphonates do? Expert Opin Drug Saf. 2006;5(6):743-5. [ Links ]

21 Allen MR, Burr DB. The pathogenesis of bisphosphonate-related osteonecrosis of the jaw: so many hypotheses, so few data. J Oral Maxillofac Surg. 2009;67(suppl 5):61-70. [ Links ]

Este es un artículo publicado en acceso (Open Access) abierto bajo la licencia Creative Commons Attribution Non-Commercial, que permite su uso, distribución y reproducción en cualquier medio, sin restricciones siempre que sin fines comerciales y que el trabajo original sea debidamente citado.