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Journal articles on the topic 'Bone cancer pain'

Author: Grafiati

Published: 13 April 2024

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1

Koyyalagunta, Dhanalakshmi, BCarolina Hernández-Porras, Ricardo Plancarte, and JuanMiguel Jimenez Andrade. "Bone cancer pain." Indian Journal of Pain 35, no. 1 (2021): 4. http://dx.doi.org/10.4103/ijpn.ijpn_4_21.

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2

Clohisy, Denis R., and Patrick W. Mantyh. "Bone Cancer Pain." Clinical Orthopaedics and Related Research 415 (October 2003): S279—S288. http://dx.doi.org/10.1097/01.blo.0000093059.96273.56.

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3

Mantyh, Patrick W. "Bone cancer pain." Current Opinion in Supportive and Palliative Care 8, no. 2 (June 2014): 83–90. http://dx.doi.org/10.1097/spc.0000000000000048.

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4

Jimenez-Andrade, Juan Miguel, William G. Mantyh, Aaron P. Bloom, Alice S. Ferng, Christopher P. Geffre, and Patrick W. Mantyh. "Bone cancer pain." Annals of the New York Academy of Sciences 1198, no. 1 (June 2010): 173–81. http://dx.doi.org/10.1111/j.1749-6632.2009.05429.x.

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5

Clohisy, Denis R., and Patrick W. Mantyh. "Bone cancer pain." Cancer 97, S3 (January 23, 2003): 866–73. http://dx.doi.org/10.1002/cncr.11144.

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6

Ungard, Robert G., Eric P. Seidlitz, and Gurmit Singh. "Oxidative stress and cancer pain." Canadian Journal of Physiology and Pharmacology 91, no. 1 (January 2013): 31–37. http://dx.doi.org/10.1139/cjpp-2012-0298.

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Breast cancers are the most common source of metastases to bone, of which cancer-induced bone pain is a frequent pathological feature. Cancer-induced bone pain is a unique pain state with multiple determinants that remains to be well understood and managed. Current standard treatments are limited by dose-dependent side effects that can reduce the quality of life of patients. Glutamate is a neurotransmitter and bone cell-signalling molecule that is released via the system [Formula: see text] cystine/glutamate antiporter from cancer cell types that frequently metastasize to bone, including breast cancers. In cancer cells, glutamate release is understood to be a side effect of the cellular response to oxidative stress that upregulates the expression and activity of system [Formula: see text] to promote the increased import of cystine. Attenuation of glutamate release from cancer cells has been demonstrated to result in reductions in associated cancer-induced bone pain in animal models. This review examines the clinical implications of attenuating cystine uptake and glutamate release in the treatment of cancer-induced bone pain.

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7

Feller, Liviu, Razia Abdool Gafaar Khammissa, Michael Bouckaert, Raoul Ballyram, Yusuf Jadwat, and Johan Lemmer. "Pain: Persistent postsurgery and bone cancer-related pain." Journal of International Medical Research 47, no. 2 (January 11, 2019): 528–43. http://dx.doi.org/10.1177/0300060518818296.

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The generation of neuropathic pain is a complex dynamic process. Factors involved include one or more dysregulated sensory neural pathways; dysregulated activity of specific neurotransmitters, synapses, receptors and cognitive and emotional neural circuits; and the balance between degenerative and regenerative neural events. Risk factors include age, sex, cognition, emotions, genetic polymorphism, previous or ongoing chronic pain conditions and the use of certain drugs. Intense pain experienced before, during and after surgery is a risk factor for the development of central sensitization with consequent persistent postsurgery neuropathic pain. Blockade of N-methyl-D-aspartate receptors with appropriate drugs during and immediately after surgery may prevent persistent postsurgical pain. Most cancers, but particularly malignant metastases in bone, can induce persistent pain. Local factors including direct damage to sensory nerve fibres, infiltration of nerve roots by cancer cells and algogenic biological agents within the microenvironment of the tumour bring about central sensitization of dorsal horn neurons, characterized by neurochemical reorganization with persistent cancer pain. In this article, the clinical features, pathogenesis and principles of management of persistent postsurgery pain and cancer pain are briefly discussed.

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8

Erdmann, A. "Cancer-related Bone Pain." British Journal of Anaesthesia 101, no. 1 (July 2008): 132–33. http://dx.doi.org/10.1093/bja/aen142.

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9

Kane, C. M., P. Hoskin, and M. I. Bennett. "Cancer induced bone pain." BMJ 350, jan29 7 (January 29, 2015): h315. http://dx.doi.org/10.1136/bmj.h315.

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10

Mohsin, Intikhab. "Cancer induced bone pain." Public Health and Emergency 1 (August 23, 2016): 29. http://dx.doi.org/10.21037/phe.2016.08.10.

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11

Gilmore, Karen, and Mark Taylor. "Cancer-Related Bone Pain." Anaesthesia 63, no. 11 (November 2008): 1274. http://dx.doi.org/10.1111/j.1365-2044.2008.05572.x.

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12

Paley, Carole A., Michael I. Bennett, and Mark I. Johnson. "Acupuncture for Cancer-Induced Bone Pain?" Evidence-Based Complementary and Alternative Medicine 2011 (2011): 1–8. http://dx.doi.org/10.1093/ecam/neq020.

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Bone pain is the most common type of pain in cancer. Bony metastases are common in advanced cancers, particularly in multiple myeloma, breast, prostate or lung cancer. Current pain-relieving strategies include the use of opioid-based analgesia, bisphosphonates and radiotherapy. Although patients experience some pain relief, these interventions may produce unacceptable side-effects which inevitably affect the quality of life. Acupuncture may represent a potentially valuable adjunct to existing strategies for pain relief and it is known to be relatively free of harmful side-effects. Although acupuncture is used in palliative care settings for all types of cancer pain the evidence-base is sparse and inconclusive and there is very little evidence to show its effectiveness in relieving cancer-induced bone pain (CIBP). The aim of this critical review is to consider the known physiological effects of acupuncture and discuss these in the context of the pathophysiology of malignant bone pain. The aim of future research should be to produce an effective protocol for treating CIBP with acupuncture based on a sound, evidence-based rationale. The physiological mechanisms presented in this review suggest that this is a realistic objective.

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13

Colvin, L., and M. Fallon. "Challenges in cancer pain management–bone pain." European Journal of Cancer 44, no. 8 (May 2008): 1083–90. http://dx.doi.org/10.1016/j.ejca.2008.03.001.

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14

Sorbie, Charles. "Bone Cancer Pain-Experimental Relief." Orthopedics 23, no. 8 (August 2000): 787–88. http://dx.doi.org/10.3928/0147-7447-20000801-06.

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15

Goblirsch, Michael J., Pawel P. Zwolak, and Denis R. Clohisy. "Biology of Bone Cancer Pain." Clinical Cancer Research 12, no. 20 (October 15, 2006): 6231s—6235s. http://dx.doi.org/10.1158/1078-0432.ccr-06-0682.

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16

&NA;. "Osteoprotegerin reduces bone cancer pain." Inpharma Weekly &NA;, no. 1239 (May 2000): 9. http://dx.doi.org/10.2165/00128413-200012390-00020.

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17

Falk, Sarah, and Anthony H. Dickenson. "Pain and Nociception: Mechanisms of Cancer-Induced Bone Pain." Journal of Clinical Oncology 32, no. 16 (June 1, 2014): 1647–54. http://dx.doi.org/10.1200/jco.2013.51.7219.

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Cancer pain, especially pain caused by metastasis to bone, is a severe type of pain, and unless the cause and consequences can be resolved, the pain will become chronic. As detection and survival among patients with cancer have improved, pain has become an increasing challenge, because traditional therapies are often only partially effective. Until recently, knowledge of cancer pain mechanisms was poor compared with understanding of neuropathic and inflammatory pain states. We now view cancer-induced bone pain as a complex pain state involving components of both inflammatory and neuropathic pain but also exhibiting elements that seem unique to cancer pain. In addition, the pain state is often unpredictable, and the intensity of the pain is highly variable, making it difficult to manage. The establishment of translational animal models has started to reveal some of the molecular components involved in cancer pain. We present the essential pharmacologic and neurobiologic mechanisms involved in the generation and continuance of cancer-induced bone pain and discuss these in the context of understanding and treating patients. We discuss changes in peripheral signaling in the area of tumor growth, examine spinal cord mechanisms of sensitization, and finally address central processing. Our aim is to provide a mechanistic background for the sensory characteristics of cancer-induced bone pain as a basis for better understanding and treating this condition.

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18

HIRD, AMANDA, SHAELYN CULLETON, and EDWARD CHOW. "Oxford Pain Management Library: Cancer-Related Bone Pain." European Journal of Cancer Care 19, no. 4 (October 14, 2009): e7-e7. http://dx.doi.org/10.1111/j.1365-2354.2008.01024.x.

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19

&NA;, &NA;. "Radioactive Relief For Cancer Bone Pain." AJN, American Journal of Nursing 94, no. 2 (February 1994): 58. http://dx.doi.org/10.1097/00000446-199402000-00032.

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20

Zhou, Ya-Qun, Zheng Liu, Hui-Quan Liu, Dai-Qiang Liu, Shu-Ping Chen, Da-Wei Ye, and Yu-Ke Tian. "Targeting glia for bone cancer pain." Expert Opinion on Therapeutic Targets 20, no. 11 (July 27, 2016): 1365–74. http://dx.doi.org/10.1080/14728222.2016.1214716.

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21

Laws, Shelena, and Kelly Conright. "Cancer-Related Incident Bone Pain #380." Journal of Palliative Medicine 22, no. 11 (November 1, 2019): 1468–70. http://dx.doi.org/10.1089/jpm.2019.0481.

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22

Thompson, Stephen W. N., and David Tonge. "Bone cancer gain without the pain." Nature Medicine 6, no. 5 (May 2000): 504–5. http://dx.doi.org/10.1038/74977.

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23

Goblirsch, M. J., P. Zwolak, and D. R. Clohisy. "Advances in understanding bone cancer pain." Journal of Cellular Biochemistry 96, no. 4 (2005): 682–88. http://dx.doi.org/10.1002/jcb.20589.

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24

Middlemiss, T., B. J. A. Laird, and M. T. Fallon. "Mechanisms of Cancer-induced Bone Pain." Clinical Oncology 23, no. 6 (August 2011): 387–92. http://dx.doi.org/10.1016/j.clon.2011.03.003.

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25

Kim, Kyung-Hoon. "Scapuloplasty Alleviates Scapular Pain Resulting from Lung Cancer Metastasis." Pain Physician 5;13, no. 5;9 (September 14, 2010): 485–91. http://dx.doi.org/10.36076/ppj.2010/13/485.

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Osteoplasty, a highly effective minimally invasive procedure that alleviates the painful effects of metastatic bone disease by injecting bone cement to support weakened bones, provides immediate and substantial pain relief. However, it is rarely performed in non-weight bearing flat bones such as the scapula. Fractures of the body of the scapula are rarely treated surgically, except for cases of marked displacement of fragments that limit the function of the scapula. According to the reported incidences of operative treatment of different scapula fracture types, 99% of all isolated scapula body fractures are treated nonoperatively A 54-year-old man had been experiencing metastatic bone pain in the lateral border, medial border, and medial infraspinatus fossa of the left scapula for the past 2 months; this pain originated from adenocarcinoma of the right lung. He could not sleep on his back even after completion of radiation therapy. We decided to perform scapuloplasty. The patient was placed in the prone position on a radiolucent table with an inflatable adjustable axillary pillow. Three 13-gauge, 10-cm long bone biopsy needles were simultaneously inserted from the 3 different entry points to fill the osteolytic lesion with the bone cement with fluoroscopic guidance under local anesthesia and intravenous analgesia. After confirming needle placement and ensuring that no contrast medium was extravasated, a total of 8 mL of the cement was injected. Immediately after the operation, the patient could lie on his back without pain. Scapuloplasty is a new variant of osteoplasty used to alleviate the painful effects of metastatic bone disease. It may be an option of shoulder motion-preserving minimally invasive procedure for alleviating intractable pain induced by lying on the back. Key words: Fluoroscopy; lung neoplasms; neoplasm metastasis; polymethyl methacrylate; pain; palliative care; scapula; surgical procedures, minimally invasive; vertebroplasty.

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26

Saad, Fred. "Bone Metastases in Advanced Prostate Cancer." Oncology & Hematology Review (US) 00, no. 00 (2005): 1. http://dx.doi.org/10.17925/ohr.2005.00.00.1v.

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Men with advanced prostate cancer are at high risk for development of bone metastases,resulting in clinically significant skeletal morbidity and severe bone pain. Studies of early-generation bisphosphonates,clodronate, and pamidronate,demonstrated transient palliative effects on bone pain in patients with bone metastases, but failed to demonstrate long-term clinical benefit.A small,open-label study of ibandronate demonstrated significant reductions in pain,but these results have not been confirmed in a larger,randomized,controlled trial. Currently,zoledronic acid is the only bisphosphonate that has demonstrated statistically significant reductions in skeletal morbidity – including durable pain reduction– in this patient population in a randomized placebocontrolled trial.Therefore,zoledronic acid therapy should be considered to prevent skeletal morbidity and improve the quality of life of prostate cancer patients with bone metastases.

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27

Scarpi, Emanuela, Daniele Calistri, Pål Klepstad, Stein Kaasa, Frank Skorpen, Ragnhild Habberstad, Oriana Nanni, Dino Amadori, and Marco Maltoni. "Clinical and Genetic Factors Related to Cancer‐Induced Bone Pain and Bone Pain Relief." Oncologist 19, no. 12 (October 23, 2014): 1276–83. http://dx.doi.org/10.1634/theoncologist.2014-0174.

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28

Berardinelli, F., M. Iannucci, V. Verratti, W. Fusco, M. Nicolai, and R. L. Tenaglia. "Bisphosphonates Treatment in Metastatic Prostate Cancer." European Journal of Inflammation 3, no. 2 (May 2005): 49–54. http://dx.doi.org/10.1177/1721727x0500300201.

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The skeleton is the third most common site for cancer to spread after the liver and lungs. Malignancies that can cause destruction of skeletal bones include multiple myeloma and metastatic diseases of the lung, prostate and other solid cancers. The clinical complications include pain, fractures, compression of the spinal cord and hypercalcemia of malignancy. Bisphosphonates are bone-seeking agents originally designed to treat loss of bone density. Accumulating data show that they are effective in diseases in which there is upregulation of osteoclastic or osteolytic activity. Bisphosphonates can reduce skeletal-related events and bone pain, as well as reduce the adverse effects of androgen deprivation therapy on skeletal integrity. However, it is clear that bisphosphonates do not represent a decisive treatment in the care of metastases but a therapeutic choice in synergy with regular anti-tumor drugs. The preclinical and clinical data to support this are reviewed here.

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29

Pan, Ruirui, Huiting Di, Jinming Zhang, Zhangxiang Huang, Yuming Sun, Weifeng Yu, and Feixiang Wu. "Inducible Lentivirus-Mediated siRNA against TLR4 Reduces Nociception in a Rat Model of Bone Cancer Pain." Mediators of Inflammation 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/523896.

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Although bone cancer pain is still not fully understood by scientists and clinicians alike, studies suggest that toll like receptor 4 (TLR4) plays an important role in the initiation and/or maintenance of pathological pain state in bone cancer pain. A promising treatment for bone cancer pain is the downregulation of TLR4 by RNA interference; however, naked siRNA (small interference RNA) is not effective in long-term treatments. In order to concoct a viable prolonged treatment for bone cancer pain, an inducible lentivirus LvOn-siTLR4 (tetracycline inducible lentivirus carrying siRNA targeting TLR4) was prepared and the antinociception effects were observed in bone cancer pain rats induced by Walker 256 cells injection in left leg. Results showed that LvOn-siTLR4 intrathecal injection with doxycycline (Dox) oral administration effectively reduced the nociception induced by Walker 256 cells while inhibiting the mRNA and protein expression of TLR4. Proinflammatory cytokines as TNF-αand IL-1βin spinal cord were also decreased. These findings suggest that TLR4 could be a target for bone cancer pain treatment and tetracycline inducible lentivirus LvOn-siTLR4 represents a new potential option for long-term treatment of bone cancer pain.

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30

Bortolin, Andrea, Estrela Neto, and Meriem Lamghari. "Calcium Signalling in Breast Cancer Associated Bone Pain." International Journal of Molecular Sciences 23, no. 3 (February 8, 2022): 1902. http://dx.doi.org/10.3390/ijms23031902.

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Calcium (Ca2+) is involved as a signalling mediator in a broad variety of physiological processes. Some of the fastest responses in human body like neuronal action potential firing, to the slowest gene transcriptional regulation processes are controlled by pathways involving calcium signalling. Under pathological conditions these mechanisms are also involved in tumoral cells reprogramming, resulting in the altered expression of genes associated with cell proliferation, metastatisation and homing to the secondary metastatic site. On the other hand, calcium exerts a central function in nociception, from cues sensing in distal neurons, to signal modulation and interpretation in the central nervous system leading, in pathological conditions, to hyperalgesia, allodynia and pain chronicization. It is well known the relationship between cancer and pain when tumoral metastatic cells settle in the bones, especially in late breast cancer stage, where they alter the bone micro-environment leading to bone lesions and resulting in pain refractory to the conventional analgesic therapies. The purpose of this review is to address the Ca2+ signalling mechanisms involved in cancer cell metastatisation as well as the function of the same signalling tools in pain regulation and transmission. Finally, the possible interactions between these two cells types cohabiting the same Ca2+ rich environment will be further explored attempting to highlight new possible therapeutical targets.

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31

Vermeirsch, Hilde, Rony Nuydens, and Theo F. Meert. "Bone Morphometric Changes and Pain Perception in Differentin vivoModels for Bone Cancer-Related Pain." Journal of Cancer Pain & Symptom Palliation 1, no. 1 (January 2005): 25–34. http://dx.doi.org/10.3109/j427v01n01_04.

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32

Kaggwa, Andrew Tabu, Protus Werunga Kituyi, Elijah Nzeki Muteti, and Ramadhani Barry Ayumba. "Cancer-Related Bone Pain: Patients’ Satisfaction with Analgesic Pain Control." Annals of African Surgery 19, no. 3 (September 2, 2022): 144–52. http://dx.doi.org/10.4314/aas.v19i3.3.

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Background: Management of cancer-related bone pain (CRBP) with analgesics poses a substantial challenge. This study aimed to determine the correlation between pain control satisfaction and prescribed analgesics. Methods: This 12-month descriptive prospective study included 96 adults who were consecutively sampled and followed up daily for 5 days. Eligible patients had histopathologically confirmed tumor, osseous lesion(s) on radiographs, and cognitive capacity to rank pain on the Numerical Rating Scale. Data were collected using questionnaires drafted from the Brief Pain Inventory. Self-assessed pain scores within the past 24 hours were reported on a scale of 0 (no pain) to 10 (worst pain). Pain control satisfaction was assessed as a single response question (satisfied, not sure, or dissatisfied). Associations were examined in multiple logistic regression models. Ethical approval and informed consent were obtained. Results: The median age was 57 (range, 19–90) years, and more males (52.1%) than females were recruited. The proportion of CRBP ranged from 83.3% to 86.5%, whereas that of moderate to severe pain ranged from 57.3% to 69.8%. Overall, 70.8% were satisfied with their pain control. Patients prescribed opioids (adjusted odds ratio, 0.027; p=0.041) had an increased likelihood of pain control satisfaction. Conclusion: Although a high percentage of patients experienced moderate to severe CRBP, a majority were satisfied with their analgesic pain control. Prescription opioids were associated with higher satisfaction. Policies that sustain ready accessibility of analgesics, particularly opioids, should be implemented.

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33

Furuse, Shingo, Tomoyuki Kawamata, Jun Yamamoto, Yukitoshi Niiyama, Keiichi Omote, Masahiko Watanabe, and Akiyoshi Namiki. "Reduction of Bone Cancer Pain by Activation of Spinal Cannabinoid Receptor 1 and Its Expression in the Superficial Dorsal Horn of the Spinal Cord in a Murine Model of Bone Cancer Pain." Anesthesiology 111, no. 1 (July 1, 2009): 173–86. http://dx.doi.org/10.1097/aln.0b013e3181a51e0d.

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Background Bone cancer pain has a strong impact on the quality of life of patients, but it is difficult to treat. Therefore, development of a novel strategy for the treatment of bone cancer pain is needed for improvement of patient quality of life. This study examined whether selective spinal cannabinoid receptor 1 (CB1) activation alleviates bone cancer pain and also examined the spinal expression of CB1. Methods A bone cancer pain model was made by implantation of sarcoma cells into the intramedullary space of the mouse femur. In behavioral experiments, the authors examined the effects of activation of spinal CB1 and inhibition of metabolism of endocannabinoid on bone cancer-related pain behaviors. Immunohistochemical experiments examined the distribution and localization of CB1 in the superficial dorsal horn of the spinal cord using specific antibodies. Results Spinal CB1 activation by exogenous administration of a CB1 agonist arachidonyl-2-chloroethylamide reduced bone cancer-related pain behaviors, including behaviors related to spontaneous pain and movement-evoked pain. In immunohistochemical experiments, although mu-opioid receptor 1 expression was reduced in the superficial dorsal horn ipsilateral to the site of implantation of sarcoma cells, CB1 expression was preserved. In addition, CB1 was mainly expressed in the axon terminals, but not in the dendritic process in the superficial dorsal horn. Conclusion Spinal CB1 activation reduced bone cancer-related pain behavior. Presynaptic inhibition may contribute to the analgesic effects of spinal CB1 activation. These findings may lead to novel strategies for the treatment of bone cancer pain.

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34

Berna, Lluis, Ignasi Carrio, Carmen Alonso, Josep Ferré, Montserrat Estorch, and Gustavo Torres. "Bone pain palliation with strontium-89 in breast cancer patients with bone metastases and refractory bone pain." European Journal of Nuclear Medicine 22, no. 10 (October 1995): 1101–4. http://dx.doi.org/10.1007/bf00800589.

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35

Sindhi, Vivek, and Michael Erdek. "Interventional treatments for metastatic bone cancer pain." Pain Management 9, no. 3 (May 2019): 307–15. http://dx.doi.org/10.2217/pmt-2018-0073.

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36

Seppa, Nathan. "Drug Eases Bone Cancer Pain in Mice." Science News 157, no. 19 (May 6, 2000): 292. http://dx.doi.org/10.2307/4012424.

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37

Archibald, Sarah. "Anti-NGF therapy for bone cancer pain." Nature Reviews Neuroscience 6, no. 7 (July 2005): 500. http://dx.doi.org/10.1038/nrn1710.

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38

Lozano-Ondoua, A. N., A. M. Symons-Liguori, and T. W. Vanderah. "Cancer-induced bone pain: Mechanisms and models." Neuroscience Letters 557 (December 2013): 52–59. http://dx.doi.org/10.1016/j.neulet.2013.08.003.

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39

Medhurst, S. J., K. Walker, M. Bowes, B. L. Kidd, M. Glatt, M. Muller, M. Hattenberger, et al. "A rat model of bone cancer pain." Pain 96, no. 1 (March 2002): 129–40. http://dx.doi.org/10.1016/s0304-3959(01)00437-7.

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40

Senior, Kathryn. "Osteoclast inhibitor may limit bone cancer pain." Lancet Oncology 1 (May 2000): 6. http://dx.doi.org/10.1016/s1470-2045(09)70271-2.

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41

Lucchesi, Maurizio, Gaetano Lanzetta, Andrea Antonuzzo, Antonio Rozzi, Iacopo Sardi, Claudio Favre, Carla Ida Ripamonti, Daniele Santini, and Grazia Armento. "Developing drugs in cancer-related bone pain." Critical Reviews in Oncology/Hematology 119 (November 2017): 66–74. http://dx.doi.org/10.1016/j.critrevonc.2017.08.005.

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42

Zhu, Yong Fang, Robert Ungard, Natalie Zacal, Jan D. Huizinga, James L. Henry, and Gurmit Singh. "Rat model of cancer-induced bone pain." PAIN Reports 2, no. 4 (2017): e603. http://dx.doi.org/10.1097/pr9.0000000000000603.

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43

Sabino, Mary Ann C., and Patrick W. Mantyh. "Clinically related behavioral models: bone cancer pain." Drug Discovery Today: Disease Models 1, no. 2 (November 2004): 127–34. http://dx.doi.org/10.1016/j.ddmod.2004.09.007.

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44

Yoneda, Toshiyuki, Masahiro Hiasa, and Tatsuo Okui. "Bone Pain Associated with Acidic Cancer Microenvironment." Current Molecular Biology Reports 4, no. 2 (March 22, 2018): 59–68. http://dx.doi.org/10.1007/s40610-018-0089-7.

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45

Slosky, Lauren M., Tally M. Largent-Milnes, and Todd W. Vanderah. "Use of Animal Models in Understanding Cancer-induced Bone Pain." Cancer Growth and Metastasis 8s1 (January 2015): CGM.S21215. http://dx.doi.org/10.4137/cgm.s21215.

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Many common cancers have a propensity to metastasize to bone. Although malignancies often go undetected in their native tissues, bone metastases produce excruciating pain that severely compromises patient quality of life. Cancer-induced bone pain (CIBP) is poorly managed with existing medications, and its multifaceted etiology remains to be fully elucidated. Novel analgesic targets arise as more is learned about this complex and distinct pain state. Over the past two decades, multiple animal models have been developed to study CIBP's unique pathology and identify therapeutic targets. Here, we review animal models of CIBP and the mechanistic insights gained as these models evolve. Findings from immunocompromised and immunocompetent host systems are discussed separately to highlight the effect of model choice on outcome. Gaining an understanding of the unique neuromolecular profile of cancer pain through the use of appropriate animal models will aid in the development of more effective therapeutics for CIBP.

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46

Oh, Kyung Seo, Seung Young Lee, Se-Hee Min, Choongun Ryu, and Hwa-Yong Shin. "Hypertrophic osteoarthropathy in renal cell carcinoma - A case report -." Anesthesia and Pain Medicine 16, no. 3 (July 31, 2021): 290–94. http://dx.doi.org/10.17085/apm.20092.

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Hypertrophic osteoarthropathy (HOA) is a rare clinical condition including an abnormal periosteal reaction in the long bones that causes painful swelling and tenderness of the extremities, digital clubbing, arthritis, synovitis, and joint effusions. Most cases are associated with tumorous conditions and most commonly with lung cancer. HOA has been rarely reported in association with other cancers. A patient with a history of recurrent renal cell carcinoma was referred to our clinic with bilateral leg pain, knee joint effusion, and arthritis. Simple radiography and bone scintigraphy confirmed a diagnosis of HOA. Oral non-steroidal anti-inflammatory drugs, joint fluid aspiration, and intra-articular injection of pain medications were found to be effective in the management of HOA pain. HOA prognosis depends on the underlying disease, therefore, cancer treatment is critical. This case demonstrates the need to consider HOA in patients with various malignancies who present with bone or joint pain of the extremities.

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47

Hiba, B. A., K. Dorra, R. Meriem, B. Chayma, K. Sonia, E. Hanen, K. Mahla, F. Raja, and C. Elhem. "AB1361 PAIN MANAGEMENT IN METASTATIC BONE DISEASE." Annals of the Rheumatic Diseases 81, Suppl 1 (May 23, 2022): 1786.2–1786. http://dx.doi.org/10.1136/annrheumdis-2022-eular.3568.

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BackgroundBone metastases are the most common cause of pain in patients with malignant disease. Bone metastasis (BM) pain management is one of the greatest challenges for oncologists, due not only to safety issues, but also to the significant impairment of patients’ quality of life and performance status.ObjectivesTo provide an overview of the epidemiology, clinicopathological features and treatment approaches of painful BM in patients followed-up at the pain treatment center (PTC) of Tunisia.MethodsWe performed a retrospective review of the medical records of all patients with BM, seen at the PTC of Tunisia in 2019. The information collected included patient demographics, clinicopathological features and treatment approaches of the BM.ResultsA total of 117 patients, with male to female ratio of 2.5 and a mean age of 61,2± 12.5 years [22-93], were included. Primary cancers were mainly lung cancer (40%), breast cancer (13,7%), prostate cancer (11,1%), malignant hemopathies (5%) and kidney cancer (3,5%). Mean cancer duration was 10.5 months [0-84]. Mean duration from the diagnosis of cancer to the diagnosis of BM was 4.2± 1.7 months [0-11].The most common BM sites were the spine (83.6%), the pelvis (28.5%) and the ribs (22.4%). BM was painful in 97% of cases. The mean number of consultations at the PTC was 5.5±2.8 [1-18].Malignant bone pain was nociceptive in 73.3% of cases, neuropathic in 9.5% and mixed (both nociceptive and neuropathic) in 33%. Mean visual analogue scale (VAS) pain was 8.7±1,5 [2-10]. Most of the patients (84.5%) were treated by opioid analgesics which was morphine in 98% of cases. The route of administration of morphine was the oral in 85.3% of cases with a median dose of 60mg/j [10-240]. Laxatives and antiemetic therapy, in prevention of side effects of morphine, were prescribed in respectivly 87% and 28% of cases. The transdermal fentanyl patch was prescribed for three hepatically impaired patients. Only 15.5% of patients had a good response to pain killers palier II (Tramadol) and did not necessitate to switch to morphin. Mean dose of Tramadol was 178±75.1 mg [75-300]. Pregabalin was indicated in 25% of cases with a mean dose of 227.5± 127.7mg [150-600].Tricyclic antidepressants were prescribed for 9.5% of the patients and the mean dose was 16 ±10 mg [10-40]. Corticoisteroids were used in almost two-third of cases with a mean daily dose of 1mg/kg/j [0,5-1.5]. However, in 14% of cases, non-steroidal anti-inflammatory drugs were prescribed instead of corticosteroids. Bisphosphonates were used in 15% of cases. Antalgic radiotherapy was indicated in one-third of cases. By a median follow-up of 3 months [0-24], mean VAS pain was 3.7±1.7 [1-9].ConclusionCurrently, the treatment of painful BM remains palliative at best with systemic therapy as well as local treatments especially when BMs become symptomatic or complicated. Consequently, a multidisciplinary approach to BM is essential, to ensure a proper integration of local and systemic therapiesDisclosure of InterestsNone declared

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Needham, P. R., N. P. Mithal, and P. J. Hoskin. "Radiotherapy for Bone Pain." Journal of the Royal Society of Medicine 87, no. 9 (September 1994): 503–5. http://dx.doi.org/10.1177/014107689408700904.

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Painful bone metastases are a common problem for cancer patients. Although current evidence supports the use of a single fraction of radiotherapy as the treatment of choice, many radiotherapists, for a variety of reasons, continue to use fractionated regimens. Over one six month period 105 patients received external beam irradiation for painful bone metastases at the Royal London Hospital (RLH). Thirty-one per cent of the patients were aged 70 or over. The treatment of 97 of these patients was assessed. They had a total of 280 sites treated over the course of their disease. Fifty-nine per cent of sites treated received a fractionated course of radiotherapy. Site significantly influenced fractionation. Overall response rates of 82% were achieved. Fractionation did not appear to influence this. Ten patients received large field irradiation. Fifteen patients had five or more sites irradiated, of whom only one received hemibody irradiation.

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Ren, Bing-xu, Xiao-ping Gu, Ya-guo Zheng, Cheng-long Liu, Dan Wang, Yu-e. Sun, and Zheng-liang Ma. "Intrathecal Injection of Metabotropic Glutamate Receptor Subtype 3 and 5 Agonist/Antagonist Attenuates Bone Cancer Pain by Inhibition of Spinal Astrocyte Activation in a Mouse Model." Anesthesiology 116, no. 1 (January 1, 2012): 122–32. http://dx.doi.org/10.1097/aln.0b013e31823de68d.

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Background Astrocytes and metabotropic glutamate receptors play important roles in nociceptive processing. However, their roles in bone cancer pain were not well understood. This study sought to investigate whether selective mGluR3 and mGluR5 agonist or antagonist develop antinociceptive effects on bone cancer pain by inhibition of spinal astrocyte activation. Methods C3H/HeNCrlVr mice were inoculated into the intramedullary space of the femur with sarcoma NCTC 2472 cells to induce bone cancer pain. Quantitative real-time reverse transcription-polymerase chain reaction and Western blot experiments examined messenger RNA and protein expression of spinal glial fibrillary acidic protein, mGluR3, and mGluR5. The authors further investigated effects of intrathecal treatment with the mGluR3 agonist (APDC), the mGluR3 antagonist (LY341495), the mGluR5 agonist (CHPG), or the mGluR5 antagonist (MTEP) on nociceptive behaviors and spinal astrocyte activation associated with bone cancer pain. Results Inoculation of sarcoma cells, but not α-MEM solution, induced progressive bone cancer pain and resulted in up-regulation of glial fibrillary acidic protein, mGluR3, and mGluR5 expression on days 10, 14, and 21 postinoculation. Intrathecal administration of APDC and MTEP attenuated bone cancer-evoked spontaneous pain, mechanical allodynia, thermal hyperalgesia, and reduced spinal glial fibrillary acidic protein expression. However, treatment with LY341495 and CHPG induced thermal hyperalgesia and spinal glial fibrillary acidic protein expression in control mice. Conclusions Spinal mGluR3 activation or mGluR5 inhibition reduced bone cancer pain. Inhibition of spinal astrocyte activation may contribute to the analgesic effects. These findings may lead to novel strategies for the treatment of bone cancer pain.

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Henry, David H., Roger Von Moos, Jean-Jacques Body, Alex Rider, Jonathan De Courcy, Grace Murray, Debajyoti Bhowmik, et al. "Bone targeting agent treatment patterns and the impact of bone metastases on patients with advanced breast cancer in the US." Journal of Clinical Oncology 33, no. 28_suppl (October 1, 2015): 93. http://dx.doi.org/10.1200/jco.2015.33.28_suppl.93.

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93 Background: Bone is the most common site of distant metastasis in patients with advanced breast cancer. Bone metastases (BMs) often lead to skeletal-related events (SREs) and may result in debilitating bone pain which impacts a patient’s quality of life. Bone targeting agents (BTAs) reduce the incidence of SREs and progression of pain due to BMs. This study aims to understand real world patients’ experience of bone pain and to assess BTAs treatment patterns. Methods: Data were extracted from the Adelphi Breast Cancer Disease-Specific Programme (DSP), a cross-sectional survey of 98 US oncologists conducted from February to May 2015 in the USA. Each physician completed comprehensive record forms capturing the following information about the next 12 patients being treated for advanced breast cancer: Presence of BMs, patient’s pain state at diagnosis of BMs, current pain state, time since diagnosis of BMs, current analgesic use and reasons for prescribing BTAs. Results: Bone pain was more prevalent (p < 0.001) in patients with BMs (67% of 485) than those without BM (7% of 791). Mean time for pain assessment was 6.2 months after BM diagnosis. Among breast cancer patients with BMs and bone pain (n = 323), 98% required analgesic medications to manage the pain, including 40% (n = 130) who were treated with strong opioids (e.g., morphine, oxycodone, hydromorphone, or methadone). Of these patients, 100 (77%) had moderate/severe bone pain. Of the patients with BMs, 69% (n = 337) were treated with a BTA and treatment was initiated within 3 months of BMs diagnosis in 91% (n = 306) of them. The reasons for prescribing a BTA within 3 months of BM diagnosis were “bone pain” (32%), “high risk of bone complications” (25%), “prior history of bone complications”(18%), “number of BMs” (11%) and “location of BMs” (4%). Conclusions: Advanced breast cancer patients with BMs are more likely to experience bone pain, and three-fourths of the patients treated with strong opioids experienced moderate/severe bone pain.The majority of patients with BMs receive a BTA prescription for the reduction of bone pain and risk of bone complications.

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