PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
32530102-1	2021	AIMS: To evaluate whether 2 years of treatment with bisphosphonates in combination with calcium/vitamin D supplements has an effect on lumbar spine and hip bone mineral density (BMD) in ankylosing spondylitis (AS) patients starting tumor necrosis factor-alpha (TNF-alpha) inhibitors or receiving conventional treatment.	Diphosphonates	52-67	tumor necrosis factor	Homo sapiens	232-259	
32530102-1	2021	AIMS: To evaluate whether 2 years of treatment with bisphosphonates in combination with calcium/vitamin D supplements has an effect on lumbar spine and hip bone mineral density (BMD) in ankylosing spondylitis (AS) patients starting tumor necrosis factor-alpha (TNF-alpha) inhibitors or receiving conventional treatment.	Diphosphonates	52-67	tumor necrosis factor	Homo sapiens	261-270	
28725947-4	2017	To date, the use of anti-TNF agents has been proved to be a valid alternative for patients unresponsive to conventional treatments, such as NSAIDs, corticosteroids, DMARDs and biphosphonates.	Diphosphonates	176-190	tumor necrosis factor	Homo sapiens	25-28	
26856585-14	2016	CONCLUSIONS: Our study demonstrated the key role of DKK1, RANKL, and TNF-alpha in regulating bone cell activity of subjects with OI untreated and treated with bisphosphonates.	Diphosphonates	159-174	tumor necrosis factor	Homo sapiens	69-78	
24067888-12	2014	Further studies to confirm these results over a longer time frame are warranted together with the possibility to explore the long-term efficacy of a combination of lower anti-TNF doses with bisphosphonates.	Diphosphonates	190-205	tumor necrosis factor	Homo sapiens	175-178	
24400722-7	2014	CONCLUSION: This patient with a medical history of Crohn"s disease and gastrointestinal remission under Adalimumab therapy presented with osteonecrosis of the jaw after suspended oral and intravenous Bisphosphonate therapy implicating that the biologic therapy with an anti-TNF-alpha antibody might promote the manifestation of osteonecrosis and compromise oral healing capacity.	Diphosphonates	200-214	tumor necrosis factor	Homo sapiens	274-283	
16142752-10	2005	CONCLUSION: The reduced efficacy of bisphosphonates to stop bone erosion in the inflamed joints of RA patients may result from local high levels of TNF up-regulating Ets-2 expression in osteoclasts, which in turn stimulates Bcl-xL expression in them and reduces their susceptibility to bisphosphonate-induced apoptosis.	Diphosphonates	36-50	tumor necrosis factor	Homo sapiens	148-151	
23275389-9	2013	There was a significant difference in the change of SASSS in patients treated with both TNF inhibitors and bisphosphonates compared with those treated with TNF inhibitors alone (P < 0.01).	Diphosphonates	107-122	tumor necrosis factor	Homo sapiens	156-159	
16142752-10	2005	CONCLUSION: The reduced efficacy of bisphosphonates to stop bone erosion in the inflamed joints of RA patients may result from local high levels of TNF up-regulating Ets-2 expression in osteoclasts, which in turn stimulates Bcl-xL expression in them and reduces their susceptibility to bisphosphonate-induced apoptosis.	Diphosphonates	36-51	tumor necrosis factor	Homo sapiens	148-151	
21441060-6	2011	Although no randomized placebo-controlled trials are available, there is general agreement that nonsteroidal antiinflammatory drugs constitute the best first-line treatment and that bisphosphonates and biotherapies such as TNFalpha antagonists are effective in the most severe forms.	Diphosphonates	182-197	tumor necrosis factor	Homo sapiens	223-231	
19692118-9	2009	Moreover, the coatings synthesized from hydroxyapatite at relatively high bisphosphonate content (7.1% wt) displayed a reduced production of Tumour Necrosis Factor alpha (TNF-alpha) and Interleukin 6 (IL-6), suggesting a down-regulatory role of alendronate on the inflammatory reaction.	Diphosphonates	74-88	tumor necrosis factor	Homo sapiens	171-180	
15274277-3	2004	In this study, we tested the effects of calcitriol (1alpha,25-dihydroxy-vitamin-D3) and the bisphosphonate pamidronate on titanium-particle- and TNF-alpha-induced release of interleukin-6 and suppression of osteoblast-specific gene expressions in bone-marrow-derived stromal cells with an osteoblastic phenotype.	Diphosphonates	92-106	tumor necrosis factor	Homo sapiens	145-154	
10413987-13	1999	The biphosphonates, etidronate and ibendronate significantly reduced the TNF response of the PE-stimulated macrophages (by 1/7 and 1/5, respectively).	Diphosphonates	4-18	tumor necrosis factor	Homo sapiens	73-76	
9351880-16	1997	In vitro, an increase in TNF alpha and a mild increase in IL-6 was seen with all bisphosphonates, with the greatest effects seen with the highest concentration of both pamidronate and zoledronate.	Diphosphonates	81-96	tumor necrosis factor	Homo sapiens	25-34