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1 inhibition alone predisposed the animals to osteonecrosis.
2 ical malignancies, are at risk of developing osteonecrosis.
3 t occurring in knees without any evidence of osteonecrosis.
4 control group in a pig model of femoral head osteonecrosis.
5 e dose modification would reduce the risk of osteonecrosis.
6 be a protective factor against alveolar bone osteonecrosis.
7 lymorphisms were associated with symptomatic osteonecrosis.
8 (11.7%) children with GG genotype, developed osteonecrosis.
9 nous microbiota protects against LIP-induced osteonecrosis.
10 genetic variation may contribute to risk of osteonecrosis.
11 dysplasias reminiscent of osteoarthritis and osteonecrosis.
12 intestinal events; malignant conditions; and osteonecrosis.
13 dicted solely by lesion size at diagnosis of osteonecrosis.
14 (range, 0.5 to 8.6 years) after diagnosis of osteonecrosis.
15 and klotho were associated with sickle cell osteonecrosis.
16 tify ALL patients at highest risk to develop osteonecrosis.
17 y, pathogenesis, diagnosis, and treatment of osteonecrosis.
18 the femoral head or, better yet, preventing osteonecrosis.
19 n mice protects against inflammation-induced osteonecrosis.
20 nders the oral microenvironment conducive to osteonecrosis.
21 ents with clinical suspicion of femoral head osteonecrosis.
22 h detection of and determining the extent of osteonecrosis.
23 on of apoptotic osteocytes may contribute to osteonecrosis.
24 oid treatment, and no other risk factors for osteonecrosis.
25 osteoarthritis, inflammatory arthritis, and osteonecrosis.
26 proton-density weighted imaging, similar to osteonecrosis.
27 therapy and in areas not usually affected by osteonecrosis.
28 reases the development of medication-related osteonecrosis.
29 ipants were followed to assess fractures and osteonecrosis.
30 marrow edema syndrome (TBMES) and avascular osteonecrosis.
31 tive therapeutic target for the treatment of osteonecrosis.
32 utual adjustment, no ARV was associated with osteonecrosis.
33 bidities contribute to risk of fractures and osteonecrosis.
34 critical role in the glucocorticoid-induced osteonecrosis.
35 ng induction and experienced excess rates of osteonecrosis.
36 ated with the glomerular filtration rate and osteonecrosis.
37 ide new insights into the pathophysiology of osteonecrosis.
38 emia (ALL) and their major adverse effect is osteonecrosis.
39 tify genetic and nongenetic risk factors for osteonecrosis.
40 ociation may allow interventions to decrease osteonecrosis.
42 nhibit osteoclasts have been associated with osteonecrosis, a condition limited to the jawbone, thus
43 ing the efficacy of ACTH in preventing human osteonecrosis, a devastating complication of glucocortic
46 to define possible genetic risk factors for osteonecrosis among children treated for newly diagnosed
48 fit and was associated with a higher risk of osteonecrosis among participants 10 years and older.
49 hether 12 polymorphisms were associated with osteonecrosis among patients 10 years and older treated
53 r bone complications including fractures and osteonecrosis and for reduced or delayed response to enz
55 nd histological assessment showed that total osteonecrosis and inflammatory infiltrate was significan
56 dexamethasone exposure were associated with osteonecrosis and may be linked by inherited genomic var
57 pensated hypothyroidism in 9 patients (10%), osteonecrosis and moderate osteopenia in 2 patients each
58 ogenous SMOC2 blocks injury-induced jaw bone osteonecrosis and offsets age-induced periodontal decay.
59 There were no cases of incident drug-induced osteonecrosis and only 1 case of femoral shaft fracture
61 ting event in the genesis of steroid-induced osteonecrosis and provides a basis for future investigat
62 ations of HIV and HAART, such as osteopenia, osteonecrosis, and infection continue to be a concern.
63 al skeletal diseases, such as bone fracture, osteonecrosis, and inflammation are characterized by exc
64 performance status scores, incidence of jaw osteonecrosis, and kidney dysfunction did not differ sig
65 ency fracture, complications of pre-existing osteonecrosis, and rapid joint destruction (including bo
66 ral insufficiency fracture, complications of osteonecrosis, and rapid joint destruction, including bo
67 sterol (P = .02) associated with symptomatic osteonecrosis, and severe (grade 3 or 4) osteonecrosis w
68 e-associated hypersensitivity, pancreatitis, osteonecrosis, and thromboembolism were prospectively re
69 dentify individuals who are at high risk for osteonecrosis, and thus allow earlier and more effective
70 ce imaging of both hips was used to diagnose osteonecrosis, and was performed at similar times from t
72 ifferentiation, were associated with risk of osteonecrosis as well as with lower albumin and higher c
73 ing earlier in the diagnosis of femoral head osteonecrosis, as well as its more widespread use in pat
74 ensitivity to asparaginase, hyperlipidaemia, osteonecrosis, asparaginase-associated pancreatitis, art
76 1 years, the overall cumulative incidence of osteonecrosis at 5 years was 7.7% (SE 0.9), correlating
77 y-six (92%) of 50 patients with femoral head osteonecrosis at both examinations were placed in the ap
80 ral epiphysis (SCFE), and avascular necrosis/osteonecrosis (AVN) in 4598 children and young adults wi
82 e increased in acute lymphoblastic leukemia, osteonecrosis became an increasingly frequent complicati
85 antly improved ONFH-induced symptoms such as osteonecrosis, bone loss, reduction in vessel perfusion,
86 osteroid use is an important risk factor for osteonecrosis, but its pathogenesis is likely multifacto
87 es occur, which could prevent morbidities of osteonecrosis by guiding the decisionmaking process for
88 buminuria, leg ulcers, priapism, stroke, and osteonecrosis) by clinical examination, laboratory tests
90 ll disease, clinical complications including osteonecrosis can vary in frequency and severity, presum
94 e persisted in the region, and a new site of osteonecrosis developed on the contralateral side of the
95 ay in healing may increase the likelihood of osteonecrosis developing in already-compromised bone.
103 rs, plesiosaurs, and humans develop dysbaric osteonecrosis from end-artery nitrogen embolism ("the be
108 e receptor GRIN3A locus) was associated with osteonecrosis (hazard ratio = 2.03; P = 3.59 x 10(-7)).
109 ory has developed a model of steroid-induced osteonecrosis in BALBcJ mice which reflects clinically r
110 adults showed a size-related development of osteonecrosis in chevron and rib bone articulations, del
112 imple dose modification, reduces the risk of osteonecrosis in children and adolescents given intensif
115 ation, oxidant stress, bone metabolism) with osteonecrosis in patients with sickle cell disease.
116 ting clinical joint outcomes of femoral head osteonecrosis in pediatric patients with leukemia or lym
117 may provide insight into the pathogenesis of osteonecrosis in sickle cell disease, help identify indi
118 t predictor of clinical joint outcome of hip osteonecrosis in survivors of pediatric hematologic mali
121 orphism (rs6092) was associated with risk of osteonecrosis in univariate (P = .002; odds ratio = 2.79
122 subchondral area was found between TBMES and osteonecrosis; in joints with osteonecrosis, this was co
123 elayed intensification significantly reduced osteonecrosis incidence compared with continuous dexamet
124 e race (OR, 11.1; P =.037), host factors for osteonecrosis included the vitamin D receptor FokI start
125 roids remained significantly associated with osteonecrosis, independently of HIV disease stage and pr
133 rticoid therapy, screening for extensive hip osteonecrosis is unnecessary because their risk is low a
135 7.2%]) of 339 HIV-infected participants had osteonecrosis lesions on magnetic resonance imaging, and
136 e wrist and hand including occult fractures, osteonecrosis, ligamentous and tendon injuries, and entr
138 ate MTT, which was only found in joints with osteonecrosis, mean +/- standard deviation PF was 18.9 m
139 25 patients with and the 39 patients without osteonecrosis (median, 447 days and 443 days, respective
141 effects, including infection, bone fracture, osteonecrosis, mood and behaviour problems, and myopathy
142 ociated toxicity (hypersensitivity [n = 13]; osteonecrosis [n = 29]; pancreatitis [n = 24]; thromboem
146 lucocorticoids in which treated mice develop osteonecrosis of the distal femoral epiphysis when admin
150 orticotropic hormone (ACTH) protects against osteonecrosis of the femoral head induced by depot methy
151 r, but their effect on risk of fractures and osteonecrosis of the femoral head is less understood.
152 s' disease (Perthes' disease) is a childhood osteonecrosis of the hip for which the disease determina
154 e between primary diagnosis and diagnosis of osteonecrosis of the hip was 1.7 years (range, 0.1 to 17
158 el alendronate period, adjudicated events of osteonecrosis of the jaw (1 event each in the romosozuma
159 (26%) of 526 patients; the most common were osteonecrosis of the jaw (17 [3%]), anaemia (6 [1%]), bo
160 hypophosphataemia (24 [5%] of 526 patients), osteonecrosis of the jaw (17 [3%], pain in extremity (12
161 as associated with higher rates of confirmed osteonecrosis of the jaw (35 [4%]) than was clodronic ac
167 agent associated with bisphosphonate-related osteonecrosis of the jaw (BRONJ), has been reported as c
169 acid group, there were 17 confirmed cases of osteonecrosis of the jaw (cumulative incidence, 1.1%; 95
170 recent years, new drugs that can also cause osteonecrosis of the jaw (e.g., some monoclonal antibodi
177 oradionecrosis (ORN), and medication-related osteonecrosis of the jaw (MRONJ) with histopathological
178 ors in the development of medication-related osteonecrosis of the jaw (MRONJ), a severe debilitating
180 perties but are linked to medication-related osteonecrosis of the jaw (MRONJ), particularly concernin
187 l fracture, atypical femoral fracture (AFF), osteonecrosis of the jaw (ONJ), and esophageal cancer.
188 ta regarding atrial fibrillation, bone pain, osteonecrosis of the jaw (ONJ), atypical fractures, and
189 issues, inappropriate femoral fractures, and osteonecrosis of the jaw (ONJ), the pathophysiological m
194 sion under Adalimumab therapy presented with osteonecrosis of the jaw after suspended oral and intrav
195 tients analysable for safety, three (1%) had osteonecrosis of the jaw and 15 (5%) hypocalcaemia.
198 or hypocalcemia, and there were no cases of osteonecrosis of the jaw and no adverse reactions to the
200 te proactive adjudication of every potential osteonecrosis of the jaw by an international expert pane
203 d case series described clinical features of osteonecrosis of the jaw in patients with cancer who wer
206 eons described 104 patients with cancer with osteonecrosis of the jaw in the medical literature and i
207 e conclude that the mechanism of Zol-induced osteonecrosis of the jaw involves disruption of DC immun
214 2%] of 697 vs 172 [24%] of 704) but rates of osteonecrosis of the jaw were low in both groups (nine [
218 his reason, the term "bisphosphonate-related osteonecrosis of the jaw" has been replaced with "medica
220 28 (5%) patients had positively adjudicated osteonecrosis of the jaw, four (1%) had atypical femur f
221 e dreaded adverse effect of bisphosphonates, osteonecrosis of the jaw, has been widely reported and d
222 res indicate worse disability), incidence of osteonecrosis of the jaw, kidney dysfunction, skeletal m
234 udies have linked bisphosphonate therapy and osteonecrosis of the jaws (ONJ), but neither causality n
237 ing bisphosphonates are at greatest risk for osteonecrosis of the jaws; these patients represent 94%
240 ely evaluated the incidence of fractures and osteonecrosis (ON) on two consecutive pediatric ALL prot
242 2 hips of 91 patients who had no evidence of osteonecrosis or diseases involving bone marrow, no hist
245 nces in the rates of infections, symptomatic osteonecrosis, or other complications during the second
246 n among mice that did versus did not develop osteonecrosis (P < 0.0001); in mice with osteonecrosis,
248 aring surface was evaluated subsequently for osteonecrosis-positive hips on both sets of images.
250 , lower baseline CD4, HCV coinfection, prior osteonecrosis, prior fracture, cardiovascular disease, a
251 rticoid (GC) induced osteoporosis (GIOP) and osteonecrosis remain a significant health issue with few
253 in situ death of isolated segments of bone (osteonecrosis) suggesting that glucocorticoid excess, th
254 , treatments are associated with symptomatic osteonecrosis that disproportionately affects adolescent
255 lop osteonecrosis (P < 0.0001); in mice with osteonecrosis, the associated vessels showed transmural
256 ween TBMES and osteonecrosis; in joints with osteonecrosis, this was comparable to background noise,
258 included allergic reactions to asparaginase, osteonecrosis, thrombosis, and disseminated fungal infec
259 To understand possible linkage of ischemic osteonecrosis to the ER stress, a surgery-induced animal
260 between glutamate receptor polymorphisms and osteonecrosis, using a large discovery cohort and 2 vali
261 y (grade 1-4) versus symptomatic (grade 2-4) osteonecrosis was 71.8% versus 17.6%, respectively.
262 imited and full examinations for presence of osteonecrosis was 98.9% (177 of 179 cases; kappa, 0.97).
268 No significant difference between TBMES and osteonecrosis was found for MTT (P = .09) and PF (P = .7
270 tic osteonecrosis, and severe (grade 3 or 4) osteonecrosis was linked to poor dexamethasone clearance
273 about the risks of bisphosphonate-associated osteonecrosis were disseminated by national regulatory a
275 wed progression into characteristic signs of osteonecrosis were included in the irreversible group.