ライフサイエンスコーパス: giant cell

1 cogen trophoblast and sinusoidal trophoblast giant cells.

2 ransform into macrophages and multinucleated giant cells.

3 oblasts I and II, and sinusoidal trophoblast giant cells.

4 extent, epithelioid cells and multinucleated giant cells.

5 GLABROUS11 (HDG11), control the identity of giant cells.

6 macrophages in the formation of foreign body giant cells.

7 ons with abnormal dendritic trees resembling giant cells.

8 DNA content in endoreduplicating trophoblast giant cells.

9 l cortical tuber and its unique constituent, giant cells.

10 ulomatous lymphohistiocytic choroiditis with giant cells.

11 tem cells, and trophoblast stem cell-derived giant cells.

12 le formation of multinucleate bone-resorbing giant cells.

13 s that included macrophages and foreign body giant cells.

14 bility to form TRAP positive, multinucleated giant cells.

15 function of various types of multinucleated giant cells.

16 rophages and the formation of multinucleated giant cells.

17 o failed to form multinucleated foreign body giant cells.

18 iation with multinucleated foreign body-type giant cells.

19 type in the placenta, polyploid trophoblast giant cells.

20 fusion to form surface-damaging foreign body giant cells.

21 ts, and abnormal distribution of trophoblast giant cells.

22 argely restricted to spongiotrophoblasts and giant cells.

23 nstead give rise to an excess of trophoblast giant cells.

24 xtraembryonic tissues, including trophoblast giant cells.

25 on the cell surface of TSCs and trophoblast giant cells.

26 Ns establish feeding sites in roots known as giant cells.

27 ng an area of carcinoma with osteoclast-like giant cells.

28 ifferentiated carcinoma with osteoclast-like giant cells.

29 amyloid by macrophage-derived multinucleated giant cells.

30 ifferentiated carcinoma with osteoclast-like giant cells.

31 the multinucleate and acytokinetic state of giant cells.

32 monolayer permeability and the formation of giant cells 3x to 5x normal size.

33 ranulomatous inflammation with multinucleate giant cells, accompanied by increased accumulation of ne

34 ranulomatous inflammation with multinucleate giant cells, accompanied by increased accumulation of T

35 ecognized in tubers beyond the classic tuber giant cell and demonstrates cell-specific abnormalities

36 OR signaling responses of LECs, resulting in giant cell and LEC permeability responses.

37 l review of surgically resected atria showed giant cell and lymphocytic infiltrates, lymphocytic myoc

38 ia (OP) pattern developed, with foreign-body giant cells and granulomas.

39 y spectral karyotyping, LMP1 induced "outre" giant cells and hypoploid "ghost" cells.

40 OSL1 expression is restricted to trophoblast giant cells and invasive trophoblast cells.

41 imitless differentiation into multinucleated giant cells and provide useful suggestions for the devel

42 how that distinct enhancers are expressed in giant cells and small cells, indicating that these cell

43 e find that Cited2 in sinusoidal trophoblast giant cells and syncytiotrophoblasts is likely to have a

44 eptible hosts addresses establishment of the giant cells and there is limited information on the earl

45 ncaseating granulomas lacking multinucleated giant cells and, in 1 patient, CD68-positive and CD1a-ne

46 arance of large polyploid cells (trophoblast giant cells), and the expression of trophoblast differen

47 ges, wound-healing macrophages, foreign body giant cells, and bone-resorbing osteoclasts.

48 Dysplastic neurons, giant cells, and dysplastic astroglia express high level

49 ass death, diminished numbers of trophoblast giant cells, and failure to yield trophoblast stem (TS)

50 Giant cells are associated with constitutive mammalian t

51 We found that multinucleated giant cells are formed in the inflamed mouse peritoneum

52 brain pathology of TSC, cortical tubers and giant cells are fully developed at late gestational ages

53 Trophoblast giant cells are instrumental in promoting blood flow tow

54 Abnormal multinucleated giant cells are present in the bone marrow of Slc4a2-def

55 hat comprise SIVE lesions and multinucleated giant cells are present in the CNS early, before SIVE le

56 Giant cell arteritis (GCA) and Takayasu's arteritis (TAK

57 Polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) are related inflammatory diso

58 Giant cell arteritis (GCA) causes autoimmune inflammatio

59 This article aims to provide a review of giant cell arteritis (GCA) clinical features, differenti

60 Granuloma formation in giant cell arteritis (GCA) emphasizes the role of adapti

61 Giant cell arteritis (GCA) is an immune-mediated disease

62 Glucocorticoid (GC) therapy for giant cell arteritis (GCA) is effective but requires pro

63 Giant cell arteritis (GCA) is the most common form of va

64 Giant cell arteritis (GCA) is the most common systemic v

65 Giant cell arteritis (GCA) is the most common type of pr

66 ies suggest that extracranial involvement of giant cell arteritis (GCA) may be more extensive than pr

67 conducted a large-scale genetic analysis on giant cell arteritis (GCA), a polygenic immune-mediated

68 In giant cell arteritis (GCA), vasculitic damage of the aor

69 (ESR), and bilateral AION were suggestive of giant cell arteritis (GCA).

70 lasms, inflammation, pituitary apoplexy, and giant cell arteritis (GCA).

71 artery biopsies taken from individuals with giant cell arteritis (GCA).

72 of adjunctive low-dose methotrexate (MTX) in giant cell arteritis (GCA).

73 d cerebrovascular accidents often complicate giant cell arteritis (GCA).

74 Associated with increased RAO were giant cell arteritis (odds ratio [OR], 7.73; CI, 2.78-21

75 -positive results than in patients with GCA giant cell arteritis -negative results ( TAB temporal ar

76 re significantly higher in patients with GCA giant cell arteritis -positive results than in patients

77 is accurate in the initial diagnosis of GCA giant cell arteritis .

78 continue to be the mainstay of treatment for giant cell arteritis and its complications.

79 lthough large vessel inflammatory disorders (giant cell arteritis and Takayasu arteritis) are the mos

80 ulated in inflamed arteries of patients with giant cell arteritis and Takayasu arteritis, and serum l

81 of large-vessel vasculitides, including both giant cell arteritis and Takayasu arteritis, and the aor

82 n clinically available tests: pentraxin-3 in giant cell arteritis and Takayasu's arteritis; von Wille

83 Because intracerebral VZV vasculopathy and giant cell arteritis are strongly associated with produc

84 ological aortic involvement in patients with giant cell arteritis correlates with the significant det

85 Giant cell arteritis has supplanted temporal arteritis a

86 and herpesviruses in temporal arteries with giant cell arteritis have yielded contradictory results.

87 Giant cell arteritis is a granulomatous vasculitis of th

88 rticoid-induced remission of newly diagnosed giant cell arteritis is of no benefit and may be harmful

89 GCA giant cell arteritis was diagnosed or excluded clinicall

90 onsent, 185 patients suspected of having GCA giant cell arteritis were included in a prospective thre

91 atory vasculopathy affecting large arteries (giant cell arteritis).

92 Giant cell arteritis, a chronic autoimmune disease of th

93 vasculitides, such as Takayasu arteritis and giant cell arteritis, affect vital arteries and cause cl

94 ymptoms and 2 of 203 (1.0%) for treatment of giant cell arteritis, and 1 of 193 (0.5%) for the pathop

95 al detachment, acute angle-closure glaucoma, giant cell arteritis, and central retinal artery occlusi

96 er virus (VZV) vasculopathy produces stroke, giant cell arteritis, and granulomatous aortitis, and it

97 g from the vasculitides (Takayasu arteritis, giant cell arteritis, and polyarteritis nodosa) to ather

98 tic arthritis, polymyalgia rheumatica (PMR), giant cell arteritis, ankylosing spondylitis, and Sjogre

99 k factors for RAO in cardiac surgery include giant cell arteritis, carotid stenosis, stroke, hypercoa

100 This issue provides a clinical overview of giant cell arteritis, focusing on diagnosis, treatment,

101 ous arteritis characterizes the pathology of giant cell arteritis, granulomatous aortitis, and intrac

102 biopsy (TAB), performed for the diagnosis of giant cell arteritis, has a low reported rate of complic

103 As in giant cell arteritis, recent evidence supports the role

104 reports have highlighted etiologies such as giant cell arteritis, trauma, neuro-syphilis and demyeli

105 00 have polymyalgia rheumatica, 228,000 have giant cell arteritis, up to 3.0 million have had self-re

106 rely affect the temporal arteries, mimicking giant cell arteritis, while, to our knowledge, the assoc

107 istochemical and gene expression analyses of giant cell arteritis-affected temporal arteries revealed

108 an isolated condition or in association with giant cell arteritis.

109 ith T cells and monocytes from patients with giant cell arteritis.

110 ic infiltrates in patients with panarteritic giant cell arteritis.

111 rosis factor-alpha is present in arteries in giant cell arteritis.

112 ion of patients with large-vessel disease in giant cell arteritis.

113 n the older individuals and in patients with giant cell arteritis.

114 unced in the age-related vasculitic syndrome giant cell arteritis.

115 f 216 respondents (5.1%; 95% CI, 2.2%-8.0%), giant cell arteritis; and 10 of 218 respondents (4.6%; 9

116 disorder; multiple myeloma; acute leukemia; giant cell arteritis; dialysis; esophageal, stomach, pan

117 Giant-cell arteritis (GCA) is a large-vessel vasculitis

118 ment of large arteries is well-documented in giant-cell arteritis (GCA), but the risk for cardiovascu

119 Giant-cell arteritis commonly relapses when glucocortico

120 Giant-cell arteritis frequently poses diagnostic and the

121 Giant-cell arteritis is associated with increased risks

122 rease likelihood of stroke or visual loss in giant-cell arteritis without increasing bleeding complic

123 n show findings relevant to the diagnosis of giant-cell arteritis.

124 ant to the diagnosis of challenging cases of giant-cell arteritis.

125 ations concerning diagnosis and treatment of giant-cell arteritis.

126 ucocorticoid-free remission in patients with giant-cell arteritis.

127 ticoid tapering was studied in patients with giant-cell arteritis.

128 he pathogenesis and organelle dysfunction of giant cells, as well as epilepsy control in patients wit

129 ence of retinal features was associated with giant cell astrocytoma (37.1% vs. 14.6%; P = 0.018), ren

130 more than 35% of patients with subependymal giant cell astrocytoma (SEGA) associated with tuberous s

131 of these proteins in tuber and subependymal giant cell astrocytoma (SEGA) specimens in TSC.

132 , and either serial growth of a subependymal giant cell astrocytoma, a new lesion of 1 cm or greater,

133 uction in volume of the primary subependymal giant-cell astrocytoma, as assessed on independent centr

134 resection or other therapy for subependymal giant-cell astrocytoma.

135 , one astrocytoma (6q), and two subependymal giant cell astrocytomas (16p and 21q).

136 nically definite TSC and either subependymal giant cell astrocytomas (n = 4) or a pilocytic astrocyto

137 Subependymal nodules (SENs) and subependymal giant cell astrocytomas (SEGAs) are common brain lesions

138 ore severe than TSC1, with more subependymal giant cell astrocytomas and angiomyolipomas, higher inci

139 of everolimus in patients with subependymal giant cell astrocytomas associated with tuberous scleros

140 pport the use of everolimus for subependymal giant cell astrocytomas associated with tuberous scleros

141 pport the use of everolimus for subependymal giant cell astrocytomas associated with tuberous scleros

142 In the brain, growth of subependymal giant cell astrocytomas can cause life-threatening sympt

143 therapy resulted in regrowth of subependymal giant cell astrocytomas in one patient.

144 50% reduction in the volume of subependymal giant cell astrocytomas versus none in the placebo group

145 TSC-related cortical tubers or subependymal giant cell astrocytomas, as well as tissue microarrays o

146 more likely to have concomitant subependymal giant cell astrocytomas, renal angiomyolipomas, cognitiv

147 of affected individuals display subependymal giant cell astrocytomas, which can lead to substantial n

148 greater relative to baseline in subependymal giant cell astrocytomas.

149 ificantly reduced the volume of subependymal giant cell astrocytomas.

150 s including angiomyolipomas and subependymal giant cell astrocytomas.

151 rked reduction in the volume of subependymal giant-cell astrocytomas and seizure frequency and may be

152 int was the change in volume of subependymal giant-cell astrocytomas between baseline and 6 months.

153 n is the standard treatment for subependymal giant-cell astrocytomas in patients with the tuberous sc

154 or older with serial growth of subependymal giant-cell astrocytomas were eligible for this open-labe

155 d into a male recipient, among the nuclei of giant cells at sites of osteolysis.

156 targets as well as a better understanding of giant cell biology.

157 Soft-tissue tumours include ganglion cysts, giant-cell cancers and fibromas of the tendon sheath, ep

158 the cell bodies of two neurons, the cerebral giant cell (CGC) and the B2 buccal motor neuron, in the

159 tified modulatory neuron called the cerebral giant cell (CGC).

160 spider silk meshes with increased numbers of giant cells compared with controls with initial decompos

161 ifferentiated carcinoma with osteoclast-like giant cells could be a marker of a poor prognosis.

162 was associated with: 1) lower multinucleated giant cell count (P = 0.04); 2) lower density of mesench

163 we have identified a new mutant with ectopic giant cells covering the sepal epidermis.

164 Resistance destroys the giant cells created in the plant's roots by the nematode

165 y in the promotion of spongiotrophoblast and giant cell differentiation and establish a new mechanism

166 gene resulted in an increase in trophoblast giant cell differentiation, a reduction of the spongiotr

167 gulation of Hox gene expression, trophoblast giant cell differentiation, paternal X chromosome inacti

168 mitotic cell cycle progression and promoting giant cell differentiation, respectively.

169 Intriguingly, formation of giant cells due to failed mitosis/cytokinesis is common

170 We previously reported giant-cell encephalitis in subtype B and C R5 simian-hum

171 : arrest of cell proliferation, formation of giant cells, excessive DNA replication in the absence of

172 od derived macrophage adhesion, foreign body giant cell (FBGC) formation and inflammatory cytokine an

173 gnaling mechanisms modulating multinucleated giant cell formation and function are necessary for the

174 crophage fusion receptor, that contribute to giant cell formation and function.

175 modulation and inhibition of multinucleated giant cell formation and function.

176 tion, macrophage biology, and multinucleated giant cell formation are incompletely understood.

177 diators of adhesion and fusion mechanisms of giant cell formation have been complicated by the wide d

178 aling responses and blocked permeability and giant cell formation in ANDV-infected monolayers.

179 demonstrated to be required for foreign body giant cell formation in the foreign body response.

180 containing NSC23766 attenuated foreign body giant cell formation in vivo.

181 Fusion-mediated giant cell formation is critical for osteoclast maturati

182 , rather than neoplastic, and able to induce giant cell formation similar to that of normal mesenchym

183 nhanced viral replication and multinucleated giant cell formation upon infection of rhesus macrophage

184 elements that are responsible for sustained giant cell formation via receptor activator of NF-kappaB

185 e of actin-based motility and multinucleated giant cell formation were observed between 12 and 18 h p

186 zed by macrophage infiltration, foreign body giant cell formation, and fibrotic encapsulation of the

187 nvolves macrophage activation, proceeding to giant cell formation, fibroblast activation, and collage

188 ANK autocrine loop that determines sustained giant cell formation.

189 ons to regulate IL-4-directed multinucleated giant cell formation.

190 participate in both RANKL- and IL-4-induced giant cell formation.

191 lacked the ability to induce multinucleated giant cell formation.

192 nction with productive viral replication and giant cell formation.

193 afts in the cell membrane, and inhibition of giant-cell formation and release of viral progeny.

194 activity of giant cell pathway genes LOSS OF GIANT CELLS FROM ORGANS, DEFECTIVE KERNEL1, and Arabidop

195 vo formed 'pseudo-organs' containing several giant cells (GCs).

196 a (I-PG) (n = 5), 3) peri-implant peripheral giant cell granuloma (I-PGCG) (n = 9), 4) T-RL (n = 44),

197 (n = 21), and 6) tooth-associated peripheral giant cell granuloma (T-PGCG) (n = 23).

198 ANDV-infected LECs became viable mononuclear giant cells, >4 times larger than normal, in response to

199 us SIV-p28(+) macrophages and multinucleated giant cells had fewer MAC387(+) monocytes/macrophages.

200 We found that the vacuolated giant cells had multiple signs of organelle dysfunction,

201 However, an animal model that replicates giant cells has not yet been described.

202 ifferentiated carcinoma with osteoclast-like giant cells have been described in the literature.

203 nvolving mainly osteoclasts and foreign body giant cells have revealed a number of common factors, fo

204 Giant cells have undergone endoreduplication, a speciali

205 Granulomas with a core containing giant cells, human CD68(+) macrophages, and high bacilli

206 Giant cell identity is established upstream of cell cycl

207 tic neoplasm and the presence of pleomorphic giant cells in an undifferentiated carcinoma with osteoc

208 We found similar vacuolated giant cells in human tuber specimens.

209 extraembryonic ectoderm, and in trophoblast giant cells in the E6.5 embryo.

210 eosinophilic macrophages and multinucleated giant cells in the lung.

211 mbryonic tissue, specifically in trophoblast giant cells in the parietal yolk sac.

212 phages and was unable to form multinucleated giant cells in this cell line.

213 y promotes fusion of human monocytes to form giant cells in vitro, we determined whether A(1)R occupa

214 and fibrin deposition than Cypher; peristrut giant cell infiltration, however, was more frequent in t

215 ntical epidermal cells to differentiate into giant cells interspersed between smaller cells.

216 ar fusion of macrophages into multinucleated giant cells is a distinguishing feature of the granuloma

217 as, aneurysmal bone cysts, osteoid osteomas, giant-cell lesions of bone, bone sarcomas, and metastase

218 a dehydration-rehydration process generated giant cell-like hybrid vesicles, whereas the injection o

219 vour differentiation towards the trophoblast giant cell lineage, whereas lack of Plet1 preferentially

220 unction of osteoclasts (OCs), multinucleated giant cells (MGCs) of the monocytic lineage, is bone res

221 es spontaneously matured into multinucleated giant cells (MGCs), a property not exhibited by monocyte

222 polesis of lymphocytes within multinucleated giant cells (MGCs), MGC death, and fibrinoid necrosis an

223 ing macrophage fusion to form multinucleated giant cells (MNG).

224 bit signs of cytopathology or multinucleated giant cell (MNGC) formation, which were observed in wild

225 tion of granulomas containing multinucleated giant cells (MNGCs) and cell death.

226 ity to induce the formation of multinucleate giant cells (MNGCs) in multiple cell types.

227 to stimulate the formation of multinucleated giant cells (MNGCs).

228 ic tumor featuring prominent osteoclast-like giant cells, mononuclear osteoclast precursors, and spin

229 Our work involved 51 patients with giant cell myocarditis (35 women) aged 52+/-12 years.

230 Giant cell myocarditis (GCM) typically causes fulminant

231 Giant cell myocarditis presented as nonfatal ventricular

232 ended for patients with cardiac sarcoidosis, giant cell myocarditis, and myocarditis associated with

233 cular tachyarrhythmias are characteristic of giant cell myocarditis, but their true incidence, predic

234 In giant cell myocarditis, the risk of life-threatening ven

235 to analyze (1) our experience in diagnosing giant-cell myocarditis and (2) the outcome of patients o

236 Giant-cell myocarditis often escapes diagnosis until aut

237 cutive patients with histologically verified giant-cell myocarditis treated in our hospital since 199

238 Patients with giant-cell myocarditis, eosinophilic myocarditis, or car

239 l biopsies are frequently needed to diagnose giant-cell myocarditis.

240 ogical examination revealed that trophoblast giant cells of aborting mice phagocytosed infected red b

241 Osteoclasts are multinucleated, giant cells of hematopoietic origin formed by the fusion

242 We show that the ectopic giant cells of sec24a-2 are highly endoreduplicated and

243 egions of the genome in parietal trophoblast giant cells (p-TGCs) of the mouse placenta.

244 hat their formation requires the activity of giant cell pathway genes LOSS OF GIANT CELLS FROM ORGANS

245 entiation towards the syncytiotrophoblast or giant cell pathway in Plet1-low and Plet1-high cells, re

246 her cell types can generate a multinucleated giant cell phenotype with bone resorbing activity.

247 nt, complement-dependent, macrophage-derived giant cell reaction that swiftly removes massive viscera

248 n leading to the formation of multinucleated giant cells remains unclear.

249 ic conditions alone enhance permeability and giant cell responses of ANDV-infected MECs and LECs thro

250 lysis of cultured cells and nematode-induced giant cells revealed a failure in mitotic exit, with the

251 ade mineralized tissue, these multinucleated giant cells secrete acid into a resorption lacuna formed

252 inflammation characterized by multinucleated giant cells, some of which displayed elastophagocytosis

253 nvasive spiral artery-associated trophoblast giant cells (SpA-TGCs) surrounding maternal blood vessel

254 r specification of spiral artery trophoblast giant cells (SpA-TGCs) that invade and remodel maternal

255 transcriptionally induced during trophoblast giant cell-specific differentiation.

256 fusogenicity on HSV and cause multinucleated giant cells, termed syncytia.

257 placentation with enrichment in trophoblast giant cells (TGCs) and other trophoblast-derived cell su

258 The mammalian trophoblast giant cells (TGCs) exploit their size to form a barrier

259 tiation defects and fail to form trophoblast giant cells (TGCs) in vitro.

260 The differentiation of murine trophoblast giant cells (TGCs) is well characterised at the molecula

261 last cell lineage and consist of trophoblast giant cells (TGCs) only.

262 ferentiation of blastomeres into trophoblast giant cells (TGCs), suggesting that geminin regulates tr

263 Mature osteoclasts are multinucleated giant cells that are generated from the fusion of circul

264 distinct but largely overlapping subsets of giant cells that are in direct contact with maternal art

265 treated LNCaP-AI cells formed multinucleated giant cells that contain clusters of nuclear vesicles in

266 ferous tubules, forming large multinucleated giant cells that underwent apoptosis.

267 es evidenced no reactivity of osteclast-like giant cells to epithelial markers but showed a positive

268 one-derived light responses combine in these giant cells to signal irradiance over the full dynamic r

269 cells with a diversity of sizes ranging from giant cells to small cells.

270 Giant cell tumor (GCT) of bone is a histologically benig

271 DT) or aggressive fibromatosis, tenosynovial giant cell tumor (TGCT) or diffuse-type pigmented villon

272 n the molecular pathogenesis of tenosynovial giant cell tumor (TGCT) or pigmented villonodular synovi

273 ing in osteosarcoma and, less frequently, in giant cell tumor of bone (GCT).

274 gmented villonodular synovitis (dtPVNS), and giant cell tumor of bone (GCTB).

275 served in DSRCT, solitary fibrous tumor, and giant cell tumor of bone suggests that future evaluation

276 PURPOSE OF REVIEW: Giant cell tumor of tendon sheath and pigmented villonod

277 Tenosynovial giant-cell tumor (TGCT) and pigmented villonodular synov

278 th the pathological features of tenosynovial giant-cell tumor.

279 located and highly expressed in tenosynovial giant cell tumors (TGCTs), and this observation allowed

280 In contrast, in 92% (49/53) of giant cell tumors of bone, we found histone H3.3 alterat

281 tension cohort of patients with tenosynovial giant-cell tumors (extension study).

282 tension study, 12 patients with tenosynovial giant-cell tumors had a partial response and 7 patients

283 Treatment of tenosynovial giant-cell tumors with PLX3397 resulted in a prolonged r

284 (CSF1) gene is elevated in most tenosynovial giant-cell tumors.

285 Diffuse-type tenosynovial giant cell tumour (dt-GCT) of the soft tissue (alternati

286 Giant cell tumour of bone (GCTB) is a very rare, aggress

287 pted seminiferous epithelium, multinucleated giant cells, uncleared apoptotic germ cells and decrease

288 Giant cells undergo endocycles, replicating their DNA wi

289 tive mTOR signaling induces the formation of giant cells via phosphorylation of S6K, and mTOR regulat

290 The percentage of multinucleated giant cells was lower in brain-injured patients without

291 SIV encephalitis lesions and multinucleated giant cells were also CD163 positive.

292 bone were present, but no foreign body-type giant cells were identified.

293 microglia are infected as are multinucleated giant cells when present.

294 essential in patterning the highly elongated giant cells, which are interspersed between small cells,

295 the oocyte of the frog Xenopus tropicalis, a giant cell with an equally giant nucleus.

296 ls except horizontal cells, which persist as giant cells with aberrant centrosome content, DNA damage

297 Numerous pleomorphic giant cells with an immunohistochemical sarcomatoid prof

298 rogenitor cells develop into highly enlarged giant cells with enlarged vacuoles.

299 enty-seven percent of these osteoclasts were giant cells with pyknotic nuclei that were adjacent to s

300 On the remaining surface, multinucleated giant cells with varying intensity of tartrate-resistant