ライフサイエンスコーパス: chronic periodontitis

1 flap debridement (OFD) for the management of chronic periodontitis.

2 ) is a keystone pathogen in the aetiology of chronic periodontitis.

3 inical parameters and OHRQL of patients with chronic periodontitis.

4 nate in the inflammatory infiltrate of human chronic periodontitis.

5 es, and influencing factors in patients with chronic periodontitis.

6 hanges, but these changes are not evident in chronic periodontitis.

7 NLRP3 transcription were modulated in human chronic periodontitis.

8 scaling and root planning (Q-SRP) in severe chronic periodontitis.

9 mically healthy individuals with generalized chronic periodontitis.

10 ting active periodontitis, and 2) predicting chronic periodontitis.

11 c anaerobe, is a major causative organism of chronic periodontitis.

12 diagnostic abilities, together or alone, in chronic periodontitis.

13 genesis of bone resorption in aggressive and chronic periodontitis.

14 s (metanephrine and total metanephrines) and chronic periodontitis.

15 gical periodontal treatment in patients with chronic periodontitis.

16 individuals without obesity with generalized chronic periodontitis.

17 mics revealed MZB1 as a potent candidate for chronic periodontitis.

18 s between 7% and less than 9%, and untreated chronic periodontitis.

19 of intrabony defects (IBDs) in patients with chronic periodontitis.

20 he oral microorganisms associated with human chronic periodontitis.

21 l osteopenic females with moderate-to-severe chronic periodontitis.

22 re related to the occurrence and severity of chronic periodontitis.

23 ith type 2 diabetes and moderate to advanced chronic periodontitis.

24 atment of intrabony defects in patients with chronic periodontitis.

25 ms of periodontal disease, most closely with chronic periodontitis.

26 sal osteopenic women with moderate to severe chronic periodontitis.

27 e characteristic of many diseases, including chronic periodontitis.

28 has never been investigated in patients with chronic periodontitis.

29 lay an important role in the pathogenesis of chronic periodontitis.

30 atment of intrabony defects in patients with chronic periodontitis.

31 ng status were recorded for 56 patients with chronic periodontitis.

32 RP) of individuals with moderate-to-advanced chronic periodontitis.

33 ss index >30 kg/m(2)) patients affected with chronic periodontitis.

34 cted, with a diagnosis of generalized slight chronic periodontitis.

35 perceived high by most patients treated for chronic periodontitis.

36 g it as a potential adjunctive treatment for chronic periodontitis.

37 pase-independent AIF is also significant for chronic periodontitis.

38 onizer of subgingival sites in patients with chronic periodontitis.

39 he most suitable salivary miRNA biomarker in chronic periodontitis.

40 miR143-3p as a novel salivary biomarker for chronic periodontitis.

41 o predict treatment outcome of patients with chronic periodontitis.

42 F + HA in treatment of IBDs in patients with chronic periodontitis.

43 abits periodontal pockets and contributes to chronic periodontitis.

44 their numbers are elevated in patients with chronic periodontitis.

45 ere, seven with moderate, and four with mild chronic periodontitis.

46 n be recommended in the management of severe chronic periodontitis.

47 Chronic periodontitis, a destructive inflammatory disord

48 s are significantly related to the status of chronic periodontitis, age, gender, and CVDs.

49 erella forsythia is strongly associated with chronic periodontitis, an inflammatory disease of the to

50 mblages from 25 individuals with generalized chronic periodontitis and 25 periodontally healthy indiv

51 y healthy patients >45 years of age (30 with chronic periodontitis and 30 without periodontitis) were

52 od from a patient diagnosed with generalized chronic periodontitis and a healthy control.

53 Forty-five patients with chronic periodontitis and a total of 164 screw-typed imp

54 A sample of 236 patients with chronic periodontitis and clinical depression were asses

55 Twenty-two patients with advanced chronic periodontitis and displaying one deep intrabony

56 IL-21 levels were compared between chronic periodontitis and healthy gingival tissues and c

57 Patients with chronic periodontitis and intraoral Porphyromonas gingiv

58 robiota of smokers versus never-smokers with chronic periodontitis and matched probing depths (PDs) u

59 Taiwan, 5,510 patients with newly diagnosed chronic periodontitis and participated in therapies were

60 in situ adaptive degradation in response to chronic periodontitis and peri-implantitis.

61 me individual were obtained from adults with chronic periodontitis and screened for their ability to

62 ntal diagnosis ranged from healthy to severe chronic periodontitis, and for whom "checkerboard" DNA-D

63 es and their associations among age, gender, chronic periodontitis, and patient-reported cardiovascul

64 vated in gingival tissues from patients with chronic periodontitis as compared with healthy tissues (

65 Infection by the chronic periodontitis-associated pathogen Porphyromonas

66 surgery needs is evaluated in patients with chronic periodontitis before and after completion of non

67 D, and clinical and microbial parameters of chronic periodontitis before and after treatment.

68 s is associated with IL-6 genetic factors in chronic periodontitis cases.

69 ears) periodontal treatment in patients with chronic periodontitis (ChP) and to compare it with the c

70 Chronic periodontitis (ChP) is a prevalent inflammatory

71 gulated and 40 downregulated known miRNAs in chronic periodontitis compared to healthy controls, of w

72 Thirteen patients with generalized severe chronic periodontitis completed the study.

73 45 patients with chronic periodontitis comprising 164 screw-typed implant

74 ival crevicular fluid (GCF) of patients with chronic periodontitis contains galactose (Gal)-deficient

75 Inflammatory conditions, such as chronic periodontitis, could disrupt this homeostasis, a

76 aggressive periodontitis (AP group), 40 with chronic periodontitis (CP group), and 50 periodontally h

77 givitis (G group, n = 20), and patients with chronic periodontitis (CP group, n = 20).

78 rs (DAI), and absent in melanoma 2 (AIM2) in chronic periodontitis (CP versus healthy) (H) tissues.

79 severe forms of the more moderate phenotype chronic periodontitis (CP) (993 cases, 1,419 controls).

80 ingivitis (n = 15), and patients with severe chronic periodontitis (CP) (n = 15) without any systemic

81 king individuals with gingivitis (n = 20) or chronic periodontitis (CP) (n = 20) and periodontally he

82 Patients with aggressive (AgP) (n = 24) and chronic periodontitis (CP) (n = 34) as well as healthy c

83 um were obtained from 47 adult patients with chronic periodontitis (CP) and 10 healthy controls.

84 samples were collected from 19 patients with chronic periodontitis (CP) and 16 control individuals wi

85 biopsies were obtained from 17 patients with chronic periodontitis (CP) and 18 periodontally healthy

86 viduals were included in this study, 20 with chronic periodontitis (CP) and 22 classified as periodon

87 onuclear cells (PBMCs) from 25 patients with chronic periodontitis (CP) and 25 healthy individuals we

88 Twenty-six patients with T2DM and chronic periodontitis (CP) and 26 without T2DM with CP w

89 One hundred ten patients with chronic periodontitis (CP) and 50 healthy controls were

90 rance Database 2000 for 71,182 patients with chronic periodontitis (CP) and 71,182 controls without p

91 ntal treatment in 40 patients with COPD with chronic periodontitis (CP) and a history of >/=1 infecti

92 ss MDA levels in the saliva of patients with chronic periodontitis (CP) and acute coronary syndrome (

93 rase reverse transcription (hTERT) enzyme in chronic periodontitis (CP) and aggressive periodontitis

94 is difficult to differentiate some cases of chronic periodontitis (CP) and aggressive periodontitis

95 hy patients and patients with gingivitis and chronic periodontitis (CP) and correlates these levels w

96 odontal clinical parameters of patients with chronic periodontitis (CP) and diabetes mellitus (DM).

97 among non-smoking and smoking patients with chronic periodontitis (CP) and generalized aggressive pe

98 ta from individuals with aggressive (AgP) or chronic periodontitis (CP) and healthy controls (HC), as

99 xidative DNA damage marker, in patients with chronic periodontitis (CP) and hyperlipidemia.

100 generalized aggressive periodontitis (GAgP), chronic periodontitis (CP) and in patients with no histo

101 ary syndrome (ACS) subjects with and without chronic periodontitis (CP) and its regulation of the inn

102 e existence of an association between severe chronic periodontitis (CP) and nailfold microvascular, g

103 Chronic periodontitis (CP) and rheumatoid arthritis (RA)

104 -8) patterns in smokers and non-smokers with chronic periodontitis (CP) and test the utility of basel

105 al papilla are investigated in patients with chronic periodontitis (CP) and TGF-beta1 29C/T gene poly

106 Patients with chronic periodontitis (CP) and those with healthy period

107 cemic and metabolic control in patients with chronic periodontitis (CP) and type 2 diabetes mellitus

108 propolis supplementation in individuals with chronic periodontitis (CP) and type 2 diabetes mellitus

109 loss (MBL) when compared with patients with chronic periodontitis (CP) and/or healthy patients (HPs)

110 DM and chronic periodontitis (CP) are associated with each othe

111 oriasis (PS), psoriatic arthritis (PsA), and chronic periodontitis (CP) are the most common chronic i

112 Rheumatoid arthritis (RA) and chronic periodontitis (CP) are the most common chronic i

113 althy individuals and patients with moderate chronic periodontitis (CP) before and 6 weeks after peri

114 e macrophage activation pathways involved in chronic periodontitis (CP) by the detection of the indir

115 Genome-wide association studies (GWAS) of chronic periodontitis (CP) defined by clinical criteria

116 s also wanted to check whether patients with chronic periodontitis (CP) exhibit different modulations

117 eralized aggressive periodontitis (GAgP), or chronic periodontitis (CP) groups.

118 Chronic periodontitis (CP) has a genetic component, part

119 The low-grade oral infection chronic periodontitis (CP) has been implicated in corona

120 oncentrations in the saliva of patients with chronic periodontitis (CP) has not been explored despite

121 y, genome-wide association studies (GWAS) of chronic periodontitis (CP) have been unsuccessful in dis

122 study investigates whether susceptibility to chronic periodontitis (CP) in a Thai population is assoc

123 RP) in the treatment of intrabony defects in chronic periodontitis (CP) in patients with type 2 diabe

124 ve periodontitis (AgP) not only differs from chronic periodontitis (CP) in terms of clinical manifest

125 and IL1B (+3954), have been associated with chronic periodontitis (CP) in whites.

126 Chronic periodontitis (CP) is a common oral disease that

127 Chronic periodontitis (CP) is a continuous, reversible s

128 Chronic periodontitis (CP) is an inflammatory condition

129 Chronic periodontitis (CP) is an inflammatory disease in

130 subgingival debridement in the treatment of chronic periodontitis (CP) is controversial.

131 Patients with chronic periodontitis (CP) may yield multiple species of

132 o both HIV infection and senescence, such as chronic periodontitis (CP) need to be studied.

133 nt genome-wide association studies (GWAS) of chronic periodontitis (CP) offer rich data sources for t

134 , thus providing evidence that the impact of chronic periodontitis (CP) on the activity of circulatin

135 ukin (IL)-1beta in patients with generalized chronic periodontitis (CP) or aggressive periodontitis (

136 terleukin (IL)-6, and IL-10 in patients with chronic periodontitis (CP) or aggressive periodontitis (

137 f individuals without periodontitis and with chronic periodontitis (CP) or generalized aggressive per

138 o be significantly elevated in patients with chronic periodontitis (CP) or oral lichen planus (OLP).

139 ) and serum of rheumatoid arthritis (RA) and chronic periodontitis (CP) patients to assess whether cy

140 er in the gingival crevicular fluid (GCF) of chronic periodontitis (CP) patients with type-2 diabetes

141 AgP) patients and compare them with those in chronic periodontitis (CP) patients.

142 ral polymorphonuclear neutrophils (oPMNs) in chronic periodontitis (CP) refractory to conventional th

143 aliva (UWS) of patients with prediabetes and chronic periodontitis (CP) remains uninvestigated.

144 ion of FcGR and TNFA gene polymorphisms with chronic periodontitis (CP) susceptibility has been found

145 A significant proportion of patients with chronic periodontitis (CP) test positive for antiCl, lik

146 s of peripheral neutrophils in patients with chronic periodontitis (CP) that generate different level

147 To elucidate molecular signatures of chronic periodontitis (CP) using gingival tissue samples

148 65 patients with DM with moderate-to-severe chronic periodontitis (CP) was recruited, and 15 individ

149 itis (GAgP) and 71 patients with generalized chronic periodontitis (CP) were compared to 88 periodont

150 oxidant/antioxidant status in patients with chronic periodontitis (CP) who experienced familial Medi

151 ar fluid of patients with moderate-to-severe chronic periodontitis (CP) who have been treated using S

152 a novel predictive marker for patients with chronic periodontitis (CP) with and without type 2 diabe

153 atment of intrabony defects in patients with chronic periodontitis (CP) with type 2 diabetes (DM) com

154 included in this study: 21 individuals with chronic periodontitis (CP), 14 individuals with generali

155 viduals were included in this study; 20 with chronic periodontitis (CP), 20 with generalized aggressi

156 ralized aggressive periodontitis (G-AgP), 20 chronic periodontitis (CP), 26 gingivitis patients, and

157 ubgingival microbiota of cats diagnosed with chronic periodontitis (CP), aggressive periodontitis (AP

158 ding periodontal health (H), gingivitis (G), chronic periodontitis (CP), and aggressive periodontitis

159 agnosed with aggressive periodontitis (AgP), chronic periodontitis (CP), and clinically healthy perio

160 MT in smokers (S) and non-smokers (NS) with chronic periodontitis (CP), and compare them with those

161 e gingival crevicular fluid (GCF) in health, chronic periodontitis (CP), and T2DM.

162 Plasma cells are of special interest in chronic periodontitis (CP), as they represent ~50% of in

163 sfatin in gingival tissue from patients with chronic periodontitis (CP), patients with CP and type 2

164 sion in gingival biopsies from patients with chronic periodontitis (CP), patients with gingivitis (GV

165 In chronic periodontitis (CP), the gene polymorphism of int

166 nts with type 2 diabetes mellitus (T2DM) and chronic periodontitis (CP).

167 urgical periodontal therapy for smokers with chronic periodontitis (CP).

168 of intrabony defects (IBDs) in patients with chronic periodontitis (CP).

169 s biomarkers in smokers and non-smokers with chronic periodontitis (CP).

170 nd adiponectin in patients with obesity with chronic periodontitis (CP).

171 of intrabony defects (IBDs) in patients with chronic periodontitis (CP).

172 d IL-6, are evaluated in human patients with chronic periodontitis (CP).

173 initial periodontal therapy in patients with chronic periodontitis (CP).

174 n average values for patients diagnosed with chronic periodontitis (CP).

175 tes in the peripheral blood of patients with chronic periodontitis (CP).

176 MDA) in blood and saliva of individuals with chronic periodontitis (CP).

177 matory processes in the oral cavity, such as chronic periodontitis (CP).

178 stase (NE) in patients with hypertension and chronic periodontitis (CP).

179 ctivity in serum and saliva of patients with chronic periodontitis (CP).

180 lood cultures from patients with and without chronic periodontitis (CP).

181 of smokers and non-smokers with generalized chronic periodontitis (CP).

182 concentrations of visfatin in patients with chronic periodontitis (CP).

183 hemokines and dendritic cells (DCs) in human chronic periodontitis (CP).

184 uals with aggressive periodontitis (AgP) and chronic periodontitis (CP).

185 vertical defects in smokers with generalized chronic periodontitis (CP).

186 ne irrigation and SRP alone in patients with chronic periodontitis (CP).

187 some additional benefit in the treatment of chronic periodontitis (CP).

188 individuals who are normal weight (NW) with chronic periodontitis (CP).

189 study its clinical effects on patients with chronic periodontitis (CP).

190 eatment of patients with type 2 diabetes and chronic periodontitis (CP).

191 ht to have a faster rate of progression than chronic periodontitis (CP).

192 types of periodontitis, aggressive (AgP) and chronic periodontitis (CP).

193 bonucleic acid (DNA) damage in patients with chronic periodontitis (CP).

194 6 months in patients with severe generalized chronic periodontitis (CP).

195 group of untreated patients with generalized chronic periodontitis (CP).

196 opsies of patients with type 2 diabetes with chronic periodontitis (CP).

197 riodontitis individuals and 25 patients with chronic periodontitis (CP).

198 (SOCS1) gene in smokers and non-smokers with chronic periodontitis (CP).

199 of intrabony defects (IBDs) in patients with chronic periodontitis (CP).

200 oup 2 (n = 20), individuals with generalized chronic periodontitis (CP).

201 SRP) in the treatment of moderate and severe chronic periodontitis (CP).

202 en with polycystic ovary syndrome (PCOS) and chronic periodontitis (CP).

203 bony defect (IBD) treatment in patients with chronic periodontitis (CP).

204 of intrabony defects (IBDs) in patients with chronic periodontitis (CP).

205 intrabony defects (IBDs) in individuals with chronic periodontitis (CP).

206 ided into two groups: 1) 24 individuals with chronic periodontitis (CP); and 2) 23 individuals withou

207 into three groups: 1) healthy (control); 2) chronic periodontitis (CP); and 3) myocardial infarction

208 lelic discrimination assay in AgP (n = 200), chronic periodontitis (CP, n = 190), and healthy patient

209 ivary cotinine) smokers and non-smokers with chronic periodontitis (CP: n = 13) or aggressive periodo

210 y individuals (control; n = 20), generalized chronic periodontitis (CP; n = 21), and generalized aggr

211 sive periodontitis [AgP], and the group with chronic periodontitis [CP]) and 15 volunteers who exhibi

212 ncluding aggressive periodontitis [AgP], and chronic periodontitis [CP]) and periodontal health.

213 n shamma users and non-users [controls] with chronic periodontitis [CP]) remains uninvestigated.

214 ls (27 healthy controls and 27 patients with chronic periodontitis [CP]) were enrolled in the study.

215 ive for poor oral hygiene, 95% sensitive for chronic periodontitis (defined as at least two sites wit

216 yromonas gingivalis, a principal pathogen in chronic periodontitis, did not induce NKT cell activatio

217 3 (IL-33) can differentiate individuals with chronic periodontitis from individuals with healthy peri

218 f these species in subjects with generalized chronic periodontitis (GChP; n = 30), generalized aggres

219 donic acid (AA) in patients with generalized chronic periodontitis (GCP) and compare these results wi

220 Finnish dentate adults: 84 with generalized chronic periodontitis (GCP), 65 with localized chronic p

221 al signs: 1) control; 2) AMI; 3) generalized chronic periodontitis (GCP); and 4) GCP + AMI.

222 IL-21 was overexpressed in chronic periodontitis gingival tissues and correlated wi

223 Group AgP), and 20 patients with generalized chronic periodontitis (Group CP) were included in this s

224 response of patients with generalized severe chronic periodontitis (GSCP) treated with one-stage, ful

225 Forty patients diagnosed with severe chronic periodontitis had subgingival samples harvested

226 (SRP) has been proposed for the treatment of chronic periodontitis; however, its effectiveness and cl

227 scaling and root planing (SRP) for treating chronic periodontitis in patients with type 2 diabetes.

228 nct to scaling and root planing for treating chronic periodontitis in smokers.

229 nces (P <0.05) were recorded by diagnosis of chronic periodontitis in the a* coordinate when comparin

230 estigated the interest of adults affected by chronic periodontitis in undergoing orthodontic treatmen

231 a higher prevalence of oral diseases (e.g., chronic periodontitis) in aged populations have received

232 tained from 32 otherwise healthy, non-smoker chronic periodontitis individuals and 25 systemically an

233 asma levels of IL-33 could not differentiate chronic periodontitis individuals and periodontally heal

234 rations of IL-33 were significantly lower in chronic periodontitis individuals than in healthy indivi

235 Chronic periodontitis is a chronic disease of the period

236 Chronic periodontitis is a local inflammatory disease in

237 Chronic periodontitis is controlled without antibiotics

238 Chronic periodontitis is induced by a dysbiotic microbio

239 Chronic periodontitis is linked to systemic inflammation

240 urther examined in localized and generalized chronic periodontitis (LCP and GCP).

241 ronic periodontitis (GCP), 65 with localized chronic periodontitis (LCP), and 81 controls without per

242 n of type I NKT cells in aggressive, but not chronic, periodontitis lesions in vivo.

243 healthy controls (n = 10) and patients with chronic periodontitis (n = 17) was investigated.

244 thy individuals (n = 2) and individuals with chronic periodontitis (n = 2) was done via immunohistoch

245 trolled trial was conducted in patients with chronic periodontitis (N = 22) presenting at least three

246 recovered from separate patients with severe chronic periodontitis (n = 50) before treatment, were su

247 Sixty patients with chronic periodontitis on 6-month PMT intervals to be fol

248 fold; caspase-3, 6.8-fold; Xiap: 2.5-fold in chronic periodontitis) (P < 0.05), highlighting their po

249 wenty patients (13 males and 7 females) with chronic periodontitis participated in this prospective,

250 ized controlled clinical trial comprising 20 chronic periodontitis patients (mean age: 35.9 years) ha

251 les of gingival biopsies were collected from chronic periodontitis patients (n = 10) and controls (n

252 ples collected from an independent set of 16 chronic periodontitis patients and 16 periodontally heal

253 e expression of IL-21 in gingival tissues of chronic periodontitis patients and correlate/associate t

254 with three parallel arms (#NCT04038801), 60 chronic periodontitis patients were randomly assigned to

255 Sixty-one chronic periodontitis patients, each contributing a 2- o

256 Forty-two chronic periodontitis patients, each contributing a 2-wa

257 ated in human gingival tissue specimens from chronic periodontitis patients, further confirming the b

258 yperreactivity in terms of ROS production in chronic periodontitis patients.

259 RF) in the treatment of intrabony defects in chronic periodontitis patients.

260 ily in ASC-deficient THP1 cells with that in chronic periodontitis patients.

261 virus may be associated with inflammation in chronic periodontitis patients.

262 ealth, gingivitis/peri-implant mucositis, or chronic periodontitis/peri-implantitis.

263 Patients diagnosed with severe generalized chronic periodontitis (periodontitis stage 3/4) were inc

264 ecession, aggressive or acute periodontitis, chronic periodontitis, periodontosis, accretions, other

265 Indications that were analyzed included: chronic periodontitis, plaque-induced gingivitis, aggres

266 hogens, including a key etiological agent of chronic periodontitis, Porphyromonas gingivalis, infect

267 eptible to periodontitis were diagnosed with chronic periodontitis prior to implant therapy.

268 Forty individuals with severe chronic periodontitis received periodontal surgery, dail

269 Fifty-two individuals with chronic periodontitis receiving non-surgical periodontal

270 s bone healing in preclinical studies and in chronic periodontitis, represents a potential treatment

271 ontal treatment (ST) in patients with severe chronic periodontitis (SCP).

272 Use of statins on adult patients with chronic periodontitis shows a positive effect on their p

273 oup with 5 periodontally healthy sites and 5 chronic periodontitis sites.

274 tment (SRP) outcomes in patients with severe chronic periodontitis (stage 3/4 generalized periodontit

275 h ex vivo-isolated blood mDCs and serum from chronic periodontitis subjects and healthy controls.

276 milar migratory profile; moreover, sera from chronic periodontitis subjects expressed elevated levels

277 Thirty-nine chronic periodontitis subjects were randomly assigned to

278 Ex vivo-isolated mDCs from the blood of chronic periodontitis subjects, but not healthy controls

279 lood neutrophils isolated from patients with chronic periodontitis, suggesting that oral neutrophils

280 A major etiological agent of chronic periodontitis, the Gram-negative bacterium Porph

281 hogen Porphyromonas gingivalis, which causes chronic periodontitis, the most prevalent dysbiosis-driv

282 val samples harvested from human healthy and chronic periodontitis tissues (Apaf-1, 19.2-fold; caspas

283 controlled trial, 85 patients diagnosed with chronic periodontitis underwent different treatment prot

284 A total of 73 individuals with chronic periodontitis underwent scaling and root planing

285 Thirty non-smoking patients suffering severe chronic periodontitis were allocated to this randomized,

286 Individuals with chronic periodontitis were classified as RP (n = 17) bas

287 Twenty-four patients with chronic periodontitis were divided randomly into three g

288 s and six females, aged 25 to 45 years) with chronic periodontitis were enrolled in the study.

289 linical study, data from 34 individuals with chronic periodontitis were evaluated after full-mouth SR

290 Twenty non-smoking patients with severe chronic periodontitis were included in the study.

291 defects in healthy non-smoking patients with chronic periodontitis were randomly divided in control (

292 17 non-T2DM subjects with generalized severe chronic periodontitis were recruited along with 20 perio

293 y-eight systemically healthy volunteers with chronic periodontitis were recruited and monitored clini

294 Thirty-five patients with chronic periodontitis were selected for the split-mouth

295 Fifty-one adult volunteers with generalized chronic periodontitis were treated by full-mouth SRP usi

296 Twenty-six patients (52 sites) with chronic periodontitis were treated either with autologou

297 of systemic antibiotics in the treatment of chronic periodontitis whereas 52.6%, 55.3%, 18.4% of the

298 nts with type 2 diabetes mellitus (t2DM) and chronic periodontitis who participated in the Diabetes a

299 al therapy in >/= 10 patients diagnosed with chronic periodontitis with a follow-up period of >/= 2 y

300 been studied predominantly in patients with chronic periodontitis with limited data available regard