ライフサイエンスコーパス: attachment loss

1 disease status (defined by pocket depth and attachment loss).

2 lth, gingivitis and mild periodontitis (<25% attachment loss).

3 forecasting patient vulnerability to future attachment loss.

4 wo interproximal sites with >/=3 mm clinical attachment loss.

5 and the presence of abfractions or increased attachment loss.

6 o interproximal sites with >or=3 mm clinical attachment loss.

7 earance of an abfraction lesion or increased attachment loss.

8 isease are moderately predictive of clinical attachment loss.

9 nificantly associated with increased risk of attachment loss.

10 n subgingival microorganisms and the risk of attachment loss.

11 0.82) was associated with decreased risk of attachment loss.

12 e teeth having >or=5 mm of proximal clinical attachment loss.

13 l protocols underestimated the prevalence of attachment loss.

14 Smoking history was associated with attachment loss.

15 isk factors for, early stages of periodontal attachment loss.

16 dontal disease was assessed by mean clinical attachment loss.

17 odontitis disease categories and periodontal attachment loss.

18 ot fracture that can lead to rapid localized attachment loss.

19 levels in smokers with moderate to advanced attachment loss.

20 4 versus 1.5, P <0.05) than subjects without attachment loss.

21 rom periodontal sites demonstrating advanced attachment loss.

22 razilian population had a high occurrence of attachment loss.

23 ith increases in risk for each millimeter in attachment loss.

24 re found to be a risk factor for periodontal attachment loss.

25 e mineral density being associated with less attachment loss.

26 loss or 3 gingivitis sites with no clinical attachment loss.

27 vergrowth and various degrees of periodontal attachment loss.

28 one mineral density of the spine and hip and attachment loss.

29 eth/Missing Teeth; and millimeters of mesial attachment loss.

30 clinical and radiographic evidence of severe attachment loss.

31 elation (r = 0.40, P<0.001) between ICTP and attachment loss.

32 ared to diminish with increasing periodontal attachment loss.

33 probing, probing depths (PDs), and clinical attachment loss.

34 GCF may be "protective" against periodontal attachment loss.

35 with IFCC units, clinical probing depth, and attachment loss.

36 nterval = -1.5 to 0.0, P = 0.05) in clinical attachment loss.

37 ffect against bone breakdown and periodontal attachment loss.

38 ding on probing, probing depth, and clinical attachment loss.

39 epths in the 4- to 5-mm range and 1- to 2-mm attachment loss.

40 vident signs of gingival inflammation but no attachment loss.

41 0.25 mm (95% CI, 0.14 to 0.36) for clinical attachment loss, 13.1% (95% CI, 8.1% to 18.1%) for bleed

42 mm versus 2.7 mm; P = 0.006) and more severe attachment loss (2.6 mm versus 1.7 mm; P = 0.015).

43 per-patient percentages of tooth sites with attachment loss (AL) > or = 2 mm and > or = 3 mm from ba

44 th (PD) >/=5 mm and >2 teeth with a clinical attachment loss (AL) >/= 6mm, and the group with mild pe

45 dy reported that the progression of clinical attachment loss (AL) >/=3 mm during a 6-year period was

46 a probing depth (PD) >or=4 mm or a clinical attachment loss (AL) >or=4 mm.

47 174 subjects, 59 with moderate mean clinical attachment loss (AL) (2.39+/-0.29 mm) and 50 with high A

48 on between duration of fluoxetine intake and attachment loss (AL) (R(2) = -0.321, P <0.05).

49 = -0.60 mm, 95% CI = -0.85 to -0.36 mm), and attachment loss (AL) (WMD = -0.35 mm, 95% CI = -0.65 mm

50 The measurements included evaluation of attachment loss (AL) and alveolar bone level (ABL) on th

51 on and increased probing depths and clinical attachment loss (AL) and could be stratified into multip

52 itis was defined by combinations of clinical attachment loss (AL) and periodontal probing depth (PD)

53 Attachment loss (AL) and probing depth (PD) were measure

54 One periodontist assessed attachment loss (AL) and probing depth (PD).

55 calized or generalized, based upon degree of attachment loss (AL) and types of affected teeth.

56 were classified as RP (n = 17) based on mean attachment loss (AL) and/or >3 sites with AL >/=2.5 mm a

57 surements of probing depth (PD) and clinical attachment loss (AL) at interproximal sites.

58 index (PI), probing depth (PD), and clinical attachment loss (AL) in patients with AgP, whereas hTERT

59 the presence of A. actinomycetemcomitans and attachment loss (AL) in sub-Saharan countries.

60 Clinical attachment loss (AL) is one of the most important measur

61 he impact of alcohol consumption on clinical attachment loss (AL) progression over a period of 5 year

62 ions between chronic smoking and periodontal attachment loss (AL) through ages 26, 32, and 38 years,

63 The quality of alveolar bone and attachment loss (AL) were measured by microcomputed tomo

64 P), probing depth (PD) >/=4 mm, and clinical attachment loss (AL) were measured; marginal bone loss (

65 Dental caries, tooth loss, and periodontal attachment loss (AL) were recorded for each of the parti

66 bleeding on probing, probing depth (PD), and attachment loss (AL) were recorded, and GCF samples were

67 Probing depth and clinical attachment loss (AL) were recorded.

68 index (GI), probing depth (PD), and clinical attachment loss (AL) were recorded.

69 bing (BOP), probing depth (PD), and clinical attachment loss (AL) were recorded.

70 Periodontal probing depth (PD) and attachment loss (AL) were summarized using the Centers f

71 inimum amount of KT is not needed to prevent attachment loss (AL) when optimal plaque control is pres

72 istributions of probing depth (PD), clinical attachment loss (AL), and bleeding on probing (BOP).

73 g teeth (M), periodontal pocket depth (PPD), attachment loss (AL), and gingival bleeding in addition

74 -probing (BOP), probing depth (PD), clinical attachment loss (AL), and marginal-bone-loss (MBL) were

75 val index (GI), probing depth (PD), clinical attachment loss (AL), and percentage of sites with bleed

76 rt evaluates periodontal probing depth (PD), attachment loss (AL), and tooth loss from 584 HIV-seropo

77 ng (BOP), probing depth (PD) >3 mm, clinical attachment loss (AL), marginal bone loss (MBL), and numb

78 Probing depth (PD), attachment loss (AL), plaque, and gingivitis (GI) were a

79 periodontal examination included periodontal attachment loss (AL), probing depth, bleeding on probing

80 os, probing depths (PD), calculated clinical attachment loss (AL), the presence of gingival recession

81 n was observed between glycemia and clinical attachment loss (AL), whereas a negative correlation bet

82 ase status was measured by the mean clinical attachment loss (AL).

83 ion included probing depth (PD) and clinical attachment loss (AL).

84 on probing (BOP) and combination of BOP and attachment loss (AL).

85 surements of probing depth (PD) and clinical attachment loss (AL).

86 g on probing (BOP); 4) probing depth; and 5) attachment loss (AL).

87 eeding indexes, probing depths, and clinical attachment loss (AL).

88 h (PD); 2) bleeding on probing (BOP); and 3) attachment loss (AL).

89 cal parameters of probing depth and clinical attachment loss (AL).

90 Clinical attachment loss (AL); probing depth; decayed, missing, a

91 ng [BOP], probing depth [PD] > or =4 mm, and attachment loss [AL] > or =3 mm) and a healthy papilla,

92 nts were categorized as healthy (no clinical attachment loss [AL] or bleeding on probing) or as havin

93 d 3) periodontal status (probing depth [PD], attachment loss [AL]).

94 probing [BOP], probing depth [PD], clinical attachment loss [AL], and marginal bone loss [MBL]) and

95 probing [BOP], probing depth [PD], clinical attachment loss [AL], and marginal bone loss [MBL]) were

96 eriodontal inflammatory parameters (clinical attachment loss [AL], marginal bone loss [MBL], plaque i

97 e variables were gingival bleeding, clinical attachment loss, alveolar bone loss, and presence of sub

98 risk factors for progression of periodontal attachment loss among male Sri Lankan tea laborers who p

99 estimates suggested a greater mean clinical attachment loss among obese individuals, a higher mean b

100 At week 8, the placebo group had 3.89 mm of attachment loss and 73.8% radiographic bone remaining.

101 ning; and the 80 microg/kg group had 1.05 mm attachment loss and 85.5% bone remaining.

102 The 15 microg/kg group had 1.99 mm attachment loss and 89.5% bone remaining; the 30 microg/

103 emaining; the 30 microg/kg group had 0.84 mm attachment loss and 92.5% bone remaining; and the 80 mic

104 althy adult subjects with varying degrees of attachment loss and a minimum of 20 teeth were examined

105 bited statistically significant increases in attachment loss and facial/lingual recession, but the di

106 dontitis and higher prevalence and extent of attachment loss and gingival recession than non-smokers,

107 as chronic periodontitis may have increased attachment loss and gingival recession when compared to

108 Individuals with both high attachment loss and high tooth loss (odds ratio [OR] 1.5

109 evalent CHD compared to individuals with low attachment loss and low tooth loss, while controlling fo

110 of stress and depression was associated with attachment loss and missing teeth.

111 l as a greater decrease in alveolar bone and attachment loss and MMP-9 immunoreactivity, with systemi

112 Attachment loss and mobility at previous examination wer

113 Generalized attachment loss and mobility of the teeth were observed.

114 1) via an algorithm that considered clinical attachment loss and probe depth and 2) via standardized

115 Attachment loss and probing depth were assessed at 2 sit

116 ng the percentages of teeth with > or = 5 mm attachment loss and probing depth, > or = 3 mm gingival

117 heir remaining teeth affected by > or = 3 mm attachment loss and probing depth, respectively.

118 investigated using a combination of clinical attachment loss and probing depth.

119 es of gingivitis exhibited associations with attachment loss and probing depth.

120 reduce the rate and/or extent of periodontal attachment loss and radiographic bone loss in a ligature

121 iodontitis aims to halt progressive bone and attachment loss and regenerate periodontal structures.

122 III data, we evaluated associations between attachment loss and serum cotinine after adjustment by s

123 ot completely remove the correlation between attachment loss and serum-cotinine level (r = 0.075, n=

124 Both subjects with attachment loss and those with attachment gain had a hig

125 e related to clinically measured periodontal attachment loss and warranted classifying their validity

126 l status (bleeding on probing, calculus, and attachment loss); and OHRQoL/oral health impact profile.

127 ontacts in centric relation (PCCR), clinical attachment loss, and abfraction lesions.

128 garding interactions among occlusal factors, attachment loss, and abfractions.

129 eatment Needs, plaque scores, probing depth, attachment loss, and bone level.

130 ntly reduces inflammation, connective tissue attachment loss, and bone resorption that are induced by

131 alveolar bone area, alveolar bone level, and attachment loss, and immunohistochemical analysis, which

132 ated with periodontal disease, more clinical attachment loss, and increased production of inflammator

133 x values, fewer furcation involvements, less attachment loss, and less alveolar crest height loss.

134 bleeding on probing, probing depth, clinical attachment loss, and marginal bone loss) were measured,

135 e index, bleeding on probing, probing depth, attachment loss, and marginal bone loss), and number of

136 bleeding on probing, probing depth, clinical attachment loss, and plaque index.

137 of plaque (PI), gingival inflammation (GI), attachment loss, and probing depth (PD) could be used to

138 is associated with oral bone loss, clinical attachment loss, and tooth loss in older men.

139 mproved, he has removed the jewelry, and the attachment loss appears to have stabilized.

140 stigating features such as probing depth and attachment loss, are needed for the appropriate classifi

141 bjects who exhibited abfractions had similar attachment loss as those subjects without abfraction les

142 ull-mouth, six-site periodontal probing, and attachment loss assessment.

143 Moderate to severe periodontal attachment loss associated with cemental or cementodenti

144 oxidative stress in relation to periodontal attachment loss associated with ligature-induced experim

145 Patterns of attachment loss at interproximal and buccal/lingual site

146 e examined clinically to assess the clinical attachment loss at six sites per tooth.

147 3 species at a site could not predict future attachment loss at that specific site.

148 to-enamel junction-gingival margin distance (attachment loss), bleeding on probing, and furcation inv

149 on findings included probing depth, clinical attachment loss, bleeding on probing (BOP), plaque index

150 each visit included probing depth, clinical attachment loss, bleeding on probing, and gingival index

151 gingival index, plaque index, probing depth, attachment loss, bleeding on probing, calculus index, an

152 d changes in probing pocket depths, clinical attachment loss, bleeding on probing, gingival index, fa

153 ons of IL-17 concentrations with periodontal attachment loss, but not with current smoking.

154 s defined as two or more teeth with clinical attachment loss (CAL) > or = 5 mm.

155 dence of tooth loss, progression of clinical attachment loss (CAL) >/= 3 mm, and progression of resto

156 odontitis [proportion of sites with clinical attachment loss (CAL) >= 3 mm] were estimated using robu

157 We focused on individuals with mean clinical attachment loss (CAL) above the 80th percentile within e

158 disease severity was represented by clinical attachment loss (CAL) and interproximal alveolar bone lo

159 iodontal disease was represented by clinical attachment loss (CAL) and was dichotomized as < or =1.5

160 16-19 ng/mL] had significantly less clinical attachment loss (CAL) gain (-0.43 mm vs. 0.92 mm, p < 0.

161 This study describes the clinical attachment loss (CAL) in an adult Brazilian population a

162 closan dentifrice for prevention of clinical attachment loss (CAL) in xerostomic patients.

163 s between systemic bone density and clinical attachment loss (CAL) of the soft tissue surrounding the

164 on of bleeding on probing (BOP) and clinical attachment loss (CAL) was estimated using the parametric

165 More severe clinical attachment loss (CAL) was observed in the 3D RSA measure

166 absence of supragingival plaque and clinical attachment loss (CAL) were assessed at the same 12 sites

167 epth, gingival bleeding on probing, clinical attachment loss (CAL), and alveolar bone loss (ABL) from

168 an percentage of sites with >/=2 mm clinical attachment loss (CAL), and PHS II, based on the median p

169 s assessed with probing depth (PD), clinical attachment loss (CAL), gingival recession (REC), and ble

170 half-mouth dental measures included clinical attachment loss (CAL), pocket depth (PD), calculus, plaq

171 se was assessed using interproximal clinical attachment loss (CAL), probing depth (PD), alveolar cres

172 d two Pd markers- probing depth and clinical attachment loss (CAL).

173 It was grouped based on clinical attachment loss (CAL): 0 to 2 mm (normal-slight), 3 to 4

174 PD], bleeding on probing [BOP], and clinical attachment loss (CAL); P < 0.05).

175 l measurements (probing depth [PD], clinical attachment loss [CAL], and bleeding on probing [BOP]) we

176 The depth of the horizontal component of attachment loss can vary depending on the external tooth

177 valid surrogate is satisfied: Does clinical attachment loss capture the effect of periodontal treatm

178 asurements of changes in lifetime cumulative attachment loss (cLCAL) and changes in probing depth (cP

179 1.04 to 2.00) of having more severe clinical attachment loss compared to those consuming <10 drinks/w

180 1.02 to 1.80) of having more severe clinical attachment loss compared to those consuming <5 drinks/we

181 ortions of lower bicuspid teeth demonstrated attachment loss compared with other sites.

182 dies demonstrated increased pocket depth and attachment loss compared with patients lacking the antib

183 Sera from patients with periodontal attachment loss contain higher concentrations of IgG ant

184 istometric analyses to analyze the amount of attachment loss, crestal bone loss, connective tissue at

185 trabecular separation, and connective tissue attachment loss (CTAL) as well as reduced bone volume th

186 ater bone volume and lower connective tissue attachment loss (CTAL) than group EP (P < 0.05).

187 ssive dynamic pathologic process that causes attachment loss, destroys the alveolar bone supporting a

188 n the estimates of prevalence of periodontal attachment loss due to different partial recording proto

189 a difference in disease activity (> or =2 mm attachment loss) from 19.3% (untreated) to 7.2% (treated

190 After establishment of attachment loss, full-mouth SRP was performed in all dog

191 Although panelists considered attachment loss, furcation invasions, and mobility as "v

192 eline including assessment of probing depth, attachment loss, gingival index, and plaque index.

193 In this study of subjects with minimal attachment loss, gingival inflammation was associated wi

194 loss was defined as > or = 10% of sites with attachment loss > 3 mm and high tooth loss was defined a

195 crease in women with four or more sites with attachment loss > or = 2 mm or > or = 3 mm (P < 0.05, 0.

196 r more sites with probing depth and clinical attachment loss > or = 5 mm following initial therapy an

197 with AgP if they had four or more teeth with attachment loss > or =4 mm or > or =5 mm, respectively.

198 of 0.82 in predicting prevalence of clinical attachment loss >/= 3 mm at one or more sites.

199 robing, probing depth >/= 4 mm, and clinical attachment loss >/= 3 mm), and, when available, a 'healt

200 ) with periodontal disease (>/= 3 sites with attachment loss >/= 4 mm) were studied.

201 with a probing depth >/=5 mm and a clinical attachment loss >/=3 mm at the same sites.

202 rproximal probing depth >/=6 mm and clinical attachment loss >/=4 mm, were randomized into two groups

203 depth >/=5 mm (1.37; 1.14 to 1.65), clinical attachment loss >/=5 mm (1.19; 1.00 to 1.41), alveolar b

204 were applied, number of teeth with clinical attachment loss >/=6 mm and presence of severe periodont

205 and 3) had a probing depth >4 mm or clinical attachment loss >2 mm for >/= 1 site.

206 elated with increased probing depth >5 mm or attachment loss >2 mm, whereas the amount of F. nucleatu

207 predicted the number of teeth with clinical attachment loss >5 mm.

208 titis (RP; probing depth >=4 mm and clinical attachment loss >=3 mm, together with the presence of bl

209 twice the frequency of moderate to advanced attachment loss (> or =3 mm).

210 of probing pocket depth (>/=5 mm), clinical attachment loss (>/=5 mm), mobility (>/=0.5 mm), and alv

211 ata (>/= 2 interproximal sites with >/= 3 mm attachment loss, >/= 2 interproximal sites with probing

212 Subjects with high levels of mean clinical attachment loss had significantly higher mean CRP levels

213 iduals without a history of periodontitis or attachment loss has been made that included all tooth ty

214 al factors affecting horizontal component of attachment loss have not been previously assessed.

215 bolite of nicotine, should not be related to attachment loss, if self-reported smoking captures the e

216 ne loss and, to a lesser extent, to clinical attachment loss, implicating postmenopausal osteopenia a

217 attachment remaining following simulation of attachment loss in 2 mm increments.

218 There was no clinical attachment loss in group A, either at baseline or after

219 radiographically intact patient with minimal attachment loss in older age; presence of "frank" period

220 s study was to determine whether the rate of attachment loss in periodontally healthy subjects in a p

221 s that clinically significant progression of attachment loss in posterior tooth sites occurs as a fre

222 ctive treatment to SRP to reduce progressive attachment loss in subjects with CP.

223 logic structure of the dentition, and severe attachment loss in the primary dentition have not been d

224 d, and is also influenced by the severity of attachment loss in the study population.

225 rable for controlling the high occurrence of attachment loss in this population.

226 itis diagnostic parameters (pocket depth and attachment loss) in both saliva and supragingival plaque

227 tooth loss are significantly associated with attachment loss incidence (ALI) and 2) quantify the effe

228 The final adjusted model indicated that attachment loss increased significantly with age (X2 = 7

229 The results demonstrated that attachment loss increased with age.

230 The prevalence of severe attachment loss increased with decreasing control of dia

231 itis) reduced the progression of periodontal attachment loss (intent-to-treat analysis) and the sever

232 The association between smoking and attachment loss is even stronger when the definition of

233 Although average buccal attachment loss is greater on ST-site teeth (P = 0.016),

234 The bias in the assessment of attachment loss is influenced by the partial recording d

235 Increasing attachment loss is related to decreasing root surface ar

236 Lifetime cumulative attachment loss (LCAL) > or =1 mm was measured on the me

237 between the outcomes of lifetime cumulative attachment loss (LCAL) and probing depth (PD) in relatio

238 robing, probing depth </= 4 mm, and clinical attachment loss </= 4 mm).

239 ooth-level bleeding on probing at sites with attachment loss<or=2 mm as the dependent variable, were

240 Subjects with mean attachment loss (MAL) > or = 3.0 mm had a higher risk of

241 An increase in attachment loss may represent active periodontal infecti

242 al examination including full-mouth clinical attachment loss measurements, probing depths, plaque ind

243 al index, probing depth, bleeding index, and attachment loss measurements.

244 seful tool for its treatment by reducing the attachment loss observed after simple enucleation of the

245 Although some attachment loss occurred, the reentry demonstrated a hig

246 odazole), eliminated kinetochore-microtubule attachment (loss of Nuf2), or stabilized microtubule plu

247 with measures of decayed teeth, periodontal attachment loss of > or = 4 mm, and the number of missin

248 y ("survived") or progressed to disease with attachment loss of >2 mm or bone loss (failed to "surviv

249 of 4 mm or greater, in sites with a clinical attachment loss of 2 mm or greater, and in sites coinfec

250 nths later, the patient returned with severe attachment loss of sudden onset and gingival recession a

251 During periods of periodontal attachment loss, one of the most significant cellular ch

252 rom either 3 periodontal sites with advanced attachment loss or 3 gingivitis sites with no clinical a

253 he monitoring period, 44 subjects had either attachment loss or attachment gain.

254 =45 years of age with minimal or no proximal attachment loss or pocketing.

255 ased odds of subsequent (year 2) periodontal attachment loss (OR = 1.67; P = 0.01 and OR = 1.50; P =

256 ed 2.5 times for each millimeter of clinical attachment loss (OR = 2.50; 95% CI: 1.24 to 5.07).

257 time were significantly associated with mean attachment loss over 20 years.

258 ression greatly improve the ability to model attachment loss over a longer period in untreated period

259 significant model resulted when the rate of attachment loss over the first 6 months, baseline PI, an

260 ave reported on risk factors for periodontal attachment loss over time in subjects with no home or pr

261 l nut use were significantly associated with attachment loss over time.

262 ositively related to severity of periodontal attachment loss (P <0.001).

263 expression was also directly correlated with attachment loss (P <0.05, Spearman test).

264 had greater overall mean PD (P = 0.001) and attachment loss (P = 0.006) and fewer bleeding on probin

265 in both arches) without appreciable clinical attachment loss (PHS Class 1).

266 ch) elderly adults with appreciable clinical attachment loss (PHS Class 4) were significantly more li

267 Periodontal measures included attachment loss, pocket depth, gingival bleeding, and nu

268 he bias and sensitivity in the assessment of attachment loss prevalence for these protocols were asse

269 Although panelists considered attachment loss, probing depths, and mobility somewhat l

270 Clinical attachment loss, probing depths, and percentage of perio

271 asurement were used to measure bone loss and attachment loss, respectively.

272 PRP evaluated, uniformly across the range of attachment loss severity level.

273 6) were observed in participants with severe attachment loss than in other participants.

274 jects under maintenance displayed more rapid attachment loss than periodontally healthy subjects in a

275 with a history of COPD had more periodontal attachment loss than subjects without COPD (1.48 +/- 1.3

276 action lesions had significantly more buccal attachment loss than teeth without abfraction lesions (P

277 individuals who have experienced periodontal attachment loss than those who are periodontally healthy

278 tient, teeth with abfractions presented more attachment loss than those without abfractions.

279 A clinical examination revealed moderate attachment loss that was localized to the palatal side o

280 Clinical examination revealed moderate attachment loss that was localized to the palatal side o

281 Using a >/= 5-mm clinical attachment loss threshold, seven studies provided data,

282 3% to 12% gain in sensitivity for 2 to 5 mm attachment loss thresholds for the three site half-mouth

283 periodontitis, such as pockets and clinical attachment loss to the OIL.

284 study if probing depth (PD) was </=3 mm and attachment loss was </=2 mm.

285 of treatment was 2 mm; whereas up to 1 mm of attachment loss was considered acceptable.

286 High attachment loss was defined as > or = 10% of sites with

287 More periodontal attachment loss was detected in African-American and His

288 Within subjects, the mean attachment loss was determined for teeth with and withou

289 he percentage of sites with no sign of early attachment loss was underestimated by up to 11%.

290 The associations with JP and the extent of attachment loss were even stronger when both P. gingival

291 and mean percentage of sites with > or =4 mm attachment loss were independent predictors for elevated

292 g in the 1980s, direct measures for clinical attachment loss were made in national health surveys and

293 gingival index, probing depth, and clinical attachment loss were measured, and gingival biopsies wer

294 Periodontitis and mean attachment loss were positively associated with bleeding

295 The results provided evidence that moderate attachment losses were informative on tooth mortality.

296 minations, including periodontal probing and attachment loss, were performed at the fourth clinical v

297 ue index, gingival index, probing depth, and attachment loss when compared with the control group.

298 imal sites, lower molars most frequently had attachment loss, whereas at buccal/lingual sites, higher

299 ere frequently associated with interproximal attachment loss, whereas lower bicuspid teeth were at ri

300 periodontal ligament breakdown, and gingival attachment loss, which are the clinical symptoms of peri