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 and the presence of abfractions or increased attachment loss.

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

5 earance of an abfraction lesion or increased attachment loss.

6 isease are moderately predictive of clinical attachment loss.

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

8 nificantly associated with increased risk of attachment loss.

9 n subgingival microorganisms and the risk of attachment loss.

10 0.82) was associated with decreased risk of attachment loss.

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

12 l protocols underestimated the prevalence of attachment loss.

13 Smoking history was associated with attachment loss.

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

15 dontal disease was assessed by mean clinical attachment loss.

16 odontitis disease categories and periodontal attachment loss.

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

18 levels in smokers with moderate to advanced attachment loss.

19 4 versus 1.5, P <0.05) than subjects without attachment loss.

20 rom periodontal sites demonstrating advanced attachment loss.

21 razilian population had a high occurrence of attachment loss.

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

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

24 e mineral density being associated with less attachment loss.

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

26 with IFCC units, clinical probing depth, and 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 GCF may be "protective" against periodontal attachment loss.

34 reater than in the group of subjects with no attachment loss.

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

36 ffect against bone breakdown and periodontal attachment loss.

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

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

39 forecasting patient vulnerability to future attachment loss.

40 wo interproximal sites with >/=3 mm clinical 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 index (GI), probing depth (PD), and clinical attachment loss (AL) were recorded.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

101 Attachment loss and destructive periodontitis were consi

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

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

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

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

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

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

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

109 Attachment loss and mobility at previous examination wer

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

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

112 Attachment loss and probing depth were assessed at 2 sit

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

137 Both the lifetime cumulative attachment loss, as well as attachment loss since young

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

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

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

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

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

143 3 species at a site could not predict future attachment loss at that specific site.

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

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

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

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

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

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

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

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

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

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

154 16-19 ng/mL] had significantly less clinical attachment loss (CAL) gain (-0.43 mm vs. 0.92 mm, p < 0.

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

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

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

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

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

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

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

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

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

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

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

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

167 age, gender, gingival index, probing depth, attachment loss, calculus index, plaque index, and micro

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

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

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

171 1.04 to 2.00) of having more severe clinical attachment loss compared to those consuming <10 drinks/w

172 1.02 to 1.80) of having more severe clinical attachment loss compared to those consuming <5 drinks/we

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

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

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

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

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

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

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

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

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

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

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

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

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

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

187 Prevalence of attachment loss > or = 3 mm was 53.1% for the population

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

205 adiographic alveolar bone height and probing attachment loss has been studied by a number of investig

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

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

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

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

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

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

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

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

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

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

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

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

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

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

220 The results demonstrated that attachment loss increased with age.

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

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

223 that the relationship between bone loss and attachment loss is complex, perhaps because changes in b

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

225 ontal disease diagnostic categories in which attachment loss is exhibited were tested for anti-PC in

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

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

228 Increasing attachment loss is related to decreasing root surface ar

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

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

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

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

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

234 An increase in attachment loss may represent active periodontal infecti

235 ate the first criterion: Are serial clinical attachment loss measurements informative on overall toot

236 Several aspects of the serial attachment loss measurements were related to tooth morta

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

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

239 t the time-dependent changes of the clinical attachment loss measurements.

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

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

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

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

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

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

246 percent of periodontal sites per person with attachment loss of 3 mm or greater (categorized as 0%, >

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

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

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

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

251 =45 years of age with minimal or no proximal attachment loss or pocketing.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

270 etime cumulative attachment loss, as well as attachment loss since young adulthood, of > or = 2 mm or

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

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

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

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

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

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

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

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

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

280 3% to 12% gain in sensitivity for 2 to 5 mm attachment loss thresholds for the three site half-mouth

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

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

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

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

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

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

287 Periodontal attachment loss was measured at two sites per tooth in r

288 We concluded that clinical attachment loss was moderately informative on overall to

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