Local Factors in Periodontal Disease

Ramfjord, Sigurd P.

doi:10.14219/jada.archive.1952.0109

Cited by 26 publications

(4 citation statements)

References 59 publications

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“…Open proximal contact can contribute to the periodontal pocket formation, Gingival recession/inflammation, calculus deposition, proximal carious lesions, food impaction, shifting of teeth (mesial drift), and faulty occlusion. [52122] The teeth with open or poorly shaped contacts had significantly higher Periodontal Index scores when compared with teeth that had sound proximal contacts. [5] The crowns with too tight proximal contacts can damage the periodontal tissue or cause improper tooth movement or interfere with the physiological displacement of the teeth and cause wedging of the teeth.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of presence of proximal contacts on recently inserted posterior crowns in different health sectors in Riyadh City, Saudi Arabia

Almalki

Al-Rafee

2019

J Family Med Prim Care

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Background:For the successful outcome of the rehabilitation of the teeth with crown, the proximal contact points play a significant role hence the aim of the present study was to evaluate the presence of proximal contacts on recently inserted crowns in posterior teeth.Methods and Materials:The cross-sectional study was conducted on recently inserted posterior crowns. Clinical assessment of proximal contact points on crowns was made with dental floss, the floss was wrapped around the index fingers of both hands and was passed through the crowns mesial and distal contact points and was categorized as acceptable, open contact points, and tight contact points.Results:In the present study 401 crowns were examined to assess proximal contacts on 788 proximal surfaces. It was found that 522 (66.2%) crowns were in normal proximal contact, 144 (18.3%) showed open proximal contacts, 122 (15.5%) showed tight proximal contacts.Conclusion:Regarding the assessment of proximal contacts, the study showed that a significant number of crowns had open or tight proximal contacts. Specialists and residents were able to perform better in providing the optimum proximal contacts.

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Section: Discussionmentioning

confidence: 99%

Evaluation of presence of proximal contacts on recently inserted posterior crowns in different health sectors in Riyadh City, Saudi Arabia

Almalki

Al-Rafee

2019

J Family Med Prim Care

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“…Easlick (57) carried out a comprehensive review of the dental focal infection theory and found that it was supported only by personal opinions. Chilton (45) noted that ‘there is very little information of a statistically reliable nature on the epidemiologic characteristics of periodontal disease’; Ramfjord (137) complained that the evidence for the effect of local factors on periodontal disease was based on ‘clinical impression rather than scientific investigation’; and Kerr (95) lamented the never‐ending changes to periodontal disease classifications, stating that ‘committee membership changes yearly as does the nomenclature as each group attempts to incorporate their personal preference or prejudice into the committee report’. In hindsight, Ramfjord (139) reflected on the mid‐1950s as a period when it became ‘painfully evident that the time was ripe to apply scientific methods to research in periodontology and that the authoritarian era was over’.…”

Section: Crisis (1950–1955): Time To Apply Scientific Methods In Perimentioning

confidence: 99%

Periodontal disease epidemiology – learned and unlearned?

Bælum¹,

López²

2013

Periodontology 2000

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The notion of periodontal disease being the major cause of tooth loss among adults was rooted in the focal infection paradigm that dominated the first half of the 20th century. This paradigm was established largely by personal opinions, and it was not until the development of periodontal indices in the mid-1950s that periodontal epidemiology gained momentum. Unfortunately, the indices used suffered from a number of flaws, whereby the interpretation of the research results took the form of circular reasoning. It was under this paradigm that therapeutic and preventive intervention for periodontal diseases became entirely devoted to oral hygiene, as poor oral hygiene and older age were understood to explain nearly all the variation in disease occurrence. In the early 1980s, studies appeared that contradicted the concepts of poor oral hygiene as the inevitable trigger of periodontitis and of linear and ubiquitous periodontitis progression, whereby periodontal epidemiology was led into a relatively short-lived high-risk era. At this time, it became evident that old scourges continue to haunt periodontology: the inability to agree in operational clinical criteria for a periodontitis diagnosis and the inability to devise both a meaningful and a useful classification of periodontal diseases based on nominalist principles. The meager outcome of the high-risk era led researchers to resurrect the focal infection paradigm, which is now dressed up as periodontal medicine. Unfortunately, these developments have left the core of periodontology somewhat disheveled and deserted.

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“…Among the researchers supporting this supposition are Rosebury (1947), Waerhaug (1952), Ramfjord (1952), Bibby (1953), Schultz-Haudt (1956), MacDonald (1960MacDonald ( , 1962, Wentz {1960), Arnim (1964), Schneider (1966, and Toto (1968). The hypothesis implicating bacteria as etiologic agents does not apply to every situation however.…”

Section: Bacteria As Etiologic Agents Of Periodontal Diseasementioning

confidence: 99%