Local Bone Loss Research Articles

Stimulation of bone resorption by lipoxygenase metabolites of arachidonic acid

We have studied the effect of leukotrienes, (LT): B 4, C 4, D 4 and E 4 and the hydroxyeicosatetraenoic acids (HETEs) 5-HETE and 12-HETE on bone respiration in vitro . Resorption was measured by colorimetric assay of calcium released from neonatal mouse calvaria maintained in organ culture for 72h. All the LTs and HETEs stimulated bone resorption, with optimum responses at picomolar or nanomolar concentrations. The responses were biphasic, with a decreasing effect at higher concentrations. In contrast, prostaglandin E 2 (PGE 2) stimulated resorption only at 10nM and above. Indomethacin partially inhibited resorption by LTB4, LTC4 and LTD4, but did not affect resorption stimulated by LTE4, 5-HETE nd 12-HETE. These results indicate that liposygenase products of arachidonic acid are highly potent bone resorbing factors and may play an important role in the localised bone loss associated with inflammatory lesions.

Tetracycline therapy in patients with early juvenile periodontitis.

Tetracycline therapy, when used in conjunction with surgery or root planing, has been shown to be effective in controlling the progression of juvenile periodontitis. However, the ability of tetracycline alone to control the disease has not been assessed. The present study evaluated the effects of tetracycline therapy, with supragingival plaque control, on clinical attachment levels and radiographic bone height in patients with clinical and radiographic evidence of juvenile periodontitis. The four patients (mean age 15.2 +/- 0.3 yrs) each demonstrated loss of attachment of greater than or equal to 2 mm at one or more probing sites and had accompanying radiographic evidence of early localized bone loss. Following an initial clinical evaluation consisting of pocket depths, attachment levels and standardized radiographs, the patients received systemic tetracycline therapy (1 gm/day for three to six weeks) and oral hygiene instruction. At the completion of antibiotic therapy, patients received a supragingival professional prophylaxis every two weeks for three months, whereupon the initial evaluation was repeated. On comparing the initial and three-month clinical and radiographic data, there were significant decreases in clinical and radiographic measurements. For a total of 85 affected probing sites around 26 teeth, 79% decreased in pocket depth by greater than or equal to 2 mm (with no sites increasing in pocket depth) and 69% gained clinical attachment (with only one site losing attachment of 1 mm). Radiographic measurements revealed an increase in both the height and area of coronal alveolar bone. The findings indicated that six weeks of systemic tetracycline therapy combined with supragingival plaque control was effective in the initial control of early juvenile periodontitis.

Bone metabolism in patients with rheumatoid arthritis.

Bone metabolism in patients with rheumatoid arthritis is reviewed. Two different entities are recognised: 1) a localised periarticular bone loss, due to inflammatory processes and 2) a generalised increased bone turnover, ultimately leading to a loss of axial bone mass. The mechanism of this loss of axial bone is not completely understood; probably immobilisation is the most important factor. The influence of certain drugs is discussed.

Dental disease in hill sheep: An abattoir survey

Heads from 478 aged sheep of a predominantly hill breed population were examined in detail for evidence of dental disease, using both soft and hard tissue measurements around incisor and cheek teeth. Almost 60 per cent of this population (all over 2 1 2 years of age and with a mean age between 7 and 8 years) had either loose or missing teeth. Malalignment of cheek teeth and/or incisors was also common. Pocketing was seen in 87 per cent of the population and was significantly correlated with tooth looseness. There was also a significant relationship between incisor and specific cheek tooth pocket depths. Whilst local alveolar bone loss was found, it was not a reflection of more general skeletal deterioration. The survey confirms the high incidence of broken mouth in the national flock and shows that wherever incisor problems occur there is a likelihood that cheek tooth disease is also present, a relationship not readily appreciated clinically.

Lymphokine-mediated bone resorption requires endogenous prostaglandin synthesis.

Enhanced synthesis of prostaglandin (PG) E by explanted fetal rat bones was initiated by lymphocyte-conditioned media but not by physiological levels of parathyroid hormone. Rapid release of PGE from bone occurred only when the lymphokine was present. Synthesis of PGE preceded and was necessary for the bone resorption caused by the lymphokine preparation. Local production of prostaglandins in response to inflammatory cell or tumor-derived factors may in part be responsible for the localized bone loss that occurs in certain pathological states.

Book Reviews

Book reviews in this article: Mechanisms of Localized Bone Loss, eds. John E. Horton, Thomas M. Tarpley & William F. Davis. The Cranium of the Newborn Infant: An Atlas of Tomography and Anatomical Sections, by Robert H. Pierce, Michael W. Mainen & James F. Bosma. Clinical Outline of Oral Pathology: Diagnosis and Treatment, by Lewis R. Eversole. 1978 Year Book of Dentistry, eds. M. L. Hale, S. P. Hazen, R. E. Moyers, D. F. Redig, H.B. G. Robinson & S. I. Silverman. Gingivitis, 2nd edn., by W. G. Cross. Sweeteners and Dental Caries, eds. James H. Shaw & Gerassimos G. Roussos. Methods of Caries Prediction, eds. Basil G. Bibby & Roald J. Shern. Self Assessment Manual # 1. Oral Surgery and Pathology, Bertram Cohen, David Mason & David Poswillo. Skin Manifestations in Visceral Cancer, Vladimir C. Andreev. Application of the International Classification of Diseases to Dentistry and Stomatology (ICD‐DA). Preventive Dentistry, Leon M. Silverstone. Color Atlas of Periodontology, J. Dermot Strahan & Ian M. Waite.

Localized Bone Loss on the Mesial of First Molars: A Potential Contributing Factor.

Journal of PeriodontologyVolume 47, Issue 8 p. 461-463 Localized Bone Loss on the Mesial of First Molars: A Potential Contributing Factor† Knox McMillan, Knox McMillan USNR Box 18, NAVSTA, Rota, Spain, F.P.O. New York, N. Y. 09540.Search for more papers by this author Knox McMillan, Knox McMillan USNR Box 18, NAVSTA, Rota, Spain, F.P.O. New York, N. Y. 09540.Search for more papers by this author First published: 01 August 1976 https://doi.org/10.1902/jop.1976.47.8.461Citations: 3 † The opinions or assertions contained herein are those of the author and are not to be understood as official or as reflecting the views of the Navy Department. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume47, Issue8August 1976Pages 461-463 RelatedInformation

Generalised and localised bone loss in patients with rheumatoid arthritis.

Osteoporosis was studied in 307 patients with "definite" or "classical" rheumatoid arthritis by measurement of the clavicular cortical thickness (C.C.T.). Bone loss, as measured by this index, fell with advancing age, and was significantly greater than in non-rheumatoid control subjects matched for age and sex. Bone loss from the clavicles was not greater in patients treated with corticosteroid drugs. Loss of bone from the clavicle correlated with osteoporosis in other parts of the skeleton, as determined by the femoral and metacarpal indices. This suggests that osteoporosis in rheumatoid arthritis is a generalised phenomenon rather than a localised process secondary to adjacent joint inflammation.

The effects of phosphonates on experimental osteoporosis

The effect of a diphosphonate, EHDP, was studied in two experimental models in the rat: local immobilization osteoporosis and systemic cortisone-induced osteoporosis. EHDP was able to prevent the local bone loss brought about by surgical immobilization of the left hind limb, but was ineffective in preventing the systemic bone loss produced by cortisone administration. The most prevalent action of EHDP is the production of large amounts of osteoid; it seems to have little effect on bone resorption. The lack of consistent findings in both models suggests that systemic bone-losing disorders cannot be extrapolated from local bone atrophy.

Ecology of alveolar bone loss

The literature is replete with evidence suggesting that, with advancing age, there is an increased alveolar bone loss. However, there is also clinical evidence that not all persons show bone loss with age. This suggests that either (1) there is physiologic bone loss, which means that it is pathologic to have no bone loss with age, or (2) that a few elderly persons without bone loss are well and the majority have pathologic bone loss. Granted that the latter is the more tenable hypothesis, the question is “Why?” Evidence has been presented to show that there is a correlation between local factors and bone loss, irrespective of host state. Data have been offered to show that there is a relationship between host state and alveolar bone loss, irrespective of local challenges. Evidence has been cited to show that the relationship of age and alveolar bone loss is heightened when viewed in the light of both host and local states. However, it should be emphasized that these are only relationships and do not necessarily prove cause and effect. A study has been presented, using vitamin C as the experimental model, to show that the host state may play a causative role in the genesis of alveolar bone loss.