How does aging affect the periodontium, periodontal disease progression, and your therapy?

What evidence is there that older people respond differently to etiologic factors or to therapy?

  1. Reynolds Mark A. : Modifiable risk factors in periodontitis: at the intersection of aging and disease. Periodontology 2000, Vol. 64, 2014, 7–19
  2.  Lindhe J, Socransky S, Nyman S, et al : Effect of age on healing following periodontal therapy. J. Clin. Periodontol. 12:774-787, 1985.

Hormonal Factors – Pregnancy

What is the effect of progesterones and estrogens on the periodontium?

Is periodontal disease more severe in _____ and why?

  1. puberty
  2. pregnant patients
  1. Kornman, K., Loesche, W: The subgingival microbial flora during pregnancy. J Periodont Res 15:111, 1980
  2. Adriaens, L., et al: Does Pregnancy have an impact on the subgingival microbiota .J Periodontol 2009; Vol 80, No 1, 72-81
  3. Mascarenhas, P., et al: Influence of sex hormones on the periodontium. J Clin Periodotnol 2003; 30: 671 – 681
  4. Taichman, L., et al: Oral Contraceptives and Periodontal Diseases: rethinking the association based upon analysis of national Health and Nutrition Examination Survey Data. J Periodontol 2005;76: 1374 – 1385


Hormonal Factors – Puberty

  1. Sutcliffe P. A longitudinal study of gingivitis and puberty. J. Periodontal Res 7:52-58, 1972.
  2. Sooriyamoorthy M, Gower DB : Hormonal influences on gingival tissue: Relationship to periodontal disease. J. Clin. Periodontol. 16:201-208, 1989.
  3. Mombelli A, Lang NP, Burgin WB, Gusberti FA. Microbial changes associated with the development of puberty gingivitis. J. Periodontal Res. 25: 331-338,1990.
  4. Oh T-J, Eber R, Wang H-L: Periodontal diseases in the child and adolescent.J Clin Periodontol 2002; 29: 400–410.


Do you make specific nutritional recommedations to your patients? If so, what are the recommendations? When are they made? Defend them.

What group(s) of patients in our society is(are) most likely to be suffering from a nutritional deficiency?

Discuss the role of nutrition in:

  1. periodontal disease progression and severity
  2. wound healing
  1. Tarana Singh Dang, Mark Walker, Dianne Ford and Ruth A. Valentine: Nutrigenomics: the role of nutrients in gene expression Periodontology 2000, Vol. 64, 2014, 154–160
  2. Kuzmanova D, Jansen IDC, Schoenmaker T, Nazmi K, Teeuw WJ, Bizzarro S, Loos BG, Velden van der U. Vitamin C in plasma and leucocytes in relation to periodontitis. J Clin Periodontol 2012; 39: 905–912
  3. Evans GH. Effect of liquid protein diet on collagen metabolism of the gingival of young rats. J. Periodontol. 54:101-106, 1983.
  4. Munoz CA, Kiger RD, Stephens JA, Kim J, Wilson AC. Effects of a nutritional supplement on periodontal status. Compendium 22:425-438, 2001.
  5. Siegel C, et al. Conditional oral scurvy due to megavitamin C withdrawal. J Periodontol. 53:453-455, 1982.
  6. Leggott P, Robertson PB, Rothman DL, et al : The effect of controlled ascorbic acid depletion and supplementation on periodontal health. J. Periodontol 57:480 – , 1986.
  7. Nishida, M., Grossi, S: Calcium and the risk for periodontal disease. J Periodontol 71; 1057 – 1066, 2000
  8. Nishida, M., Grossi, S et al: Dietary Vitamin C and the risk for periodontal diseas. J Periodotntol 71; 1215 – 1223, 2000
  9. Neiva, R., et al: Effects of vitamin – B complex supplementation on periodontal wound healing. J Periodontol 2005; 76: 1084 – 1091
  10. El-Sharkawy H, Aboelsaad N, Eliwa M, Darweesh M, Alshahat M, Kantarci A, Hasturk H, Van Dyke TE. Adjunctive treatment of chronic periodontitis with daily dietary supplementation with omega-3 Fatty acids and low-dose aspirin. J Periodontol. 2010 Nov;81(11):1635-43.
  11. Iwasaki M, Yoshihara A, Moynihan P, Watanabe R, Taylor GW, Miyazaki H. Longitudinal relationship between dietary ω-3 fatty acids and periodontal disease. Nutrition2010 Nov-Dec;26(11-12):1105-9
  12. Esaki M, Morita M, Akhter R, Akino K, Honda O. Relationship between folic acid intake and gingival health in non-smoking adults in Japan. Oral Dis. 2010 Jan;16(1):96-101.


Other Nutritional Factors

  1. Tezal M, Grossi SG, Ho AW, Genco RJ. The effect of alcohol consumption on periodontal disease. J Periodontol 72:183-189, 2001.
  2. Tezal, M., Ho A., Grossi, S., Genco, R. Alcohol consumption and periodontal diesease . The Third National Health and Nutrition Examination Survey. J Clin Periodontol, 2004, Jul; 31 (7): 484 -8
  3. Amaral, C et al. The relationship between alcohol dependence and periodontal disease. J Periodontol 2008; 79: 993 – 998
  4. Bartold, P et al: Periodontitis and rheumatoid arthritis. A Review. J Periodontol 2005; 11 (suppl): 2066 – 2074


What diagnostic signs are indications of HIV / AIDS?

What effect does HIV / AIDS have on periodontal diseases?

  1. Patton LL, McKaig RG, Eron Jr. JJ. Oral manifestations of HIV in a southeast USA population. Oral Diseases 4:164-169, 1998
  2. Scheutz F., et al. Is there an association between periodontal condition and HIV infection? J Clin Periodontol. 24: 580-587, 1997.
  3. Smith GLF, Cross DL, Wray D. Comparison of periodontal disease in HIV seropositive subjects and controls. (I). Clinical features. J Clin Periodontol 22:558-568, 1995.CC
  4. Robinson PG, Boulter A, Birnbaum W, Johnson NW. A controlled study of relative periodontal attachment loss in people with HIV infection. J Clin Periodontol 27:273-276, 2000
  5. Vastardis S, Yukna RA, Fidel PL Jr, Leigh JE, Mercante DE. Periodontal disease in HIV-positive individuals: Association of periodontal indices with stages of HIV disease. J Periodontol 74: 1336 -1341, 2003
  6. Murray PA, Grassi M, Winkler JR : The microbiology of HIV-associated periodontal lesions. J. Clin. Periodontol. 16:636-642, 1989.
  7. Zambon JJ, Reynolds HS, Genco RJ. Studies of the subgingival microflora in patients with acquired immunodeficiency syndrome. J. Periodontol. 61:699-704, 1990
  8. Rams TE, Andriolo M Jr, Falk D, et al: Microbiological study of HIV-related periodontitis. J. Periodontol. 62: 74 – 81, 1991
  9. Ryder MI. Periodontal management of HIV-infected patients. Periodontology 2000. 23: 85-93, 2000.
  10. Navazesh M, Mulligan R, Kono N, Kumar SK, Nowicki M, Alves M, Mack WJ Oral and systemic health correlates of HIV-1 shedding in saliva. J Dent Res. 2010 Oct;89(10):10



How does aging affect the periodontium, periodontal disease progression, and your therapy?

What evidence is there that older people respond differently to etiologic factors or to therapy?



Reynolds 2014           ARTICLE               

Keywords: Modifiable risk factors, periodontitis


P: Review article – Modifiable risk factors in periodontitis “Aging and disease”

Aging and inflammation disease

– Not fully understood
– Free radical theory of aging: the accumulation of free radicals contributes to cellular damage and the development of pathologic disorders. Inflammation is one of the manifestations of oxidative stress
– IL-6 is a central mediator of systemic inflammation, regulating the body temperature set point and the acute phase response. Circulating IL-6 is detectable within 1 hr after surgery or accidental injury. Elevation in IL-6 and in other serum markers of inflammation have been associated with increased mortality in community-dwelling elderly adults

Sex steroids in aging and disease

– In general, women generate more robust and potentially protective humoral and cell-mediated immune responses, whereas men frequently mount a more aggressive and potentially damaging inflammatory immune response to microbial stimuli.
– Estrogen deficiency is a major pathogenetic factor in the bone loss associated with the menopause and postmenopausal osteoporosis.
– Study examining sex steroids in relation to aging, immune function and risk for periodontitis highlighted the pleiotropic effects of sex-steroid hormones on tissues and organs as well as the clinical significance of such alterations on risk for common age-related diseases. Reductions in estrogen represent a major risk factor for osteoporosis and other chronic conditions in women which may help to explain the association between osteoporosis and alveolar bone loss

Smoking and alcohol consumption

– Cigarette smoke contains a complex chemical mixture of combustion compounds that can induce DNA damage, inflammation and oxidative stress.
– Alcohol abuse adversely affects the risk for infectious diseases such as tuberculosis and pneumonia. The overall implact of alcohol consumption on infectious diseases appears to be substantial attributable largely to the adverse effects of alcohol on the immune system.
– The effect of alcohol appears greatest for persons consuming more than 40 g of pure alcohol per day.
– Alcohol consumption may be associated with increased severity of clinical attachment loss.

Obesity, DM, and metabolic syndromes

– Contribute to both inflammation and chronic disease.
– Adipocytes are metabolically active and synthesize and release a number of proinflammatory molecules.
– These chronic conditions share common inflammatory cascades and events as periodontitis.


– Periodontitis and other common chronic inflammatory diseases share a relatively small set of common modifiable risk factors, which can contribute to increases in systemic markers of inflammation and modify gene regulation through a variety of biologic mechanisms.  Interventions that target modifiable risk factors have the potential to improve risk profiles for periodontitis as well as for other chronic diseases

Lindhe 1985           ARTICLE          

Keywords: Age, periodontal healing

Purpose: To analyze the effect of age on healing of the periodontal tissues following treatment.

M&M: 2 groups of pts, Group A: 62 patients (13 <40y; 26 40-49y; 23>49y.o.). Treated with SRP or MWF. Re-eval at 6 mos.

Group B: 14 yr. longitudinal study. 6pts 26-29y.o.; 15 pts >60yo. with at least 50% loss of periodontal support. Treated w/ SRP & Surgery (Gingivectomy or reversed bevel flap) to eliminate pockets. Recall every 3-6 mos. w/ yearly re-evals. PI, GI, PD, AL measured at each visit.

Result: Group A: response to tx appeared similar in all 3 groups of patients. NSSD b/w groups pertaining to decreased PD or AL alterations (35% had no alteration of AL, 25-30% had some loss & 35-40% had some gain). NSSD b/w youngest & oldest for any parameters.

Group B: At baseline- PD-21-26%<4mm; 25-31%=4-6mm; 47%-54%>6mm. 14 yrs after treatment, 96% of sites in young & 95% in older patients had PD <4mm. 3 sites in older group lost 3-4mm & 1 site in young group lost 5-6mm of attachment over 14 yrs.

Discussion: The concept that a younger individual with mod-advanced perio disease has a worse prognosis than an older individual with similar lever of disease is probably less related to the healing capacity of this individual than the risk of re-infection over a longer life span.

BL: Younger & older groups responded to treatment with the same degree of resolution in GI, PD, & AL. After 14 yrs of maintenance both groups showed a similar low tendency to develop recurrent disease. Changes in parameters were b/w 0.1 and 0.3 mm.

Hormonal Factors – Pregnancy

What is the effect of progesterones and estrogens on the periodontium?

Is periodontal disease more severe in _____ and why?

  1. puberty
  2. pregnant patients


Kornman 1980           ARTICLE

Keywords: pregnancy, subgingival flora

P: To study the subgingival flora in pregnant and non-pregnant women to see if alterations in flora are related to pregnancy associated gingivitis.

M&M: 20 pregnant women without perio dz and 11 non-pregnant controls. The subG bacterial flora from 2 gingivitis sites was cultured and characterized monthly during pregnancy and again post-partum. Control group was seen monthly for 4 months for subG plaque samples. A portion of each plaque sample was tested for bacterial uptake of C14-estradiol and C14-progesterone. Blood was drawn at every visit from both pregnant and non-pregnant: plasma levels of estrogens and progesterone were measured 4 times in each control as well as pre- and post-partum. Bleeding Score (using stimudents), gingival index, and plaque index were determined at each sampling period.

R: Clinical measurements revealed an increase in gingivitis in pregnant subjects. Mean number of bleeding sites increased significantly between 13-28 weeks of gestation with a peak at 21-24 weeks. There was an increase in the gingival index, but no change in the plaque index between these visits.

2nd Trimester: SS increase in g-vitis, ratio of anaerobic to aerobic bacteria, and the proportional levels of Pi.

3rd Trimester: Gingivitis, ratio of anaerobic to aerobic bacteria, & levels of Pi decreased. The uptake of estradiol & progesterone by plaque samples increased significantly until 24 weeks, and then decreased throughout the 3rd trimester.

Uptake of estradiol or progesterone by plaque from the non-pregnant group did not change. Plasma estrogens increased 4 times in the 3rd trimester (21.2 ng/ml), but remained constant in the 1st & 2nd trimesters (5.8 to 6.4), and post partum. Control levels ranged from 0.16 to 0.20. Plasma progesterone was 6 times greater in the 3rd trimester (200.4) than the 1st & 2nd (24.2 to 41.5 ng/ml). Control levels ranged from 6.28 to 8.48 ng/ml

Conclusion: Pregnancy and specifically steroid hormones appear capable of influencing the normal bacterial flora and inducing alterations in the subgingival ecology.


Adriens et al, 2009          ARTICLE

Keywords: pregnancy, subgingival flora

P: To study whether pregnancy has an impact on the subgingival microbiota
M: 20 pregnant women without dental or medical interventions, > 18 years of age. Full mouth exam (PD, CAL) was performed at 12 weeks of pregnancy and 4-6 weeks postpartum. BOP and subgingival bacterial samples were taken at weeks 12, 28, and 36 of pregnancy and at the 4-6 weeks postpartum. All exams were done with a standardized probe, and a single examiner. DNA-DNA hybridization method was used for microbiological examination.

  • BOP reduction (weeks 12 40%, 4-6 weeks postpartum 27%).
  • NSSD in PD between week 12 of pregnancy and 4-6 weeks postpartum.
  • Total bacterial counts SS decreased between week 12 and postpartum.
  • SS Increased bacterial counts over time were found for Neisseria mucosa.
  • Lower counts (SS) were found for Capnocytophaga ochracea, Capnocytophaga sputigena, Eubacterium saburreum, Fusobacterium nucleatum naviforme, Fusobacterium nucleatum polymorphum, Leptotrichia buccalis, P. micra , P.i, P. melaninogenica, S. aureus, S. anginosus, S. intermedius, S. mutans, S. oralis, S. sanguinis, Selenomonas noxia, and Veillonella parvula.
  • No changes occurred in total bacterial counts between weeks 12 and 28 of pregnancy. Between weeks 12 and 36, significant reduction occurred in the total bacterial counts, which decreased further at 4 to 6 weeks postpartum.
  • Counts of Aa, Pg, Tf, and Td did not change.
  • Counts of Pg and Tf at week 12 were associated with gingivitis.

BL: Subgingival levels of bacteria associated with periodontitis did not change during pregnancy. Pg and Tf counts were associated with BOP at week 12. A decrease was found in 17 of 37 species from week 12 to postpartum. Only counts of N. mucosa increased.

Mascarenhas 2003          ARTICLE

Keywords: endocrinology, sex hormones, oral systemic connection, estrogen, androgen

P: To discuss how sex hormones may influence the periodontium and periodontal wound/ bone healing.

M+M: Review of the literature was conducted in Medline, Premedline, and Pubmed. Publications up to 2002 were selected for further analysis. In addition, a manual search was also performed including specific related journals and books.



Estrogens can influence the differentiation of stratified squamous epithelium as well as synthesis and maintenance of fibrous collagen. Estrogen receptors found in osteoblast-like cells.

Clinically estrogen sufficient patients have been reported to have more plaque without increased gingival inflammation compared to healthy controls. This suggests that inflammatory mediators may be affected by estrogen hormone level, which may be attributed to the production of prostaglandins (PGs) by the involvement of estradiol and progesterone.

It is speculated that normal estrogen levels essential for periodontal protection. The amount of circulating estradiol seems to be inversely correlated with the prevalence of periodontal disease (Plancak et al. 1998).



Progesterone is active in bone metabolism and may play an important role in the coupling of bone resorption and bone formation. It may exert its actions directly on bone by engaging osteoblast receptors or indirectly by competing for a glucocorticoid receptor. (Feldman et al. 1975, Chen et al. 1977).



An increased matrix synthesis occurs on periodontal cells under testosterone influence. Androgens may protect the periodontium via a positive anabolic effect on periodontal cells (positive determinants of OPG serum levels), a negative effect on the production and presence of mediators of inflammation, and an inhibitory effect on osteoclastic function.



Women are more susceptible than men, especially in older age groups, however they seek dental care more frequently than men. Females during menopause show higher frequency of alveolar bone loss as well as decrease crestal and subcrestal bone density.


Puberty: Children in puberty experience an increased inflammatory response as a result of the influence of sex hormones. There are higher bacterial counts, especially Pi and Capnocytophaga species.

Menstrual Cycle:

Generally the periodontium does not exhibit significant changes during the menstrual cycle. Gingival bleeding and increased exudates as well as ulcerations of the oral mucosa and vesicular lesions have also been noted in the luteal phase of the menstrual cycle.


Pregnant women in good health are unlikely to experience any significant gingival responses that would have serious clinical implications. Increase in Pi and Pg has been showed. Susceptibility to infections can be explained by hormonal changes that cause suppression on T-cell activity, decreased PMN chemotaxis and phagocytosis, altered lymphocyte response and depressed antibody production.


Menopause and Postmenopause:

Signs of generalized osteoporosis and lower bone density of the mandible correlates with an increased incidence of periodontal disease, higher BOP and more CAL loss. During the peri-menopausal transition (2-7 years) the concentration of circulating estrogen decreases, while FSH and LH increase, therefore compromising the anti-inflammatory effect of estrogen in the periodontium. It is believed that ovarian deficiency and not aging are the predominant causes of bone loss during the first two decades after menopause.


Contraceptives can increase inflammation and gingival exudates, as well as increase prevalence of dry socket and accelerated progression of periodontal disease when used long term.

Hormone replacement therapy:

Should be suggested for women during menopause since several pathologic conditions common during this period of time can be avoided or at least reduced in severity. HRT reduces BOP and CAL loss in postmenopausal women as well as the risk of fatal myocardial infarction, ischemic heart disease and stroke by 20-40% and even reduce Alzheimer’s disease.

Effect on wound healing:

Sex hormones have a regulatory effect on growth factors involved in wound healing, including stimulation of proliferation, migration and morphogenesis of pluripotent cells. More research is needed to improve understanding of how sex hormones influence the overall periodontal and implant healing.

BL: Sexual hormones play an important role in influencing periodontal disease progression and wound healing. Not all patients and their periodontium respond in the same way to similar amounts of circulating hormones. The influence of sex hormones can be minimized with good plaque control as well as with hormone replacement therapies, however, the true mechanism of how these interactions actually occur have yet to be determined.



Taichman, L,  2005          ARTICLE

Keywords: Contraceptives, oral/adverse effects; gingivitis; National Health and Nutrition Examination Survey III; periodontal diseases, epidemiology, etiology.

P: Historically, high doses of oral contraceptive have been associated w/ perio dz. This is a cross sectional study to determine whether an association exists among users of currently available “low dose” OCs and perio dz in females, 17 -50 y/o.

M&M: Data used is from NHANES I (1971 to 1974) and NHANES III (1988 to 1994). Gingivitis defined as presence of BOP at one of more sites. Periodontitis defined as at least 2 sites with 4mm or more CAL as well as 2 sites with PD of 4mm or more.

R: The prevalence of OC use in NHANES I was 22% and in NHANES III, 20%. The incidence of moderate periodontitis was 13.1 (NHANES I) vs 10.7 (III). There was SS lower of perio dz for current users of OC vs non-users. NSSD in prevalence of gingivitis between the two. Current OC users had an OR 0.36 for having periodontal dz in (I) and 0.73 in (III) after adjusting.

C: Analysis of data failed to show high dose OC’s are associated with gingivitis or periodontitis and there may be no detrimental association for low dose OCs.

Hormonal Factors – Puberty


Sutcliffe 1972           ARTICLE

Purpose: To employ longitudinal information on the gingival health of 127 children in order to study the changes in gingivitis between the ages of 11 and 17 years in relationship with oral cleanliness.

Materials and methods: 73 boys and 54 girls. At the first examination all of the children were aged between exactly 11 years and 11 years and 11 months. These children were seen at every one of six subsequent examinations which were separated by intervals of approximately 12 months.

Subjects were examined for gingivitis on the labial surfaces and papillae of the anterior teeth in both jaws. Same surfaces were also evaluated for the amount of debris and were recorded as clean or dirty.

Results: In both sexes the prevalence of gingivitis tended to fall with age


The site prevalence of gingivitis rose to peak levels at the age of 12 years, after which it tended to decline with age.

Girls tended to reach their maximum gingivitis experience earlier than the boys. Mean age of maximum experience in girls was 12 years and 10 months which was significantly different that the mean age of 13 years and 7 months found in boys. There was a tendency of the maximum gingivitis experience to occur around age of 12.

The maximum mean number of inflamed gingival sites per child was 14.1 sites which was between 60 and 70% greater than the mean values found in the preceding year and in the following year.

Although in general distributions of mean numbers of inflamed gingival sites and of the proportions of mouths with dirty teeth were remarkably similar, there was a disparity at the time of maximum site inflammation where the mean number of inflamed sites was higher than might have been expected from the proportion of dirty mouths. This is consistent with the hypothesis that at the time of puberty there is an increased tissue reaction to local irritation.

Conclusion: Gingivitis was found to increase with an age variation that suggests a link with puberty. The increase was apparently the result of an increased tissue response to irritation which suggests that the cause was related to the concentration of circulating sex hormones.

Soorriyamoorthy 1989           ARTICLE
Keywords: plaque; steroid hormones; gingival inflammation; gingival hyperplasia; probing attachment loss

Purpose: To survey the influence of corticosteroids, androgens, estrogens and progesterone on gingival tissues and to show the relationship of such influences to periodontal disease. Review Article.

  • The clinical changes in plaque induced gingivitis are accentuated by circulating levels of corticosteroids, androgens, estrogens and progesterone.
  • These hormones act by partial immune suppression, increased fluid exudation, increased bone resorption and increased fibroblast synthetic activity.
  • P. Intermedia counts have shown to be high in people taking oral contraceptives and in second trimester of pregnancy without showing gingival inflammation.
  • This is a result of competitive binding between progesterone and naphthoquinone (essential nutrient), as they have similar structure.
  • Therefore, high counts of P. intermedia may be a better indicator of altered systemic hormonal condition than just clinical observations.

BL: Main hormonal effect results in: false pocketing (psuedopockets) rather than a change in attachment levels, except in cases of progressive periodontal disease.



Mombelli 1990          ARTICLE

Keywords: Subgingival microbes, puberty, bleeding

P: To monitor longitudinal changes in the composition of subgingival microbiota of children between 11 and 14 and study their association with changes of clinical parameters related to gingival health.

M&M: 22 boys and 20 girls between 11-14 years of age volunteered to be in the study. Throughout 4 years, 10 samples were taken from each mesial aspect of both upper first molars. To determine the subject’s pubertal development, pubic hair development, testicular volume, breast development and Rx of the hand-wrist were taken. Prior to collecting the samples, the PI was recorded and the supragingival plaque was removed with a curette. Five sterile paper points inserted into the sulcus for ten seconds and removed. Following, the GI was recorded and the PBI by means of using a Sim-U-Dent and waiting 30 seconds to see if bleeding occurs. Part of the sample was studied under darkfield microscopy, enumerating up to 200 organisms. The other part was plated and cultivated in an anaerobic environment. The proportions of the morphotypes were then studied under a darkfield microscope. Later, the data was compared between bleeding and non-bleeding sites, as well as at what point in time the sample was taken.

R: The bleeding tendency increased significantly at the start of the pubertal phase. Bone age, testicular volume, and breast development had a significant association with PBI and chronological age. At the same time, A. odontolyticus and Capnocytophaga sp. increased. Significantly different concentrations of the following bacteria were found when compared in the presence or absence of bleeding: Fusobacterium, Capnocytphage, A. naeslundii, A. viscous (only one more present in non-bleeding sites), Eikenella, P. intermedius, B melaninogenicus, (B MEL WAS RENAMED TO PORPHYROMONAS GINGIVALIS) motile rods, fusiform organisms, small, medium and large spirochetes. P. gingivalis is not listed because it was not found in any sample, while cocci and non-motile rods were not listed because they were ubiquitous. Samples taken before a rise in PBI contained Capnocytophaga more frequently than prepubertal samples. Samples taken at a high PBI just before a decrease of PBI, contained black pigmenting bacteroides more frequently.

BL: Capnocytophaga is present at the initiation of puberty gingivitis, while there is a shift in the subgingival flora associated with bleeding.


Oh 2002          ARTICLE

Keywords: dental plaque, aggressive periodontitis, intra oral lesions, treatment

P: Review article “Periodontal diseases in the child and adolescent”


Dental plaque-induced gingival disease

– Most common periodontal infection among children and adolescents
– Children developed gingivitis less readily than adults
– No clear cut age at which the gingival reaction to bacterial insult in children becomes similar to that in adults

Aggressive periodontitis

– Onset before age 35 years, rapid disease progression, somewhat different distribution of lesions than in adult periodontitis, and distinct etiologic characteristics



Common intraoral lesions and management

1) Primary herpetic gingivostomatitis
– HSV-1
– Transmission via oral-genital or oral-oral direct mucocutaneous contact of infected secretions
– Affects children under 10 years of age with a peak incidence at 2-4 years of age

2) Recurrent herpes simplex
– Following primary infection by HSV, the virus ascends through sensory or autonomic nerves and persists in neuronal ganglia
– 30-40% of population, secondary manifestations may occur as a result of precipitating factors such as sunlight, trauma, fever, stress

3) Recurrent aphthous stomatitis
– Small 0.5-1.0 cm or large 1-3 cm
– Small lesions heal in 7-10 days without scarring

4) Candidiasis
– Overgrowth of a superficial fungus, Candida albicans
– Diffuse, curdy, or velvety white mucosal plaques that can be wiped off

5) Angular cheilitis
– Painful condition beginning as an inflammation of the commissure of the lips followed by erosion, ulceration, and fissuring
– Associated with Candida albicans and Staphylococcus aureus

6) Geographic tongue (benign migratory glossitis)
– Desquamation of superficial keratin and the filiform papillae
– 1-2% of population with 0.6% prevalence in US schoolchildren
– Can become symptomatic exhibiting a burning sensation



Do you make specific nutritional recommendations to your patients? If so, what are the recommendations? When are they made? Defend them.

What group(s) of patients in our society is(are) most likely to be suffering from a nutritional deficiency?

Discuss the role of nutrition in:

  1. periodontal disease progression and severity
  2. wound healing


Tarana Singh 2000           No ARTICLE

Keywords: nutrient, gene, interactions, diet

Purpose: To study nutrient–gene interactions and how diet affects the inflammatory mechanisms underlying severe periodontitis.

Nutrigenomics aims to reveal the relationship between nutrition and the genome and to provide the scientific basis for improved public health through dietary means. It is extremely likely that interactions between genotype and diet are important in determining the risk of the most common complex diseases, including periodontal disease.

Type 2 diabetes and periodontal disease- a possible role for nutrigenomics:
-Significant association between the variant genotypes of both interleukin-1A (interleukin-1A-889) and interleukin- 1B (interleukin-1B+3954 and interleukin-1B-511) and periodontitis in subjects with type 2 diabetes, which was not seen in nondiabetic controls

The role of the micronutrient zinc, a zinc transporter gene and the risk of developing type 2 diabetes:

  • Recent genome-wide association studies have identified a genetic-susceptibility locus for type 2 diabetes comprising a nonsynonymous single nucleotide polymorphism (C ⁄ T; rs13266634) in a beta cell-specific zinc-transporter gene. This zinc- transporter gene (SLC30A8, coding for ZnT8) may be important in insulin storage and release.
  • Zinc has a specific role in beta cell function takes on new significance with respect to potential strategies to prevent or treat type 2 diabetes and potentially periodontal disease.
  • Type 2 diabetes and periodontal disease, lead us to hypothesize that zinc supplementation may alter periodontal disease progression through changes in expression of the ZnT8 transporter gene.
  • Increasing the extracellular zinc concentration has a positive effect on glucose-induced insulin secretion, indicating a potential benefit of zinc supplementation on susceptibility to type 2 diabetes in individuals carrying the risk allele

Conclusion: The observed differences in the response of an individual to dietary modification can be attributed to differences in their genetic make-up, which emphasizes the importance of exploring the role of nutrient–gene interactions in the development of chronic diseases.


Kuzmanova 2012           ARTICLE

Keywords: leukocytes, periodontitis, plasma, vitamin C

P: To examine if vitamin C concentrations in plasma, PMNs and peripheral blood mononuclear cells (PBMCs) are lower in perio pts vs no dz.

M&M: 21 untreated perio patients and 21 controls evaluated for age, gender, race and smoking habits were selected. Perio dz measured by presence of radiographic bone loss >1/3 of the root length at >/= 1 tooth per quadrant and >/= 20 teeth. Dietary vitamin C intake was assessed by a self-administered dietary record. Preprandial blood glu samples were obtained and analyzed for vitamin C concentrations in plasma, PMNs and PBMCs by means of high-pressure liquid chromatography (HPLC).

R: Plasma vitamin C was lower in periodontitis patients compared with controls (8.3 and 11.3 mg/l, respectively, p = 0.03). Only in the control group a positive correlation was present between vitamin C intake and plasma values. No differences could be determined between pts and controls regarding vitamin C dietary intake and levels in PMNs and PBMCs. In the test group, pocket depth appeared to be negatively associated with the vitamin C concentration in PMNs.

C: A relationship between low plasma vitamin C levels and periodontitis was shown, though the dz cannot be explained by insufficient vitamin C storage capacity of leucocytes; the question remains through which mechanism low plasma vitamin C levels are related to periodontitis.

Cr: no mention of standardization of radiographs



Evans, Yukna, 1983           ARTICLE

Keywords: liquid protein diet, nutrition, collagen metabolism
Background: The liquid protein diet (LPD) was used to lose weight. The liquid protein preparations are formulated from hydrolysates made from collagen or gelatin derived from cowhides and other sources of connective tissue known to be materials of poor protein quality. The individual who strictly followed the LPD would consume several ounces of a hydrolyzed gelatin drink as sole caloric source, providing less than 400 calories/day. In addition a potassium supplement , a multi vitamin/mineral preparation and non-caloric fluids or water would be taken. This diet has been implicated in the deaths of 50 females in 1978.
P: To study the effects of LPD on gingival collagen metabolism of developing gingiva in young rats.
M & M: 117 (23 day-old) rats were included. 3 groups . Group 1: 49 rats fed with 20 % LPD. Group 2: 33 rats pair fed with group 1, but receiving a 20% casein diet. Group 3: 27 rats fed a 20% casein diet ad libitum. Rats were sacrificed on days 35 and 48. Gingival tissues from the palate were biopsied.

R: Body-weight changes at day 48 showed a 20% decrease in the LPD group, while pair-fed and ad libitum groups increased 47% and 267%, respectively. 14 rats in the LPD group died and some started losing hair at 12 d. No mortality in the other groups. Collagen content per gram of gingiva was NSSD among the 3 groups. The gingival collagen content of the 3 groups at days 35 and 48 were not significantly different from that of the beginning of the experiment. Gingival collagen synthesis revealed significant differences among all three groups at days 35 and 48. At day 48, collagen of the gingiva was highest in the pair-fed group, followed by the LPD and ad libitum groups.

BL: While LPD effects on the overall body condition were profound, LPD exerts minimal effect on gingival collagen metabolism in young rats.



Munoz 2001           No ARTICLE

Keywords: nutrition, systemic health, oral systemic connection

P: To compare the effect of certain nutritional and plant-derived supplement(Perio Therapy) and a placebo tablet in the reduction of gingivitis, bleeding, probing depths, and attachment levels in a 60-day, randomized, parallel clinical trial for patients with periodontal disease.

M+M: Double-blind trial. 63 healthy patients that had mean GI>1.7 and had moderate periodontal disease in at least one quad and three PDs of 4-5mm but not >7mm. Randomly divided into two groups: control (31 pts) given placebo and experimental (32 pts) given a vitamin tablet containing seven active ingredients: Folic Acid, Vit B12,Vit C, Purple Cone Flower, CoQ10, Black Pepper, and Grape Seed. The clinical parameters assessed were the gingival index (GI), bleeding index (BI), periodontal pocket depth (PD), and attachment levels (AL), and were recorded at baseline and 60 days. Pts took the assigned tablet at breakfast and at dinner after brushing their teethh twice daily.

R: Clinical reduction in the GI, BI, and PD for the experimental group. There were NSS changes for AL with either the experimental or the placebo group. PDs of ≥ 4 mm in patients receiving the experimental treatment, had improvements in the GI (1.75 to 1.55 ) and PD( 4.5mm to 3mm) from baseline to 60 days, but NSSD in the BI and AL. There were NSSD in any of the indices when the data were compared between men and women.

BL: A plant derived supplement (PerioTherapy) offers pts a noninvasive, systemic, adjunct to add to their OH regimen.

CR: Study funded by Pharmaden, makers of PerioTherapy.



Siegel 1982          ARTICLE

Keywords: nutrition, systemic health, oral systemic connection

D: To present a case report of a 49-year-old male presenting with sudden onset of petechial hemorrhages, oral capillary fragility and discrete ulcerations that could not be attributed to any hemorrhagic disorder (lesions confined to oral cavity). There were no oral or systemic signs of scurvy. No vesicles and other clinical signs and symptoms ruled out primary herpes.

Patient gave a history of daily intake of megadose of Vit C (1000mg/day) for more than 1 year. Symptoms appeared about 10 days following cessation. Pt. was instructed to resume the full megadosage of Vit C immediately, and 1 week later the lesion disappeared. A diagnosis of conditioned oral scurvy due to megadose of vitamin C withdrawal was made. (Rebound or “conditioned” scurvy: upon cessation of the megavitamin dose, the excretion and/or catabolism of vit C continues). No lab assay was done due to the cost. Patient volunteered to stop taking Vit C and the lesions appeared again.

Authors’ suggested treatment:
1) Resume 1000mg Vit C/day for 2 weeks
2) Decrease dosage to 750 mg/day for 2 weeks
3) Decrease dosage to 500 mg/day for 2 weeks
4) Decrease dosage to 100 mg/day and maintain indefinitely

Pt. reported free of symptoms after following the recommended regimen



Leggott 1986          ARTICLE

Keywords: ascorbic acid, plaque accumulation, gingival health, periodontal probing, supplementation

Purpose: To assess changes in plaque accumulation, gingival health and periodontal probing depth in health y subjects under experimental conditions that established controlled period of ascorbic acid depletion and supplementation.

Materials and methods: 11 healthy nonsmoking men aged 19 to 28 years old participated in the 3-month study. They were selected on the basis of relatively good existing oral health, a natural dentition of at least 20 teeth, minimal supragingival and subgingival calculus and no mucosal disease.

The study was divided in 4 periods. Period I ascorbic acid supplements of 60mg/day were provided to allow body levels of the vitamin to stabilize in preparation for the collection of baseline clinical, biochemical, dietary and demographic data. After period IV subjects were given ascorbic acid to replete tissue stores of the vitamin. Plasma and urine ascorbate levels were obtained to reflect recent intake. PI, GI, Gingival Bleeding Index (BI) and PD of Ramfjord teeth were recorded.
Results: No mucosal lesions, severe periodontal disease or other oral signs associated with clinical descriptions of scurvy were observed in any of the subjects at any point of the study.
Ascorbic acid concentrations responded rapidly to changes in Vit C intake. Decrease was more rapid in period IV than period II.
Plaque scores and PDs remained relatively constant throughout the study period. Percentage of non bleeding sites decreased slightly during first depletion period, increased significantly during period III and decreased significantly during period IV. Mean GI was 1.08±0.30, 1.26±0.24, 0.74±0.25 and 1.6±0.22 for periods I, II, III and IV respectively and bleeding indices for the same periods were 1.42±0.57, 1.89±0.44, 1.06±0.50 and 2.26±0.46.

At the end of period III healthy sites were about 30% and bleeding sites less than 5% while after period IV healthy sites were less than 2% and sites with BOP more than 50%.
Conclusion: ascorbic acid depletion was not associated with severe periodontal disease but measures of gingival inflammation and bleeding varied with changes in plasma and leukocyte ascorbate levels. Results suggest that ascorbic acid status may influence early stages of gingival inflammation, particularly crevicular bleeding.



Nishida 2000           ARTICLE

Keywords: National Health and Nutrition Survey III; periodontal disease/prevention and control; risk factors; smoking/adverse effects; vitamin C/therapeutic use

P:  To investigate the association between dietary calcium intake and severity of periodontal disease.
M&M: 12,419 subjects,3 age groups (20-39, 40-59, >60). Dietary calcium intake was determined from a 24-hour dietary recall, conducted by nutritionists. Calcium supplements were not considered in this study. In order to examine whether a dose-dependent increase in perio disease was present, the daily calcium intake was categorized into 3 levels: 2-499mg, 500-799mg and 800mg and above. Perio exam included measurements of gingival bleeding, calculus, probing depth and clinical attachment level carried out in 2 randomly selected quadrants per subject, one maxillary and one mandibular. AL (attachment loss) > 1.5mm was used to define periodontal disease. Tobacco use and total serum calcium were assessed.

R: Lower dietary intake of calcium increased the risk of periodontal disease, a dose-response relationship was seen. The younger age group (20-39 years) in both males and females and the middle age group (40-59 years) in females showed a statistically significant association between lower dietary calcium intake and increased periodontal disease. A statistically significant association between low total serum calcium and periodontal disease was found in younger females aged 20-39 years.

BL: Low dietary intake of calcium results in more severe periodontal disease.



Nishida 2000    ARTICLE

Keywords: National health and nutrition survey III, periodontal diseases/prevention and control, risk factors, smoking/adverse effects, vitamin C/therapeutic use

P: To investigate the association between dietary vitamin C and periodontal disease, defined by clinical attachment level (CAL), in a sample of the U.S. population provided by NHANES III. Also, to examine the association of vitamin C with periodontal disease comparing smokers and non-smokers.

M+M: NHANES III (sample of 12,419 adults, between 20-90 years old) used to gather data. Dietary vitamin C intake was estimated from a 24 hour recall conducted in mobile examination center by nutritionists. Individuals with periodontal disease were defined as those having CAL of 1.5mm or greater. Subjects were analyzed for the relationship between dietary vitamin C intake and periodontal disease by using multiple logistic regression analysis. In addition, to see whether a dose-dependent decrease in periodontal disease was present, the continuous vitamin C variable was replaced by 5 intervals of vitamin C intake (0-29mg, 30-59mg, 60-99 mg, 100-179 mg, and 180mg or greater). Data were also analyzed separately for each tobacco use group, 31.0% of the subjects were smokers. .

R: After adjusting for age, gender, gingival bleeding, and tobacco consumption, there was a dose-response relationship between the levels of dietary vitamin C and periodontal disease with an OR of periodontal disease being 1.30 for the lowest vitamin C intake group (0-29mg/day) and an OR of 1.16 for the group taking 100-179mg/day. Current and former smokers with less dietary vitamin C had OR of 1.28.

Mg vitamin C consumed: OR:
0-29 mg 1.30
30-59 mg 1.26
60-99 mg 1.21
100-179 mg 1.16


BL: Those taking lowest levels of vitamin C, and those who also smoke may be at greater risk to have periodontal disease.



Neiva 2005             ARTICLE

Keywords: Vitamin B complex, wound healing, attachment level

P: To determine if vitamin-B complex supplementation following periodontal access flap surgery (AFS) improves wound healing.

M&M: 30 pts with generalized moderate to advanced periodontitis with 2 teeth in a quadrant presenting a PD of 5 mm or greater with BOP were selected to perform access flap surgery (AFS). All pts already had initial therapy performed and had adequate OH. Roughly half were smokers. Pts were given either vitamin-B complex (B1,2,3,5,6,7,12, and folic acid) pills or placebo pills and were instructed to take them immediately after surgery and each morning until the 30-day post-op appointment. Post-op appointments were performed at 7, 14, and 30 days after surgery, at which GI and PI scores were taken. Periodontal maintenance appointments were scheduled at 90 and 180 days after surgery, at which GI, PI, CAL, PD, and BOP were measured. Healing and tissue maturation were evaluated through microbiological assessments (BANA) at baseline, 90 and 180 days.

R: There was no significant difference in PI or GI between groups. BOP was significantly less in the test group at days 7, 14 and 180, but no significant difference was observed at 30 or 90 days. No significant difference in PD was observed between groups at 90 or 180 days. With respect to CAL at 180 days, the control group had a decrease of 0.52 +/- 0.23 mm, while the test group had a gain of 0.41 +/- 0.12 mm (statistically significant). Smoking did not affect CAL changes. PD in sites > 3mm were significantly decreased in both groups, while there was a slight increase in shallow sites. There was also no significant difference between groups at any time in the BANA test. Less PD reduction was found in non-smokers vs smokers in the control group, but there was no difference between smokers and non-smokers in the test group (0.4mm).

BL: Supplementation with vitamin-B complex in AFS results in statistically significant CAL gains (0.9mm) versus placebo. There is no difference between groups with respect to PD, BI, PI or the BANA test.



El Sharkawy, 2010             ARTICLE

Keywords: host, modulation, therapy, fish oil, aspirin

Purpose: To test an innovative strategy using host modulation therapy for periodontal treatment.

M&M: Egyptian study. 80 healthy subjects with advanced chronic periodontitis. Two groups (40 patients each). The control group was treated with SRP plus placebo. The experimental group received SRP followed by a dietary supplement of fish oil (900 mg) and 81 mg aspirin daily. Saliva samples were collected at baseline, 3 and 6 months for evaluation of RANKL  and MMP8. Clinical perio parameters were also collected at the same time intervals.

Results: A significant reduction in probing depth and a significant attachment gain was seen after 3 and 6 months in the test group when compared to the control group from baseline. Salivary RANKL and MMP8 levels showed significant reductions in the test group in response to treatment at 3 and 6 months compared to controls. The test groups also showed more of a shift in the frequency of pockets < 4 mm.

Conclusion: The results of this study suggest that dietary supplementation with fish oil and baby aspirin may provide a sustainable, low cost intervention to augment periodontal therapy.

Iwasaki 2010            ARTICLE

Keywords: ω-3 fatty acids, periodontal condition, nutrition, longitudinal study, elderly

BG: Fish oil has anti-inflammatory actions that may benefit periodontal health. Dietary fish or fish oil rich in ω-3 fatty acids (FA), mainly docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), can attenuate chronic inflammatory diseases by various mechanisms. DHA has demonstrated anti-inflammatory effects by interference with interleukin-1 signaling pathways leading to cyclooxygenase-2 induction in endothelial cells

P: To investigate the longitudinal relation between dietary ω -3 fatty acids (FAs), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA) to periodontal disease
–‘periodontal disease event’ signifies >/=3mm CAL loss in 1 year

M: 36 pts completed the study. All were > 74 y/o, were randomly selected and were followed over a period of 1 month. The dietary intakes of DHA, and EPA were calculated based on the Standard Food Composition Tables in Japan every 3 days. Dental examinations were carried out at baseline and once a year for 5 years. CAL was measured at six sites per tth.

R: DHA intake was associated w/ tooth loss: a mean of 22.3 +/- 6.9 in the upper third of DHA intake vs 15.2 +/-9.6tth in the lower third. A similar relationship was found for EPA intake: 22.1 +/- 7.5tth in the upper third vs 14.7 +/- 9.6 in the lower. Low DHA intake was significantly associated with more periodontal disease progression. The mean number of periodontal disease events for participants who were in the lower third of DHA intake was approximately 1.5 times larger than the upper third after adjusting for possible confounders (gender, smoking, BMI). No SSD between EPA consumption at baseline and periodontal disease events , though there was a tendency for the lowest EPA group to have more disease events.

BL: The findings suggest there may be an inverse, independent relation of dietary DHA intake to the progression of periodontal disease in older people.

Esaki 2010            ARTICLE

Keywords: folic acid; gingivitis; non-smoker; adults

B: Folic acid is a B group vitamin, with deficiencies affecting cell production and mitosis. Folic acid deficiency is the most common nutrient deficiency in the world.

P: To investigate epidemiologically any correlation of gingival health characterized by gingival bleeding tendency and dietary folate levels.

M&M: 497 non-smoking Japanese adults with 20 teeth or more were used for analysis. Questionnaire survey was conducted to record dietary habits, medication, drinking habits and health related activities. Dietary records were subsequently processed for nutrition content by computer analysis. After that clinical exam was done, which included BMI, PD, BOP, and calculus. Periodontal status was assessed using Community Periodontal Index (CPI). Oral cavity was divided in 6 sextants and 10 index teeth were evaluated in each participant. The index teeth were 17, 16, 11, 26 and 27 in maxilla and 37, 36, 31, 46 and 47 in the mandible. CPI score was recorded (healthy=0, BOP=1, calculus=2, PD 4-5mm = 4, PD ≥6mm=4). The highest score in the six sextants was used as individual CPI score.

Statistical analysis was done, including multiple regression analysis.

R: 61% of subjects had dietary levels lower than recommended standards. The mean value for BOP was 23.7% Older age, male gender, irregular dental visits and no inter-dental cleaning were identified as important correlates of CPI scores. There were SS negative correlations of calcium, iron, vit A, vit c and folic acid with BOP%. The negative association between folate level and bleeding on probing remained statistically significant in multiple regression analysis (standardized beta = -0.204, P < 0.001). No significant correlation was found between CPI scores and folate intake level.

BL: This investigation demonstrated a significant relationship between folic acid deficiency and gingival bleeding in a non-smoking Japanese population, and suggests that nutritional deficiencies can affect gingival health.



Other Nutritional Factors


Tezal 2001            ARTICLE

Keywords: alcohol effects, periodontal disease, pathogenesis, host modifications

Purpose: Assess the relationship between alcohol consumption and severity of periodontal disease

Methods and Materials: Cross-sectional study examining alcohol consumption assessed by self-reported questionnaires among 1,426 subjects (25-74yrs), which asked about number of drinks/week. “One drink” defined as 12 oz of beer, 4 oz of wine, 1 oz of hard liquor. Periodontal exam included supra-gingival plaque (0 absent, 1 present), calculus, gingival bleeding (GB: 0 no bleeding, 1 some bleeding), PD, CAL, alveolar bone loss (BL). Subgingival plaque samples were tested for Bf (Tannerella forsythia), Aa, Pg, Pi, Cr, Fn, Es, and Capnocytophaga species (Cs).

Results: 96% reported drinking habits (recorded in # of drinks/week)

1136≤5 drinks, 235 ≥ 5 drinks; 1215 ≤10 drinks, 156 ≥ 10 drinks. The findings suggested there exists a possible dose response relationship between alcohol consumption and periodontal inflammation. OR for> 10 drinks/wk and gingival bleeding was 1.62. OR and and CAL was 1.44 for subjects who fell into the category of >10 drinks/week. Alcohol consumption was NSSD related to bone loss or to any of the sub-gingival microorganisms.  Number of males and smokers higher in high drinking groups.

High drinking groups presented higher level in periodontal parameters.

Possible mechanism:

  1. Adverse host response (complement deficiency and defective neutrophil function)
  2. Liver toxicity (pro thrombin production, Vit K activation, and clotting mechanism may be disrupted)
  3. Altered protein metabolism and tissue healing
  4. Alcohol stimulates bone resorption and blocks bone formation (in vitro studies)
  5. May have direct toxic effects on periodontal tissues.

BL:  Alcohol may be a risk indicator for periodontal disease.  Longitudinal studies are needed to determine whether alcohol is a true risk factor for periodontal disease.


Tezal,Grossi 2004            ARTICLE

Keywords: alcohol; epidemiology; periodontal disease

P: The aim of the study is was to assess the relationship between alcohol intake and severity of perio dz in a large sample of U.S. population
M&M: Cross sectional NHANES study , n= 13,198. All subjects 20 years old had at least 6 natural teeth. Number of drinks in the past 12 months was assessed by interviewed questionnaires. Alcohol intake was analyzed using cut off points of 5 or less,10,15,20 or more drinks/wk. Severity of perio dz was represented by CAL as 1.5 mm as the cut off point. Independent effect of alcohol was analyzed adjusting for the effect of age, gender, race, education, income, smoking, diet, diabetes, gingival bleeding and # of remaining teeth. Information on plaque was not available.

R: There was SSD relationship between # of drinks /wk and CAL. OR for the risk for attachment loss using 5, 10, 15, and 20 drink/wk as cut off point were 1.22, 1.39, 1.54, and 1.64 respectively. However, differences in PDs and CAL were only 0.12mm and 0.18mm, respectively, between those that had 5 drinks or less/wk and those with 20 drinks/wk. There was no difference in # of remaining teeth between any of the groups (all had an avg of 23).

C: Alcohol consumption may be associated with CAL and the relationship appears to be dose dependent.
Cr: Since information on plaque was not available, we do not know if alcohol consumption is related to CALoss directly or indirectly (pts may brush less when intoxicated). The differences in PD, CAL, and # of tth remaining not clinically significant. Article written in a very slanted fashion.



Amaral 2008            ARTICLE

Keywords: Alcohol dependence; alcoholism; epidemiology; periodontal disease; periodontitis

Purpose: To evaluate the relationship between the severity of periodontal disease and alcohol dependence in a population drawn from a hospital in Rio de Janeiro.

Materials and methods: 50 alcoholic and 49 non-alcoholic subjects. Questionnaires were used as alcohol screening tests, to record sociodemographic data (age, education, income, smoking and living conditions).
Subjects should have more than 15 teeth and had not been submitted to antibiotic medication or periodontal therapy during the previous 6 months.
Visible plaque (VP), BOP. PD and CAL were recorded in 6 sites/tooth.

Results: Alcoholic group had a higher mean age but not significant differences were found for income, education and living conditions between the groups.
The mean PD (3.2mm vs 2.7mm) and CAL (3.5mm vs 2.9mm) and the mean percentage of sites with PD or CAL≥4mm were statistically greater for the alcohol dependent group (32.4% vs 16.6%).
NSSD were found between the two groups for VP and BOP.

Conclusion: Alcohol dependence and periodontal disease were associated when controlling for age, plaque, income, education, living conditions, and smoking in this cross-sectional study.



Bartold, 2005            ARTICLE

Keywords: Arthritis, rheumatoid; periodontitis

Purpose: To explore the common pathologic mechanisms of periodontitis and rheumatoid arthritis (RA)


  • There have been recent reports suggesting a significant association between these two common chronic inflammatory conditions.
  • Rheumatoid arthritis is a chronic destructive inflammatory disease characterized by the accumulation and persistence of an inflammatory infiltrate in the synovial membrane that leads to synovitis and the destruction of the joint architecture resulting in impaired function.
  • RA has an initiating event leading to significant synovial inflammation and tissue destruction.
  • Both periodontitis and RA have three types of disease.
  • Periodontitis can:
  1. manifest very little or no disease progression
    2. moderate progression
  2. rapid progression
  • RA can be:
  1. self-limited
    2. easily controlled
    3. progressive
  • The etiology of periodontal disease is a more specific inflammatory response to specific pathogens residing in the subgingival biofilm.
  • The cause of RA is unknown, as it can develop secondarily to several different stimuli and through different effectors pathways.
  • Both diseases have a genetic risk in their development: more than 50% of the variance in several features of chronic periodontitis can be explained by genetic factors; HLA genes and gender constitute about 30% of the genetic risk for RA.
  • Evidence suggest a strong relationship between the extent and severity of periodontal disease and RA.
  • Individuals with advance RA are more likely to experience more significant periodontal problems compared to non-RA.
  • A possible common pathway in RA and periodontitis is RANKL, OPG and TNF-related apoptosis inducing ligand but further studies are needed to prove this and the possible association of periodontitis and RA.

BL: The clinical implications of the current data dictate that patients with RA should be carefully screened for their periodontal status.




What diagnostic signs are indications of HIV / AIDS?

What effect does HIV / AIDS have on periodontal diseases?


Patton 1998            ARTICLE

Keywords: HIV seropositivity, opportunistic infections, epidemiology

P: To examine different oral manifestations of HIV by gender, race, risk behaviors, substance use and immune status in a previously unstudied population in southeast USA.

M&M: 238 people over 18 that identified themselves as black or white, no Hispanics participated in the study. Pts were evaluated clinically by UNC periodontists and were interviewed by a trained social research assistant. Also, the subjects’ UNC Hospital’s medical record was reviewed to determined the subject’s medical status at the time of evaluation (CD4 count, neutrophil count, HIV associated malignancies, etc).

R: The population was 41% white and 59% black. Half of the subjects had a CD4 count of < 200. Tobacco usage was reported by 55%, consuming more than 7 alcoholic drinks in the previous week was present in 63%, and 20% participated in recreational drug use. An oral lesion was present in 48% of the subjects, with hairy leukoplakia (OHL) being 26% and candidiasis (OC) accounting for 20% of them. Lesions were more prevalent in whites (54%) than blacks (44%), and more so in males (51%) than females (37%). Neither of these differences was statistically significant. People with oral lesions were 4 times more likely to have a CD4 count of < 200 and, those that consumed more than 7 drinks in the past week were more likely to present oral lesions in general and with HIV-associated periodontal disease (linear gingival erythema, NUG, NUP). Tobacco smoking was significantly associated with OC.

BL: OC and OHL are associated with HIV and, smokers are at a higher risk for OC infections.

-This study population does not represent a random sample of HIV-infected individuals in this region



Scheutz, 1997            ARTICLE

Keywords: HIV seropositivity, opportunistic infections, epidemiology

P: to examine the association between HIV infection and periodontal disease in the Sub-Saharan African population.

M&M: 119 HIV+, 73 AIDS patients and 156 HIV- controls fit criteria of >18 years old, no recent history of antibiotics, no prophy in the last 3 months, no history of anti-viral treatment. BOP, PD, Attachment Loss measured on teeth 3, 9, 12, 19, 25, 29.

R: NSD in % of BOP sites, PD, or Attachment Loss among 3 groups. Caries was more common in HIV+ and AIDS patients. Multiple logistic regression showed no association between BOP, PD or CAL with regard to lymphocyte and CD4+ T-cell counts among HIV+ and AIDS patients.

BL: Neither BOP, PD, or AL was significantly different among non-infected, infected, or AIDS patients. (surprising)

Smith, 1995 (I)            ARTICLE

Keywords: HIV, seropositive, herpes, zoster, virus, simplex, pneumocystis, Kaposi’s sarcoma

Background: Other studies have reported prevalence of gingivitis from 0-50% and periodontitis from 0-22% in HIV sero-positive individuals.

Purpose: To investigate the prevalence & severity of periodontal disease in HIV sero-positive & assumed sero-negative individuals in Edinburg, Scotland.

M&M: 29 HIV (+) subjects with diagnosis recorded on an average 3 years prior to study were examined at baseline & at 3 months intervals. 29 control subjects were examined at baseline only. Medical & social histories were taken; oral exam, plaque, redness, necrosis, sequestration, suppuration, and PD were examined at 6 sites on all teeth except 3rd molars. Supra gingival plaque was removed from all mesial surfaces. Subgingival plaque samples were taken. At recall, clinical exam was performed, & samples only from sites calculated to have lost >3 mm attachment loss between visits. Also, a sample was taken from a site without attachment loss at the end of study.

Results: In the test group, 12 patients had CDC stage II & 17 had CDC stage IV, most with HIV-related & unrelated diseases. At 1st visit, 5 had history of herpes zoster virus (HZV); 4 herpes simplex virus (HSV); 3 pneumocystis; 2 Kaposi’s sarcoma. Orally, 11(37%) had hairy leukoplakia; 7(23%) candida; 4(13%) recurrent oral ulcers; 2(7%) HSV, 1(3%) Kaposi’s sarcoma. At baseline, NSD between groups with regards to mean attachment level, but HIV patients had more severe attachment loss on lower anterior teeth, & some had an increased mean attachment loss for their age. HIV patients had higher mean percentage of sites with redness & suppuration. 9(31%) patients had widespread attachment loss with special damage to lower anterior teeth. Mean PD decreased in 14 (48%) patients between initial and second visit. Attachment loss ≥3mm was observed in only 20/2814 sites in HIV patients longitudinally.

Discussion: The decrease in PD can be explained by scaling, OHI & awareness of periodontal problems as a result of HIV infection, but after 3 months, patients lapsed back, & plaque index was higher.

BL: Although the results of this study indicated a tendency for mean CAL loss increase across CDC stages, the presence of widespread periodontal disease or the incidence of active sites were not restrictive in patients with increased immunosuppression.

Comment: Most of the patients were on antimicrobial, antiviral or antifungal drugs. The sample is not completely representative of the HIV population due to the fact that many HIV drug users were poor attendees or not interested in taking part of the study. The length of the study was never clear. No data about results of subgingival plaque sampling. It was not possible to determine if periodontal breakdown occurred before or after HIV infection.

CDC: Center for disease control and prevention.



Robinson, 2000             ARTICLE

Keywords: HIV, periodontitis

P: To compare changes of CAL in subjects with and without HIV.

M&M: Data obtained as follow up on a study looking at oral hairy leukoplakia and EBV. Relative attachment loss on 6 index (Ramfjord) teeth was compared between 19 subjects with HIV (12 smokers) and 19 (2 smokers) controls w/o HIV infection over 12-18 month follow ups (only 13 HIV+ & 15 HIV– pts remained at 18 months). Controls were on hospital workers who were assumed not to have HIV. Baseline variables, age, sex, tobacco use and assumed route of HIV acquisition were collected (CD4+ count).

R: At baseline, mean CD4 count was 339 cells/mm3 (range 36-670). 73.7% of subjects of the test group had loss of CAL of ≥4mm compared to 15.8% for the control. Mean maximum relative attachment loss was similar in both groups after 12 months, 1.89mm for the test group vs. 1.82mm for the control, but significantly greater in the test group after 18 months, 2.18mm vs. 1.67mm for the control.

BL: The data are not compelling evidence of greater periodontal destruction associated with HIV infection. Large scale cohort studies or meta-analyses would be more conclusive.

Crit: Most subjects in test group smoked vs most did not in control. Control group included people who were assumed to not have HIV, not tested. Did not stratify over different CD4 ranges, so included pts with full blown AIDS as well.



Vastardis et al, 2003            ARTICLE

Keywords: cell count, HIV infections, gingivitis/ epidemiology, periodontal diseases/ complications, periodontal diseases/ epidemiology, periodontal index

P: To report the prevalence and severity of periodontal disease in a population of HIV+ patients and to investigate the association between clinical periodontal indices and the stage of HIV disease as expressed by CD4 cell counts.

M&M: 39 male (24 Caucasians, 15 African Americans), 25-54 years of age, HIV + patients (18-55 years old) were recruited. Participants were interviewed to obtain medical and sociodemographic information and were given a clinical screening for oral pathology and a periodontal examination. Information was gathered regarding: age, race, medical history, history of alcohol use, tobacco, and/or drugs. CD4 cell counts were measured by flow cytometry. Periodontal exam: PD, AL, BOP, gingival inflammation, GI, PI. For PD, the numbers and % of sites with PD >4 mm were recorded.


  • 29 pts had at least one PD > 4mm. One pt had NUP at time of exam.
  • 24 patients were current smokers, 9 never smoked, 6 patients were past smokers.
  • Cytology: 9 patients had severe immunological suppression (CD4 cell counts < 200 cells/μl), 19 patients had moderate immunological suppression (CD4 counts from 200-500 cells/μl) and 11 had mild immunological suppression (CD4 >500cells/μl)
  • Patients with CD4 < 200cells/μl had SS lower bleeding index compared to patients with CD4 > 200 cells/μl, as well as lower number of sites with probing depths > 4mm and AL> 4mm.
  • No correlation was found between CD4 cell counts and any of the periodontal indices when all patients were evaluated. When patients with CD4 counts <500cells/μl were evaluated alone, a correlation was found (positive correlation close to significance) between CD4 cell counts and bleeding index, modified gingival index, and the number of sites with attachment levels >4mm.
  • Heavy smokers had significantly more sites with attachment loss of > 4mm when compared to never smokers.

D:Patients with severe immunosuppression presented with a significantly lower bleeding index and fewer sites with attachment levels >4mm compared to individuals with moderate or mild immunosuppression. Individuals with moderate immunosuppression had similar BI to those with mild immunosuppression. Overall correlations between CD4 cell counts and periodontal disease were NSS.


– Patients with CD4 counts >500 cells/μl and a normal immunological response showed no association between CD4 cell count and periodontal indices.

– Patients with CD4 counts < 500 showed a positive linear association between clinical indices and their CD4 counts.

– Patients with CD4 counts <200 (severely immunocompromised) showed less periodontal disease compared to those with a normal immune system.



Murray, 1989            ARTICLE

Keywords: immunity, HIV, oral microbiota, oral systemic connection

P: To evaluate microbiota of HIV-gingivitis and HIV-periodontitis.

M+M: 89 total male subjects (23-52 yrs old), 45 patients HIV+ (sought perio tx) and 44 HIV – controls (19 pts had been treated for periodontitis and on 3 month maintenance; 25 pts seeking tx for periodontitis). Clinical parameters measured were PI, GI, and PDs. Subgingival plaque samples taken from 2 or 3 sites in each subject. Each sampled site was clinically and radiographically classified as HIV associated gingivitis, HIV-associated periodontitis, healthy in an HIV-seropositive subject, or healthy, conventional gingivitis or classical periodontitis in a control subject.

Healthy or conventional-gingivitis: sites were defined as having no loss of attachment, PD<4 mm, no radiographic evidence of bone loss, and no erythema of the attached gingiva or alveolar mucosa.

Classical periodontitis: sites defined as those with 6 mm or greater PD and more than 50% bone loss. HIV-associated gingivitis: presented as a band-like marginal erythema, usually accompanied by petechial or diffuse redness extending into the vestibular mucosa.

HlV-associated periodontitis: included HlV-gingivitis with blunted or cratered papillae, loss of attachment, soft tissue ulceration and necrosis, radiographic evidence of bone loss, and BOP with a tendency towards spontaneous bleeding.

Two paper point subgingival samples were obtained from each patient, and supragingival samples were curetted. Total of 225 subgingival plaque samples obtained. Plaque samples were examined by anaerobic culture technique and indirect immunofluorescence.

R: Pg., Pi, Fn, Aa were detected significantly more in HIV-periodontitis and HIV-gingivitis sites as compared to HIV+ healthy and controls. Microbiota in HIV-periodontitis is similar to non-HIV periodontitis. Microbiota in HIV-gingivitis is very different than non-HIV gingivitis, but similar to HIV-periodontitis.

BL: HIV-gingivitis is very similar to HIV-periodontitis and may be direct precursor to HIV-periodontitis (Pi, Pg, Fn). Early detection and treatment of HIV-gingivitis lesion may prevent rapid and extensive breakdown of periodontal tissues associated with HIV-periodontitis.



Zambon 1990            ARTICLE

Keywords: AIDS/complications; periodontitis/microbiology; dental plaque/microbiology; gingivitis/microbiology; HIV/complications

P: To examine the predominant cultivable microflora in plaque of patients with AIDS.

M&M: Predominant cultivable microflora in 21 subgingival plaque samples from 11 AIDS patients with periodontitis. Presence of putative periodontal pathogens (Aa, Pi, Pg and W. recta) examined by immunofluorescence in 128 subgingival plaque samples from 50 AIDS patients (including 32 with periodontitis and 18 with gingivitis).

R: Microflora in AIDS patients with periodontitis revealed many of the same Gram – anaerobic species as associated with periodontitis (defined as mod–severe gingival inflammation, 6 or more tth with PD of 6mm or greater, radiographic evidence of bone loss) in otherwise normal subjects as well as species which have been less frequently associated with subgingival plaques.
– Predominant flora: Fusobacterium nucleatum (11.4%).
-Staphylococus epidermidis (8.7%)
-Streptococcus sanguis = most frequent species (18.5%)
-Actinomyces naeslundii (7.5%)
-Lactobacillus acidophilus (12.2%)
-Actinomyces viscosus (4.7%)
-Pg (12%)

Gingivitis and periodontitis AIDS patients had similar rates of Aa, Pi and Pg, while Wr was seen 4x more than those in AIDS perio pts. Subgingival candida was found in an average of 55% of sites in 62% of patients. There were also bacterial species found in AIDS perio pts (several enteric microorganisms; E. faecalis, C. dificile, etc) not typically found in healthy subjects, and their role is yet to be determined.

BL: Sub G plaque in AIDS patients harbors high proportions of the same perio pathogens associated with periodontitis in non-HIV infected patients, as well as high proportions of opportunistic pathogens.



Rams 1991            ARTICLE

Keywords: plaque/microbiology, periodontitis, HIV/microbiology, periodontitis/microbiology

Purpose: To examine the microflora of HIV-periodontitis lesions and normal periodontal sites in 14 persons, using nonselective and selective culture techniques.

Materials and methods: 13 males and one female, mean age of 35.9 years, with HIV-periodontitis were selected. All of them were presented with laboratory evidence of HIV – infection. 8 of them presented with AIDS, 3 with AIDS – related complex and 3 of them asymptomatic HIV – positive.

None of the patients presented with diabetes, renal disorders, heart disease, severe liver dysfunction, surgically placed prosthesis or a dental prophylaxis within the prior 3 months. T4 values ranged from 24 to 374/mL.

In each patient 3 periodontitis sites were identified with severe attachment loss or ANUG-like tissue necrosis and 3 normal sites with minimal or none attachment loss or gingival inflammation. GI, Modified Papillary Index (PBI), PDs and AL were recorded.
Subgingival plaque samples were obtained using fine absorbent paper points to identify bacterial isolates and yeasts.
Statistical analysis was performed, and a value of P≤0.05 was required for statistical significance.

Results: Patients had 24.6 teeth on average and 58.5% demonstrated 7mm or more of periodontal attachment loss. Differences between HIV-periodontitis and normal control sites were statistically significant in GI and PBI scores


In HIV-related periodontitis spirochetes comprised 20.1% of total bacterial counts and 0.7% in normal periodontitis.
Gram- anaerobic rods averaged 37.3% of the total isolates in HIV-related periodontitis..
W. recta was identified in 13/14 patients. Bacteroides intermedius was present in 50% of the patients in 7% average proportions.
Candida albicans was found in 6/14 patients but generally in low proportions. The composition of microbial samples from ANUG-like necrotizing sites did not differ significantly from HIV-periodontitis sites.

In normal periodontal sites Gram+ anaerobic and facultatively anaerobic cocci comprised 39.5% of the microflora.
Gram – facultatively anaerobic rods averaged 10>7% of the microflora..

Conclusion: A.a., P. micros and Gram- anaerobic rods were the predominant subgingival isolates in HIV-periodontitis.

The species are found in normal periodontitis patients too, so disease progression in HIV patients may occur with similar pathologic characteristics but in an accelerated mode.

However HIV – periodontitis sites can also harbor yeasts, pseudomonads, enteric rods, and other non-oral bacteria atypical for periodontitis. If those organisms contribute to perio the disease entity may contain features uncharacteristic of common adult periodontitis.



Ryder 2000            ARTICLE

Keywords: HIV infection; periodontitis; patient management

Purpose: Periodontal management of HIV-infected patients


  • The dental practitioner plays an important role in recognizing periodontal and oral manifestations of HIV infection at different stages of the disease in order to refer patients for viral and immunological testing. About 40% of all HIV infected individuals show one or more HIV-associated oral manifestations, and over 90% by the time the patient reaches the late stages of immunosupression of this disease.
  • The most widely employed classification system today in monitoring the progression of HIV infection is the revised US CDC and Prevention system that employs a matrix of three ranges of CD4 lymphocyte counts (>500, 200-499, and <200) combined with a series of three clinical syndrome classifications.
  • Oral lesions now widely accepted as indicators of decreasing immunocompetence are: oral candidiasis, hairy leukoplakia, extensive apthous ulceration and ANUG, linear gingival erythema (associated with earlier stage HIV infection), NUP (associated with severely depressed CD4 count, progression to AIDS).


Navazesh 2010             ARTICLE

Keywords: HIV-1 shedding, saliva, oral health

P: To correlate the presence of HIV-1 RNA in saliva samples from women and correlate it with demographic, lifestyle, medical and oral health characteristics.

M&M: Saliva from 127 women enrolled in the Women’s Interagency HIV study was collected and the HIV-1 RNA was measured by a commercial NASBA/NucliSens assay. Demographic (age, ethnicity, education), lifestyle (smoking, drugs use, HIV exposure), and health (bmi, diabetes, AIDS status, CD4+ count, HIV-1 RNA in plasma) data were recorded. Anti-viral therapy as well as oral health (salivary glands, salivary flow rate, CAL, PD, # of teeth, etc.) was taken into account as well. All of this data was collected at baseline, and every 6 months, in some cases as many times as 7 visits, accounting for 354 subject-visits. Statistical analysis was performed.

R: At baseline, 38% of the women had detectable RNA in saliva. The number of visits was associated with likelihood of HIV shedding in saliva, indicating prevalence of HIV shedding in follow-up visits. Higher HIV-1 RNA in plasma was positively correlated with higher quantities of HIV-1 RNA in saliva. The risk of shedding increased significantly with decreasing CD4 counts. History of diabetes and a high proportion of gingival bleeding were associated with likelihood of shedding as well. Anti-retroviral therapy and higher stimulated salivary flow rates were correlated with a lower prevalence of HIV shedding.

BL: A low CD4 counts, diabetes and gingival bleeding are associated with HIV-1 RNA shedding in saliva, while anti-retroviral therapy and high stimulated salivary flow were negatively associated with shedding.