Table 3.
Experimental studies on vitamin effects on periodontal disease.
| Subjects/Animals; Age; N | Experimental Design (Duration) | Results Data (p-Value) | Main Results/Conclusions | Ref. |
|---|---|---|---|---|
| RCT (DB) B-complex supplement for 30 d (50 mg of B1, B5, B2, B3, and B6; 50 μg of B12 and B7; and 400 μg of B9) after access flap surgery (180 d) | ΔCAL: 0.41 > −0.52 mm (p = 0.024) | B-complex led to superior CAL gains when compared to placebo whereas PPD improved in similar manner among groups | [50] | |
| ΔPPD: −1.50 ± 0.21 = −1.57 ± 0.34 mm (N.S.) | ||||
| Calculus formers from Staff & patients from a Faculty of Odontology (Sweden); Age not provided; N = 60 | Chew on 0 or 5 sugar free gum/day contained 60 mg or 0 mg vitamin C (CO) (3 m per treatment) | Calculus index, Erosion scores, GB, visible PI, & saliva secretion rates (p < 0.05) | Vitamin C & non-vitamin gum reduced visible plaque, but No. of bleeding sites only with the first one | [53] |
| Children with ≤1 fully erupted tooth following routine prophylaxis; 5–20 y; N = 267 | Chew on tablets containing vitamin C or mannitol (DB) (28 d) | RPI (N.S.) Teeth lost (N.S.) | No effect | [54] |
| Chronic periodontitis patients with ≤20 teeth receiving non-surgical treatment & health Subjects (Syria); 23–65 y; N = 60 | Adjunctive dose of vitamin C or none (4 w after non-surgical treatment) | Plasma TAOC, PPD, CAL, % BOP, PI & GI | Non-surgical treatment increases plasma TAOC & improves clinical measures, but vitamin C supplements have no effect | [55] |
| Patients with vary degrees of gingivitis (USA); 25–60 y; N = 41 | Vitamin C-supplemented or non-supplemented diet (14 d), after receiving scaling & curettage therapy in one quadrant or not | Levels of vitamin C in blood & gingiva, microscopy evaluation of gingival biopsies | Vitamin C supplementation increased Vitamin C levels in blood | [56] |
| Male Wistar rats; 8 w; N = 35 | Ligatures placement or not placement (6 w) combined or not with vitamin C supplementation (last 2 w) | Plasma levels of vitamin C & ROM, gingival GSH/GSSG & levels of 8-OhdG Genetic expresion study in gums 1 |
Vitamin C increased plasma vitamin C level, improved GSH/GSSG & decreased 8-OHdG level (61% lower) & down-regulated some inflammation genes expression (p < 0.01) | [57] |
| Male Wistar rats; N.A.; N = 36 | Ligatures placement or not placement (7 w) combined or not with supplemens of vitamin C (last 2 w) | Serum levels of BAP, gingival MPO activity, RANKL expression, BDI in mandible | Either supplement led to lower MPO activity, & RANKL expression, but higher AP; & improved BDI at the periodontitis areas | [58] |
| Male Wistar rats; 8 w; N = 24 | 1 or 2 folds vitamin C-supplemented high-cholesterol diet, non-supplemented, or standard diet (12 w) | Alveolar BMD, TRAP-positive osteoclastic cells & 8-OHdG level in periodontal tissues 8-OHdG (1663 & 1675 mg/cm in vitamin C groups vs. 1430 (−80) mg/cm in cholesterol group, p < 0.001 and vs. 1556 mg/cm in control groups, p < 0.05), osteoclast differentiation (1.1 & 0.8 vs. 4.2 No. of tartrate-resistant acid phosphatase [TRAP]-positive osteoclasts/0.1 mm, p < 0.05) &decreased serum 8-OHdG expression (0.12 & 0.10 vs. 0.14 ng/mL, p < 0.05) |
Vitamin C supplements reduced the effect of high-cholesterol diet on BMD, osteoclast differentiation & decreased 8-OhdG and osteoclast differentiation kit | [59] |
| Male rats with non-osteogenic hereditary disorder (ODS od/od) & without it (ODS +/+); 5 w; N = 28 | Vitamin C-deficient, minimally supplemented or sufficient supplemented diet in non-osteogenic disorder group (4 w) | Plasma level of vitamin C, histological observations of periodontium, BMD & cephalometric evaluation | Vitamin C deficiency influenced periodontal ligament & craniofacial growth | [60] |
| Male Wistar rats; 180–220 g; N = 72 | Vitamin E supplements or placebo; combined with ligatures placement or sham-operations (9 d) | ABL & malondialdehyde formation, SOD activity, iNOS & TNF-α levels (1.89 ± 0.35 vs. 3.13 ± 0.42 mM of malondialdehyde, p < 0.01) | Vitamin E prevented malondialdehyde formation & reduced the immunoreactivity to iNOS levels | [61] |
| Male rice rats; 92–119 d; N = 32 | Vitamin E supplemented or non-supplemented diet (122 d), combined with stress by a rotational device (last 90 d) | ABL (0.369 ± 0.091 vs. 0.436 ± 0.036 mm of CEJ-ABC, p = 0.017), | Vitamin E had a protective effect on bone loss which was most pronounced at sites most susceptible to loss | [62] |
1 Genetic expression analysis for 86 genes implicated on: oxidative or metabolic stress, heat shock, proliferation and carcinogenesis, growth arrest and senescence, and necrosis or apoptosis. Abbreviations: 8-OHdG: 8-hydroxydeoxyguanosine, ABL: alveolar bone loss; BAP: bone alkaline phosphatase, BDI: Bone Density Index, BI: Bleeding index, BMD: Bone mass density, BOP: Bleeding on probing, CAL: Clinical attachment level, CO: Cross-over, d: days, DB: Double-bind, GB: gingival bleeding, GI: Gingival index, GSH/GSSG: reduced glutathione to oxidized glutathione ratio, IL: Interleukin, iNOS: Inducible nitric oxide synthase, m: moth, MPO: Myeloperoxidase, ODS: Osteogenic disorder Shionogi, PI: Plaque index, PPD: Periodontal probing depth, RANKL: Receptor activator of nuclear factor κB ligand, RCT: Randomized controlled trial, ROM: Reactive oxygen metabolites, RPI: Russell’s periodontal index, SOD: Superoxide dismutase, TAOC: total antioxidant capacity, TNF-α: Tumor necrosis factor alpha, TRAP: Tartrate-resistant acid phosphatase, US: United Sates of America, w: weeks, y: years.