Abstract
Central giant-cell granulomas are benign, but occasionally aggressive, lesions that traditionally have been treated surgically. 21 cases of central giant-cell granuloma of the jaw were treated with intralesional injection of corticosteroids. The treatment protocol adopted was intralesional injection of 20 mg/ml triamcinolone hexacetonide diluted in an anaesthetic solution of 2% lidocaine/epinephrine 1:200,000 in the proportion 1:1; 1.0 ml of the solution was infiltrated for every 1 cm 3 of radiolucid area of the lesion, totalling 6 biweekly applications. Ten patients had aggressive lesions and 11 nonaggressive. Two patients showed a negative response to the treatment and underwent surgical resection, 4 showed a moderate response and 15 a good response. 8 of the 19 who had a moderate-to-good response to the drug treatment underwent osteoplasty to reestablish facial aesthetics. In these cases, only mature or dysplastic bone was observed, with the presence or absence of rare giant multinucleated cells. The advantages of this therapy are its less-invasive nature, the probable lower cost to the patient, lower risk and the ability to treat the lesion surgically in the future, if necessary.
Conventional treatment for central giant-cell granuloma (CGCG) involves surgery. The procedures recommended in the literature vary according to the lesion. In recurrent or aggressive lesions, en bloc resection, including healthy bone, is a treatment option, but it results in large surgical defects, which are undesirable in children or young adults. For the remaining lesions, the treatment indicated is simple curettage, curettage accompanied by peripheral osteotomy or cryotherapy with liquid nitrogen . Treatment by surgical curettage is widely recommended and nonsurgical methods, such as radiotherapy daily systematic doses of calcitonin and intralesional injections with corticosteroids are increasingly used. New therapies are undergoing tests, K aban et al. applied antiangiogenic therapy with α interferon, through the subcutaneous route, after enucleation of aggressive lesions in 8 patients and observed no evidence of recurrence during follow-up, from 1 to 6 months.
Therapy involving calcitonin, initially described by H arris , has been validated by several authors using different administration strategies. The prolonged treatment period required restricts its use to multiple, recurrent or particularly aggressive lesions.
Intralesional injections of corticosteroids seem to be a more viable approach. The technique is simple, low cost, relatively quick and avoids expressive aesthetic and functional defects . This treatment results in lesion reduction until the resolution of the case, eliminating or reducing the size of surgical resection. Intralesional corticotherapy was first reported by J acoway et al. and the mechanism of action of steroids in giant-cell lesions is not fully understood. Steroids appear to inhibit osteoclast activity, resulting in rapid resolution, including bone regeneration and the recovery of normal functioning . Treatment with steroids is based on the microscopic similarity between CGCG and sarcoidosis. Supported by their study regarding the effect of dexamethasone on osteoclasts, H irayama et al. affirmed that the drug had a direct effect on osteoclast formation and activity, stimulating the proliferation and differentiation of the precursors of these cells and inhibiting the activity of mature osteoclasts.
T erry and J acoway published a protocol for CGCG treatment that consisted of intralesional injections of a solution of equal parts of triamcinolone acetonide (Kenalog-10, 10 ml/mg) and local anaesthetic (0.5% marcaine with epinephrine 1:200,000). The suggested dose is 1.0 ml/cm 3 of radiolucency. The injection is administered in distinct sites all over the lesion, in a weekly regime, for at least 6 weeks. According to K urtz et al. , the intralesional injection of corticoids is preferable to systemic administration, since higher drug concentrations are achieved in the tissue. The authors affirmed that steroids should be reserved for selected cases, especially for large lesions, in which surgery could cause functional and aesthetic defects in the patient.
C arlos and S edano analysed the effect of intralesional corticoid injections on 4 patients; in 3 cases, residual lesions remained without presenting recurrence or side effects associated with steroid therapy during the mean follow-up of 5 years and 4 months. According to the authors, the dosage used did not compromise adrenal gland function, since higher daily doses would be required to induce glandular suppression. They suggested that this treatment approach could be used as an alternative to surgical removal of the lesion, principally in cases of extensive lesions, where surgical resection could compromise important structures.
Several other studies have published favourable results using this approach . Although these studies involved fewer than 50 patients treated with corticosteroids , most cases showed significant regression within 3–5 months, though in some cases, curettage of the residual lesion was required. This seems to be a promising treatment for CGCG and more studies should be developed to assess it.
The drug used in the cases reported in the literature was triamcinolone acetonide, a topical or intraarticular medication widely used in the treatment of joint disease. At the time of the present study, this medication was not readily available locally. Triamcinolone hexacetonide was chosen because it is a similar drug, with a higher potency than acetonide. When used in joint infiltrations, the formation of intraarticular osteophytes is a side effect with both drugs. It is thought that the antiinflammatory, immunosuppressor and anti-transcriptional action in inflammatory cells permits greater osteogenic activity in the bone cells at the site of infiltration, leading to the formation of osteophytes. This could be one explanation for osteogenic induction in CGCG of the maxilla.
Research aimed at elucidating the etiopathogenesis of this disease and establishing conservative treatment protocols that minimize or eliminate surgical procedures is of prime importance. The objective of this study was to assess the therapeutic response of 21 patients with CGCG in the jaws, treated with intralesional applications of 20 mg/ml triamcinolone hexacetonide, and evaluate their clinical and radiographic response to the treatment.
Materials and methods
The study involved 21 patients, aged 5–25 years at the time of diagnosis, verified by clinical, laboratory, radiographic and histopathological examination. The inclusion/exclusion criteria were: discard cherubism and hyperparathyroidism brown tumour using analysis of familial history, clinical, radiographic and laboratory examination (parathormone, alkaline phosphatase, calcium and potassium levels) and ascertain that sufficient data are available to classify the lesion as aggressive or nonaggressive (cortical destruction or expansion, uni- or multi-locular images, presence of tooth dislocation and or dental resorption). Table 1 presents the data regarding sex, age and lesion site. The patients were followed-up for 3–8 years. In 4 cases the lesion ceased to evolve to resolution and maintained an area of radiolucency, so complementary curettage was performed. In 2 cases, the lesion did not regress so the patients were treated conventionally by surgical resection ( Table 1 ).
| Case | Age (years) | Sex | Site | Treatment | Clinical type | Follow-up | Response to the drug | Time between the end of infiltrations and osteoplasty/curettage (in months) |
|---|---|---|---|---|---|---|---|---|
| 1 | 20 | M | Maxilla | Corticosteroids + osteoplasty | Aggressive | 7 years | Good | 03 |
| 2 | 7 | M | Mandible | Corticosteroids | Nonaggressive | 5 years | Good | – |
| 3 | 23 | F | Mandible | Corticosteroids | Aggressive | 6 years | Good | – |
| 4 | 20 | M | Maxilla | Corticosteroids + osteoplasty | Nonaggressive | 4 years | Good | 12 |
| 5 | 19 | F | Mandible | Corticosteroids | Nonaggressive | 7 years | Good | – |
| 6 | 9 | M | Mandible | Corticosteroids | Aggressive | 8 years | Good | – |
| 7 | 5 | M | Maxilla | Corticosteroids + osteoplasty | Aggressive | 4 years | Moderate | 12 |
| 8 | 15 | F | Mandible | Corticosteroids + osteoplasty | Aggressive | 4 years | Moderate | 06 |
| 9 | 12 | M | Mandible | Corticosteroids | Nonaggressive | 7 years | Good | – |
| 10 | 24 | F | Maxilla | Corticosteroids + osteoplasty | Nonaggressive | 4 years | Good | 12 |
| 11 | 24 | M | Mandible | Corticosteroids + curettage | Nonaggressive | 7 years | Good | 03 |
| 12 | 20 | F | Mandible | Corticosteroids + Surgical Resection | Aggressive | 6 years | Negative | – |
| 13 | 7 | M | Mandible | Corticosteroids + curettage | Nonaggressive | 5 years | Moderate | 08 |
| 14 | 9 | F | Maxilla | Corticosteroids | Nonaggressive | 6 years | Good | |
| 15 | 25 | M | Mandible | Corticosteroids + osteoplasty | Nonaggressive | 4 years | Good | 12 |
| 16 | 10 | F | Mandible | Corticosteroids | Nonaggressive | 6 years | Good | – |
| 17 | 18 | F | Mandible | Corticosteroids + curettage | Aggressive | 4 years | Moderate | 06 |
| 18 | 23 | F | Maxilla | Corticosteroids + Surgical Resection | Aggressive | 6 years | Negative | – |
| 19 | 6 | M | Maxilla | Corticosteroids + osteoplasty | Aggressive | 4 years | Good | 12 |
| 20 | 13 | M | Maxilla | Corticosteroids | Aggressive | 4 years | Good | – |
| 21 | 17 | F | Mandible | Corticosteroids + osteoplasty | Nonaggressive | 4 years | Good | 12 |
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