Problems encountered using dermal fillers, particularly calcium hydroxylapatite, as a treatment in acne scarring.
This article aims to establish the efficacy and safety profile of dermal fillers, especially calcium hydroxyapatite (CaHA) in the treatment of atrophic acne scars.
Twenty-seven subjects with differing degrees of atrophic acne scarring were treated with the CaHA filler over a 12-month period. Thirteen patients were treated with low molecular weight cross-linked hyaluronic acid in a comparative study.
Most atrophic acne scars responded well to CaHA dermal filler treatment. Icepick scars were not treated. At 12-month evaluation, 22% of subjects showed a 75% improvement, while 48% showed a 50% improvement. This compared to an average 0% improvement for the hyaluronic acid cohort. Eleven hyaluronic acid patients (85% of total) showed a 0–25% improvement in treated atrophic scars at 12 months.
Dermal fillers, especially CaHA, can provide a safe and efficacious method of treating atrophic acne scars. This compound appears to provide a longer-lasting effect owing to volume replenishment and possible neocollagenesis. The efficacy of hyaluronic acid in repairing atrophic acne scars is not demonstrable.
Acne occurs in approximately 95% of 16–17-year-old boys and 84% of 16–17-year-old girls1. Although the condition usually resolves by the mid-20s, 1% of men and 5% of women still bear the signs of moderately severe acne scarring at 40 years of age2. Some studies show scarring of some degree may affect up to 95% of patients with acne3. The same study found that keloidal or hypertrophic truncal scarring were more common in men. This form of scarring is usually treated by using such measures as intralesional steroids, silicone sheeting, or vascular laser treatment. Atrophic scarring will often appear many years later, and can cause great distress in patients during their courtship years4. Affected patients report more social inhibition, unhappiness, anxiety, and even suicidal thoughts as a result of their facial appearance5.
For many years different treatment modalities have been used for the revision of atrophic acne scarring, with varying degrees of success. Many controlled trials have demonstrated that moderate to severe atrophic acne scars can be safely improved through ablative fractional CO2 laser resurfacing (fractional laser skin resurfacing; FLSR)6. Although FLSR is still the most popular therapeutic modality for the correction of acne scars, it is not always effective in all types of atrophic lesions7 — the more common type of defects encountered after inflammatory acne. The use of higher energy levels might have improved the results, and also possibly induced significant adverse effects7. Over the past decade, non-ablative laser resurfacing8–10, radiofrequency (RF)11, and microneedling12 have been shown to create some improvement in the appearance of these atrophic scars. A number of autologous and non-autologous techniques attempting dermal and subcutaneous augmentation have been tried to improve the facial aesthetic appearance. The autologous methods have included dermal grafting, fat transfer13,14, and implantation of autologous fibroblasts, such as Isolagen®15.
There has been interest in non-autologous augmentation by way of injections of hyaluronic acid (HA), polymethylmethacrylate microspheres (PMMA), and calcium hydroxylapatite (CaHA)16, 17. CaHA, the main mineral component of Radiesse® (Merz Aesthetics, San Mateo, CA), is a synthetic analogue of the inorganic salt found in the human body as a constituent of bone and teeth. The CaHA microspheres (25–45 μ) are suspended in an aqueous carboxymethylcellulose carrier gel, composed of cellulose, glycerin, and sterile water. None of these materials should elicit a chronic inflammatory, infectious or immune response. Multiple clinical and histologic studies have tended to document its safety, efficacy, and longevity in tissue17, 18.
By its very composition, CaHA is designed to provide immediate correction and long-term biostimulatory neocollagenesis. Over time, the gel is absorbed, fibroblasts appear and the process of neocollagenesis begins, stimulating the gradual growth of the patient’s own collagen. The carboxymethylcellulose gel carrier volumises the ‘lost’ space and acts as a replacement filler; the microspheres stimulate neocollagenesis so that, as the gel dissipates, the spheres anchor into the soft tissue. There, they serve as a scaffold for new collagen growth as early as 4 weeks post-injection, and then continue for up to at least 12 months17, 18. CaHA is not permanent, however. The CaHA microspheres are metabolised into calcium and phosphate ions through normal metabolic processes over 24 months. CaHA will not promote osteogenesis in soft tissues, does not migrate, and does not obscure diagnostic x-rays.