Skeletal Radiology

, Volume 41, Issue 4, pp 477–481

Progressive craniofacial bone loss after cosmetic surgery at the forehead

Authors

  • Annie P. Prasad
    • Department of Radiology and Biomedical ImagingUniversity of California San Francisco
  • Vijay George
    • Department of PathologyUniversity of California San Francisco
  • Anne Porzig
    • Division of Endocrinology and Metabolism, Department of MedicineUniversity of California San Francisco
  • Andrew E. Horvai
    • Department of PathologyUniversity of California San Francisco
  • Andrew Gross
    • Division of Rheumatology, Department of MedicineUniversity of California San Francisco
  • Dolores Shoback
    • Division of Endocrinology and Metabolism, Department of MedicineUniversity of California San Francisco
    • Department of Radiology and Biomedical ImagingUniversity of California San Francisco
Case Report

DOI: 10.1007/s00256-011-1330-0

Cite this article as:
Prasad, A.P., George, V., Porzig, A. et al. Skeletal Radiol (2012) 41: 477. doi:10.1007/s00256-011-1330-0
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Abstract

We present the case of a 59-year-old woman with a history of plastic surgery at the forehead who complained of progressive indentations at the frontal skull. CT and MR scans revealed significant bone thinning, presenting as lytic skull lesions, which progressed over a period of 3 years. Biopsies were obtained from the lytic lesions and histology showed fibrotic tissue, synthetic residue of previous cosmetic procedure, and no evidence of infection or neoplasm. Progressive cranial bone resorption places the patient at increased risk for cerebral injury. This case highlights a potential complication after cosmetic facial surgery, with bony resorption resulting in both skull deformation and increased risk for cerebral injury.

Keywords

Bone resorptionCraniofacial anomaliesCosmetic surgery complicationsCTMRI

Introduction

The coronal brow lift is a cosmetic surgical procedure and one of the earliest forms of a brow lift. It is performed by making coronal incisions on the hair-bearing scalp as well as the anterior hairline and frontal forehead skin [1, 2] and is a common method of correcting eyebrow ptosis and forehead rhytids [1, 3, 4]. Risks are usually fairly insignificant, and include scar alopecia (4% of patients), asymmetry (less than 1% of patients), and numbness (less than 1% of patients) [5, 6]. However, the tension created by tight skin closure increases the risk of scarring, hair loss, and necrosis [7]. With a coronal approach, it is nearly impossible to preserve the deep division of the supraorbital nerve, which may cause numbness, itchiness, and paresthesias to the area [8], and the access incisions necessary may cause vascular and lymphatic circulation disruption as has been demonstrated in a study of zygomatic fractures [9]. Vascular injury associated with the coronal brow lift may limit tissue perfusion, a necessary component of the healing process, which may potentially affect the underlying skull bone and cause bony resorption [9].

We present the case of a 59-year-old woman who underwent a coronal brow lift 5 years previously and subsequently suffered bone resorption of the frontal skull with progressing severe indentations. Histology showed evidence of prior cosmetic surgery, but osseous findings were non-specific. Follow-up over 3 years demonstrated progressive bony resorption, but no evidence of infection or neoplasm.

Case report

In 2006, a 54-year-old woman underwent a brow lift with coronal incisions in the subgaleal plane. Periosteal violation was not reported, but delayed healing at the site of incision was noted, and over a period of several months, the skin defects healed, and no abnormalities were noted. Of note, the patient also experienced a minor infection behind the right ear, which was insignificant and disappeared with topical treatment. In 2007, the patient underwent five photofacial treatments—non-ablative laser treatment to even out pigmentation of the face. Past medical history for the patient included hysterectomy, unilateral oophorectomy, and other nonfacial cosmetic procedures. The patient also had a history of osteoporosis (lumbar spine T-score of −2.6 in 2007), as well as fibromyalgia and irritable bowel syndrome. Medications at the time of presentation in 2009 included ibandronate (150 mg per month) over a period of 6 months, hyoscyamine (0.125 mg per day), and various vitamin and calcium supplements. In 2008, the patient had complained for the first time of increasingly painful indentations at the forehead, which began on the right side of the face and progressed to the left side. She also complained of headaches.

Imaging

In 2009, a skull radiograph showed focal erosion of the frontal bone (Fig. 1). Erosions were well defined and did not suggest underlying infection or neoplastic growth. Repair with hydroxyapatite cement augmentation was considered at this time, along the path of the already-existing coronal scars from plastic surgery, but no action was taken because of concern for lesion progression.
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Fig. 1

Lateral radiograph of the skull from 2009 demonstrating focal, well-defined indentations of the frontal calvarium (arrow)

In 2010, MRI and CT studies were obtained, which showed interval progression of resorption of the left and right frontal bones of the skull (Figs. 2 and 3). The CT scans and MRIs obtained showed that the surrounding fat planes were normal, and there was no inflammation of the surrounding soft tissue, indicating no osteomyelitis or tumor. The focal bony indentations, however, were substantial and were associated with substantial thinning of the calvarium; outer table and diploë are completely resorbed with only a thin remnant of the inner table, which is in close proximity to the frontal lobe of the brain. The CT was repeated 4 months later, and progression of the indentations was noted. The imaging shows loss of the outer plate of the cortex in the affected area is consistent with loss of viability of the devascularized outer cortex that depends on blood supply from the periosteal area. The most recent CT obtained in 2011 showed stable abnormalities with no significant increase in bone resorption.
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Fig. 2

Axial CT image (bone window) of the calvarium from 2010 showing focal thinning, in particular at the left side (arrow), however, well-defined margins with no sign of subcutaneous or bony mass lesion. Also note that the outer table has been completely resorbed and that there is no diploë/bone marrow space left; there is only a thin remnant of the inner table of the calvarium

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Fig. 3

a, b Sagittal T1-weighted MR image from 2010 depicting focal indentation of the calvarium (arrow in a and b) affecting the outer plate and diploë. Inner plate is barely visible and appears in increased proximity to the frontal part of the brain

Histology and cultures

After the patient reported the indentations in 2009, open biopsies were obtained from the right and left frontal region. Microscopically, both areas showed fibrovascular tissue with scarring and serous fluid-filled cavities consistent with prior cosmetic surgery (Fig. 4a). Synthetic residue of the previous cosmetic procedure was also found but no sign of foreign-body reaction or granulomas. Very focally, a few fragments of lamellar bone were entrapped in the fibrous tissue (Fig. 4b). The fragments of bone present were acellular. Osteoclasts were present along the surfaces of the fragments, consistent with ongoing resorption of dead bone. No significant inflammatory infiltration and no neoplasm were identified. Separately submitted 1-mm fragments of lamellar bone were also examined microscopically but were unremarkable (not shown). Bone cultures did not reveal any evidence of infection. Given the presence of these findings in the area of the indentations after the cosmetic surgery, it was felt that these phenomena were related.
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Fig. 4

Histologic findings of frontal area. Hematoxylin and eosin-stained sections demonstrate fibrovascular tissue with focal scar and serous fluid-filed cystic spaces consistent with prior surgery at the site (a, original magnification 40×). Focally, a few fragments of lamellar bone were entrapped in the fibrous tissue with minimal reaction (b, original magnification, 200×)

Laboratory and clinical tests

Secondary etiologies of accelerated bone resorption were excluded with a normal serum and urine protein electrophoreses, normal CBC, 25-hydroxy vitamin D 83 ng/ml, 1,25 vitamin D 67 pg/ml (18–72) calcium 9.4, phosphate 3.4, and PTH 23, C-telopeptide 177 pg/ml (40–465), and bone-specific alkaline phosphatase 11.1 mcg/l (5.6–29.0), and alkaline phosphatase 56 U/l (29–111). Lumbar spine T-score progressed from −2.6 in 2007 to −2.8 in 2009, while left and right hip T-scores improved from −2.0 and −2.1, respectively, to −1.9 and −1.6, respectively. It was concluded that the patient did not have a neoplastic disorder or Paget’s disease.

Clinical management and course

The patient was seen by endocrinology, rheumatology, and plastic surgery at our institution but given the indolence of the findings and slow course of abnormalities, no interventional therapy was initiated. However, because of the similarity of the findings with parietal thinning, which is typically found in older women and has been related to osteoporosis, the patient was started on a brief trial of teriparatide in May, 2010, while continuing calcium 1,200 mg daily and vitamin D 1,000 IU daily. Teriparatide was discontinued within 4 months because of a rash on the abdomen, chest, and face (which an outside dermatologist thought was contact dermatitis), and because the patient found compliance with daily injections to be challenging. No bone turnover markers were drawn while on teriparatide therapy. Two months after stopping teriparatide, a C-telopeptide level was 552 pg/ml (40–465 pg/ml), a threefold increase from 177 pg/ml prior to teriparatide. The increase in bone turnover markers and progression on CT prompted the initiation of yearly IV zoledronic acid. The stable CT findings in 2011 supported this clinical management decision.

Discussion

This case impressively demonstrates a potential complication of forehead cosmetic surgery, which may resemble focal scleroderma. To the best of our knowledge, a similar case has not been published in the literature. A number of other differential diagnoses were obtained, which, however, were all less likely. Initially it was hypothesized that bisphosphonate treatment could have contributed to the loss of skull because its potent anti-remodeling activity could have blocked the normal coupled osteoblastic response to bone resorption. This might be considered similar to the role of bisphosphonate in actively remodeling bone in the jaw in bisphosphonate-related osteonecrosis of the jaw. However, upon questioning, the patient admitted to only having taken the ibandronate a total of six times, which was reasoned to be insufficient to suppress bone turnover substantially. Furthermore, her markers of bone turnover were not dramatically low during her course, almost always being within the normal premenopausal range for serum C-telopeptide (after a brief trial of teriparatide, C-telopeptide increased) and bone-specific alkaline phosphates.

It is interesting to note that accelerated bone resorption is associated with chin implants, another facial cosmetic surgery procedure. According to Abrahams et al., the facial bone structure is especially susceptible to resorption because of the thin nature of the affected bones [10]. In the study by Abrahams et al., patients with chin implants experienced clinically significant bone resorption: in one cohort, nine of 12 patients had resorption, and in another, 12 of 14 patients. Although the resorption noted in this case is not related to implants, Abrahams et al. notes a finding that when facial cosmetic surgery affects skin overlying muscle or bone, it can alter mechanical loading of the structures and the surgically altered pressure can provide stress to the area, increasing chances of bone erosion [10].

Localized linear scleroderma (“En coup de sabre” subtype) is a rare form of scleroderma that also targets the forehead and typically causes depressions in the forehead [11, 12]. Although not in every case, bone loss and resorption in the frontal skull have been noted, similar to those found in our case [11]. Histopathology generally, however, shows an increase of collagen and a decrease of elastic fibers in the affected tissue, as well as epidermal atrophy [11], which was not seen in our patient. Because our patient had normal histology and no inflammation, linear localized scleroderma was excluded. However, the obliteration of vasculature post-cosmetic surgery is a similar mechanism compared to this found in scleroderma, which typically leads to hypoperfusion of tissue with necrosis. Both scleroderma and Raynaud’s syndrome lead to acroosteolysis, which is related to sclerosis of the subcutaneous tissue and/or lack of arterial perfusion. Though this eventually leads to bony necrosis, this is a different mechanism from osteonecrosis found with avascular necrosis of the epiphyses of long bones or bisphosphonate-related osteonecrosis of the jaw. There was no necrosis at the time of surgery in 2006 and biopsy was obtained in 2009, which showed scant bone and small fragments of dead bone. The pain and indentations came to clinical attention in 2008 and may have been ongoing for some time, suggesting a slow process of bone resorption again similar to scleroderma. However, at no time were focal mass lesions demonstrated that would be expected with foreign-body reaction or granuloma.

The cosmetic procedure was done in the subgaleal plane. The subgaleal vascular plane supplies blood both to the galea aponeurotica and the periosteum [8]. If revascularization to the affected area is not obtained post-operatively, necrosis and bone resorption are likely as demonstrated in the zygomatic fracture reduction study [9]. To the best of our knowledge, this is the first report of calvarial bone resorption, as a result of widely popularized brow lift surgery. We hypothesize that in this case, the vessels in the subgaleal plane were disrupted and the blood supply to the periosteum was affected, not only explaining the scarring and thinning of the periosteum (without direct periosteal violation), but also compromising perfusion of the bone and leading to bone loss due to necrosis secondary to compromised blood flow. This case highlights the potential of bone death after surgery whenever blood supply is disrupted, whether directly or indirectly, which has been previously noted in cases involving other surgical procedures [9, 10].

In conclusion, we present the case of a 59-year-old woman with focal bone loss at the calvarium after forehead cosmetic surgery. This case implies that there may be serious complications associated with craniofacial plastic surgery that may require post-surgical plates or other post-operative reinforcing and potentially non-aesthetic solutions, as substantial bone loss in the frontal skull provides a serious potential danger to the brain, should trauma occur.

Conflict of interest

The authors declare that they have no conflicts of interest in this study.

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